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ATP + 1D-myo-inositol 1,4,5-triphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
r
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
ATP + 1D-myo-inositol 2,4,5-trisphosphate
ADP + 1D-myo-inositol 2,4,5,6-tetrakisphosphate
-
recombinant, catalytically active fragment of isoform C, in the presence of Ins(1,3,4,5)P4, authentic side activity of isoform C
-
?
ATP + D-2-deoxy-myo-inositol 1,4,5-trisphosphate
ADP + D-2-deoxy-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
additional information
?
-
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
specific for phosphorylation of the 3-position
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
target enzyme of cellular regulation, enzyme controls the rate of InsP3 metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
role in limiting the availability of InsP3 for Ca2+ release in smooth muscle relaxation
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
important alternative route for inositol 1,4,5-trisphosphate metabolism in skeletal muscle
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
the enzyme plays a key role in maintaining Ca2+ homeostasis by regulating the concentrations of 1D-myo-inositol 1,4,5-trisphosphate and 1D-myo-inositol 1,3,4,5-tetrakisphosphate, the enzyme has an important regulatory function in the inositol phosphate metabolism which is important for several cellular functions and signaling, overview
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
r
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
r
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulatory mechanism of isoenzyme B involving phosphorylation by both protein kinase C and CaM kinase II
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulation mechanism of isoenzyme A involving CaM kinase II-mediated phosphorylation
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
role of the 3 isoforms as direct InsP3 metabolizing enzymes and direct regulators of Ca2+ responses to extracellular signals
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulation mechanism of isoenzyme A in brain involving CaM kinase II-mediated phosphorylation, role of Ins(1,4,5)P3 3-kinase in brain
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
key enzyme in inositol phosphate signaling pathway
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
the enzyme plays a key role in maintaining Ca2+ homeostasis by regulating the concentrations of 1D-myo-inositol 1,4,5-trisphosphate and 1D-myo-inositol 1,3,4,5-tetrakisphosphate, the enzyme has an important regulatory function in the inositol phosphate metabolism which is important for several cellular functions and signaling, overview
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
substrate and product binding site structure
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
role in rapidly metabolizing the pool of Ins(1,4,5)P3 that is generated when phospholipase C-coupled receptors are activated, the product Ins(1,3,4,5)P4 can protect Ins(1,4,5)P3 against hydrolysis and therefore increase its effectiveness, detailed consequences of Ins(1,3,4,5)P4 generation in the cell, all 3 isoenzymes are regulated by calmodulin, 2 isoenzymes are regulated by a Ca2+/calmodulin-dependent protein kinase II
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
enzyme phosphorylates the 3'-position of the inositol ring to convert the substrate to the product
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
reducing the influx of calcium released from endoplasmic reticulum via IP3 receptor signaling
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
multiple regulation mechanisms of enzyme isoform A and B
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
domain structure of IP3K-C
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulatory mechanism of isoenzyme B involving phosphorylation by both protein kinase C and CaM kinase II
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulation mechanism of isoenzyme A involving CaM kinase II-mediated phosphorylation
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
environment of the active site, proposed binding site model for Ins(1,4,5)P3
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
also phosphorylates the 1,2-cyclic form of myo-inositol 1,4,5-trisphosphate
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
specific for phosphorylation of the 3-position
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
specific for phosphorylation of the 3-position
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
enzyme is specific for phosphorylating the position 3 of the myo-inositol ring and requires vicinal phosphates in the 4 and 5 positions
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
isoform A: N-terminal 66-amino acid F-actin-binding region
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
differential expression and regulation of the two enzyme isoforms A and B provides multiple mechanisms for regulating the cytosolic level of inositol 1,4,5-trisphosphate in cells, regulation mechanisms
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate have separate second messenger roles, perhaps both relating to Ca2+-signaling events
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
phosphorylation of IP3 in dentritic spines to produce IP4 is important for modulating the compartmentalization of calcium at synapses, control of calcium signals, the rapid, localized synthesis of IP4 may have complex effects on cytosolic calcium and on the molecular mechanisms that control learning and memory
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
IP3K regulates the intracellular level of the 2 second messengers Ins(1,4,5)P3 and Ins(1,3,4,5)P4
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulation mechanism of isoenzyme A in brain involving CaM kinase II-mediated phosphorylation, role of Ins(1,4,5)P3 3-kinase in brain
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
IP3K isoform C: nucleocytoplasmic shuttling, particular role in nuclear inositol trisphosphate phosphorylation and cellular growth, enzyme seems to function during the intervalls between signaling events, keeps the resting Ins(1,4,5)P3 very low and provides a basal Ins(1,3,4,5)P4 production in the absence of stimulatory signals from the exterior
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
enzyme occupies a central position in inositol phosphate metabolism by terminating the Ca2+ mobilizing of InsP3 and by generating InsP4
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol tris/tetrakisphosphate pathway
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
isoform B may play a significant role in the regulation of Ins(1,4,5)P3 levels, and consequently in Ca2+ responses following stimulation of cells with Ins(1,4,5)P3-elevating agonists
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate mobilizes Ca2+ from the intracellular stores of permeabilized cells, enzyme is Ca2+-regulated
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
important regulatory role in inositol phosphate signaling by promoting the formation of additional inositol polyphosphate isomers
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involved in inositol polyphosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involved in inositol polyphosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involved in inositol polyphosphate metabolism
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
the enzyme plays a key role in maintaining Ca2+ homeostasis by regulating the concentrations of 1D-myo-inositol 1,4,5-trisphosphate and 1D-myo-inositol 1,3,4,5-tetrakisphosphate, the enzyme has an important regulatory function in the inositol phosphate metabolism which is important for several cellular functions and signaling, overview
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate 3-kinase reaction of the inositol polyphosphate multikinase, EC 2.7.1.151
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
InsP3K activity is a determinant of the extent of basal Ras activation in mast cells and of the Ras activation that follows antigenic crosslinking of the FcepsilonRI
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
reducing the influx of calcium released from endoplasmic reticulum via IP3 receptor signaling
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate 3-kinase reaction of the inositol polyphosphate multikinase, EC 2.7.1.151
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate 3-kinase reaction of the inositol polyphosphate multikinase, EC 2.7.1.151
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
the enzyme plays a key role in maintaining Ca2+ homeostasis by regulating the concentrations of 1D-myo-inositol 1,4,5-trisphosphate and 1D-myo-inositol 1,3,4,5-tetrakisphosphate, the enzyme has an important regulatory function in the inositol phosphate metabolism which is important for several cellular functions and signaling, overview
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involvement of a calmodulin-dependent protein kinase II-mediated phosphorylation in enzyme regulation, enzyme decreases the Ins(1,4,5)P3 concentration, this second messenger binds to the InsP3 receptor to release Ca2+ from intracellular stores, the activation of enzyme may be involved in the Ca2+-dependent down regulation of the InsP3-mediated Ca2+ release, enzyme may play a key role in regulating signals arising from the phospholipase C-related transduction system
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involved in inositol polyphosphate metabolism
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
additional information
?
-
-
the enzyme might be involved in oxidative damage resistance
-
-
?
additional information
?
-
-
the 3 isoenzymes A, B and C can be distinguished by their N-terminal sequence, sensitivity to Ca2+/calmodulin and localization on transfection in COS-7 cells
-
-
?
additional information
?
-
-
the enzyme might be involved in brain development, memory, and learning
-
-
?
additional information
?
-
-
the enzyme binds to F-actin in the cellular actin cytoskeleton with its F-actin domain at the N-terminus, the C-terminal fragment cannot bind to F-actin
-
-
?
additional information
?
-
ITPKA is a bifunctional protein; it phosphorylates Ins(1,4,5)P3 by its kinase activity and cross-links F-actin by its F-actin bundling activity
-
-
-
additional information
?
-
-
ITPKA is a bifunctional protein; it phosphorylates Ins(1,4,5)P3 by its kinase activity and cross-links F-actin by its F-actin bundling activity
-
-
-
additional information
?
-
-
isozyme B controls positive selection of T cells and modulates Erk activity, the enzyme is important in Ras signaling which is important for Erk activation, overview
-
-
?
additional information
?
-
-
isozyme B controls positive selection of T cells and modulates Erk activity, the enzyme is important in Ras signaling which is important for Erk activation, overview
-
-
?
additional information
?
-
-
not: GTP, 5'-guanylylimidodiphosphate
-
-
?
additional information
?
-
-
the enzyme might be involved in brain development, memory, and learning
-
-
?
additional information
?
-
the enzyme binds to F-actin in the cellular actin cytoskeleton with its F-actin domain at the N-terminus, the C-terminal fragment cannot bind to F-actin
-
-
?
additional information
?
-
-
the enzyme contains a catalytic domain and a 4-helix substrate binding domain, both are in an open conformation with respect to each other, thus substrate recognition and catalysis involve a dynamic conformational cycle
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ATP + 1D-myo-inositol 1,4,5-triphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
r
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
additional information
?
-
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
target enzyme of cellular regulation, enzyme controls the rate of InsP3 metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
role in limiting the availability of InsP3 for Ca2+ release in smooth muscle relaxation
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
important alternative route for inositol 1,4,5-trisphosphate metabolism in skeletal muscle
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
the enzyme plays a key role in maintaining Ca2+ homeostasis by regulating the concentrations of 1D-myo-inositol 1,4,5-trisphosphate and 1D-myo-inositol 1,3,4,5-tetrakisphosphate, the enzyme has an important regulatory function in the inositol phosphate metabolism which is important for several cellular functions and signaling, overview
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
r
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
r
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulatory mechanism of isoenzyme B involving phosphorylation by both protein kinase C and CaM kinase II
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
role of the 3 isoforms as direct InsP3 metabolizing enzymes and direct regulators of Ca2+ responses to extracellular signals
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulation mechanism of isoenzyme A in brain involving CaM kinase II-mediated phosphorylation, role of Ins(1,4,5)P3 3-kinase in brain
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
key enzyme in inositol phosphate signaling pathway
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
the enzyme plays a key role in maintaining Ca2+ homeostasis by regulating the concentrations of 1D-myo-inositol 1,4,5-trisphosphate and 1D-myo-inositol 1,3,4,5-tetrakisphosphate, the enzyme has an important regulatory function in the inositol phosphate metabolism which is important for several cellular functions and signaling, overview
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
role in rapidly metabolizing the pool of Ins(1,4,5)P3 that is generated when phospholipase C-coupled receptors are activated, the product Ins(1,3,4,5)P4 can protect Ins(1,4,5)P3 against hydrolysis and therefore increase its effectiveness, detailed consequences of Ins(1,3,4,5)P4 generation in the cell, all 3 isoenzymes are regulated by calmodulin, 2 isoenzymes are regulated by a Ca2+/calmodulin-dependent protein kinase II
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
enzyme phosphorylates the 3'-position of the inositol ring to convert the substrate to the product
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
reducing the influx of calcium released from endoplasmic reticulum via IP3 receptor signaling
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulatory mechanism of isoenzyme B involving phosphorylation by both protein kinase C and CaM kinase II
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
differential expression and regulation of the two enzyme isoforms A and B provides multiple mechanisms for regulating the cytosolic level of inositol 1,4,5-trisphosphate in cells, regulation mechanisms
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate have separate second messenger roles, perhaps both relating to Ca2+-signaling events
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
phosphorylation of IP3 in dentritic spines to produce IP4 is important for modulating the compartmentalization of calcium at synapses, control of calcium signals, the rapid, localized synthesis of IP4 may have complex effects on cytosolic calcium and on the molecular mechanisms that control learning and memory
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
IP3K regulates the intracellular level of the 2 second messengers Ins(1,4,5)P3 and Ins(1,3,4,5)P4
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
regulation mechanism of isoenzyme A in brain involving CaM kinase II-mediated phosphorylation, role of Ins(1,4,5)P3 3-kinase in brain
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
IP3K isoform C: nucleocytoplasmic shuttling, particular role in nuclear inositol trisphosphate phosphorylation and cellular growth, enzyme seems to function during the intervalls between signaling events, keeps the resting Ins(1,4,5)P3 very low and provides a basal Ins(1,3,4,5)P4 production in the absence of stimulatory signals from the exterior
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
enzyme occupies a central position in inositol phosphate metabolism by terminating the Ca2+ mobilizing of InsP3 and by generating InsP4
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol tris/tetrakisphosphate pathway
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
isoform B may play a significant role in the regulation of Ins(1,4,5)P3 levels, and consequently in Ca2+ responses following stimulation of cells with Ins(1,4,5)P3-elevating agonists
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate mobilizes Ca2+ from the intracellular stores of permeabilized cells, enzyme is Ca2+-regulated
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
important regulatory role in inositol phosphate signaling by promoting the formation of additional inositol polyphosphate isomers
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol phosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involved in inositol polyphosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involved in inositol polyphosphate metabolism
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involved in inositol polyphosphate metabolism
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
the enzyme plays a key role in maintaining Ca2+ homeostasis by regulating the concentrations of 1D-myo-inositol 1,4,5-trisphosphate and 1D-myo-inositol 1,3,4,5-tetrakisphosphate, the enzyme has an important regulatory function in the inositol phosphate metabolism which is important for several cellular functions and signaling, overview
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
InsP3K activity is a determinant of the extent of basal Ras activation in mast cells and of the Ras activation that follows antigenic crosslinking of the FcepsilonRI
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
reducing the influx of calcium released from endoplasmic reticulum via IP3 receptor signaling
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
inositol 1,4,5-trisphosphate is a second messenger
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
the enzyme plays a key role in maintaining Ca2+ homeostasis by regulating the concentrations of 1D-myo-inositol 1,4,5-trisphosphate and 1D-myo-inositol 1,3,4,5-tetrakisphosphate, the enzyme has an important regulatory function in the inositol phosphate metabolism which is important for several cellular functions and signaling, overview
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involvement of a calmodulin-dependent protein kinase II-mediated phosphorylation in enzyme regulation, enzyme decreases the Ins(1,4,5)P3 concentration, this second messenger binds to the InsP3 receptor to release Ca2+ from intracellular stores, the activation of enzyme may be involved in the Ca2+-dependent down regulation of the InsP3-mediated Ca2+ release, enzyme may play a key role in regulating signals arising from the phospholipase C-related transduction system
-
-
?
ATP + 1D-myo-inositol 1,4,5-trisphosphate
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
involved in inositol polyphosphate metabolism
-
-
?
additional information
?
-
-
the enzyme might be involved in oxidative damage resistance
-
-
?
additional information
?
-
-
the enzyme might be involved in brain development, memory, and learning
-
-
?
additional information
?
-
ITPKA is a bifunctional protein; it phosphorylates Ins(1,4,5)P3 by its kinase activity and cross-links F-actin by its F-actin bundling activity
-
-
-
additional information
?
-
-
ITPKA is a bifunctional protein; it phosphorylates Ins(1,4,5)P3 by its kinase activity and cross-links F-actin by its F-actin bundling activity
-
-
-
additional information
?
-
-
isozyme B controls positive selection of T cells and modulates Erk activity, the enzyme is important in Ras signaling which is important for Erk activation, overview
-
-
?
additional information
?
-
-
isozyme B controls positive selection of T cells and modulates Erk activity, the enzyme is important in Ras signaling which is important for Erk activation, overview
-
-
?
additional information
?
-
-
the enzyme might be involved in brain development, memory, and learning
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
(2'S)-1D-1,2-O-[(2'-phosphoryloxy)propane-1',3'-diyl]-myo-inositol 4,5-bisphosphate
-
synthetic bicyclic inositol trisphosphate S epimer, IC50 is 0.156 mM
1D-myo-inositol 1,3,4,5-tetrakisphosphate
1D-myo-inositol 1,4,5-trisphosphate
2,3-diphosphoglycerate
-
-
2-[3,5-dimethyl-1-(4-nitrophenyl)-1H-pyrazol-4-yl]-5,8-dinitro-1H-benzo[de]isoquinoline-1,3(2H)-dione
BIP-4, BIP-4 is competitive to Ins(1,4,5)P3 and shows high selectivity for the Ins(1,4,5)P3 binding pocket, BIP-4 does not block the actin bundling activity of ITPKA
-
3',4',7,8-tetrahydroxyflavone
7-methylsulfanyl-3-phenyl-[1,3,4]thiadiazolo[2,3-c][1,2,4]triazin-4-one
55% inhibition at 0.04 mM
D-2-deoxyinositol 1,3,4,5-tetrakisphosphate
-
strong inhibition of isozyme A, IC50 is 0.0054 mM
D-2-deoxyinositol 1,4,5-trisphosphate
-
strong inhibition of isozyme A, IC50 is 0.0017 mM
D-3-deoxyinositol 1,4,6-trisphosphate
-
strong inhibition of isozyme A, IC50 is 0.0014 mM
D-6-deoxyinositol 1,3,4,5-tetrakisphosphate
-
strong inhibition of isozyme A, IC50 is 0.0051 mM
D-myo-inositol 1,4,5-trisphosphate
-
strong inhibition, purified recombinant enzyme, IC50 value is 0.003 mM in absence of Ca2+
D-myo-inositol 2,4,5-trisphosphate
-
IC50 is 0.117 mM
D-scyllo-inositol 1,2,3,4-tetrakisphosphate
-
purified recombinant enzyme, IC50 value is above 0.1 mM in absence of Ca2+
D-scyllo-inositol 1,2,4-trisphosphate
-
purified recombinant enzyme, IC50 value is 0.044 mM in absence of Ca2+
epigallocatechin-3-gallate
heparin
-
mixed-type inhibition
inositol phosphate
-
inhibitory effects of all possible 38 regioisomers of synthetic inositol phosphates, only inositol trisphosphates and tetrakisphosphates inhibit, not or very weak: inositol monophosphates, bisphosphates and pentakisphosphates, the recognition of myo-inositol phosphate regioisomers is highly structure-selective
L-scyllo-inositol 1,2,3,4-tetrakisphosphate
-
purified recombinant enzyme, IC50 value is above 0.1 mM in absence of Ca2+
L-scyllo-inositol 1,2,4-trisphosphate
-
purified recombinant enzyme, IC50 value is 0.006 mM in absence of Ca2+
N-(1,2-benzoxazol-3-yl)-4-methylbenzamide
68% inhibition at 0.04 mM, mixed type inhibitor, that is nearly completely taken up by H1299 cells and remains stable after cellular uptake, the compound exhibits a robust stability and a high membrane permeability. The inhibitor provides the possibility to partly inhibit the metastasis-promoting effect of ITPKA in lung tumor cells. Inhibition mechanism of BAMB-4, overview
N-(4-ethoxyphenyl)pyrazolo[1,5-a]pyridine-3-carboxamide
87% inhibition at 0.04 mM
N-(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide
protein kinase A
-
isoforms A and B are differentially regulated via phosphorylation by the cAMP-dependent protein kinase, isoform A: stimulation in the presence or absence of Ca2+/calmodulin, isoform B: no effect on activity in the absence of Ca2+/calmodulin, 45% inhibition in the presence of Ca2+/calmodulin
-
RS-20
-
calmodulin antagonist, prevents the Ca2+/calmodulin-mediated activation
-
scyllo-inositol 1,2,3,5-tetrakisphosphate
-
weak inhibition, purified recombinant enzyme, IC50 value is 0.028 mM in absence of Ca2+
scyllo-inositol 1,2,3-trisphosphate
-
purified recombinant enzyme, IC50 value is 0.027 mM in absence of Ca2+
scyllo-inositol 1,2,4,5-tetrakisphosphate
-
weak inhibition, purified recombinant enzyme, IC50 value is 0.039 mM in absence of Ca2+
scyllo-inositol 1,3,5-trisphosphate
-
purified recombinant enzyme, IC50 value is 0.090 mM in absence of Ca2+
TSH
-
thyroid-stimulating hormone, inhibits at a physiological concentration, inhibition is mimicked by dibuturyl cyclic AMP and forskolin, mechanism
1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
marked product inhibition, isoforms A and B
1D-myo-inositol 1,3,4,5-tetrakisphosphate
-
product inhibition, IC50 is 0.013 mM
1D-myo-inositol 1,4,5-trisphosphate
-
substrate inhibition of the catalytic domain
1D-myo-inositol 1,4,5-trisphosphate
-
recombinant, catalytically active fragment of isoform C, substrate inhibition by high concentrations
3',4',7,8-tetrahydroxyflavone
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
3',4',7,8-tetrahydroxyflavone
-
the point mutant K336Q reveals a drastically reduced inhibition by THF. Substitution of Lys336 leads to a 260fold increase in the IC50. On the other hand, kinetic parameters of the enzyme with respect to both substrates are nearly unchanged. This region shows high homology between IP3K isoforms.
3',4',7,8-tetrahydroxyflavone
-
inhibition of isozyme A, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
3',4',7,8-tetrahydroxyflavone
-
3',4',7,8-tetrahydroxyflavone
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
3',4',7,8-tetrahydroxyflavone
-
aurintricarboxylic acid
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
aurintricarboxylic acid
-
-
aurintricarboxylic acid
-
inhibition of isozyme A and isozyme B, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
aurintricarboxylic acid
-
aurintricarboxylic acid
-
strong inhibition, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
aurintricarboxylic acid
-
Ca2+
-
-
Ca2+
-
at concentrations higher than 0.01-0.1 mM
Ca2+
-
at higher concentrations
Ca2+
-
isoforms A and B, above 0.01 mM
chlorogenic acid
-
-
chlorpromazine
-
calmodulin-antagonist, inhibits Ca2+-activated enzyme activity
chlorpromazine
-
calmodulin-antagonist, inhibits Ca2+-activated enzyme activity
EGTA
-
Ca2+/calmodulin-activated enzyme
EGTA
-
Ca2+/calmodulin-activated enzyme
EGTA
-
Ca2+/calmodulin-activated enzyme
EGTA
-
Ca2+/calmodulin-activated enzyme
ellagic acid
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
ellagic acid
-
inhibition of isozyme B, slight inhibition of isozyme A, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
epicatechin-3-gallate
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
epicatechin-3-gallate
-
-
epicatechin-3-gallate
-
slight inhibition of isozyme A and isozyme B, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
epicatechin-3-gallate
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-triphosphate
epigallocatechin-3-gallate
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
epigallocatechin-3-gallate
-
-
epigallocatechin-3-gallate
-
inhibition of isozyme A, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
epigallocatechin-3-gallate
-
epigallocatechin-3-gallate
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-triphosphate
epigallocatechin-3-gallate
-
gossypol
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
gossypol
-
inhibition of isozyme A and isozyme B, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
gossypol
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
hypericin
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
hypericin
-
inhibition of isozyme A and isozyme B, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
hypericin
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-triphosphate
KN-62
-
calmodulin-dependent protein kinase II inhibitor; prevents the carbachol- or UTP-mediated activation
KN-62
-
calmodulin-dependent protein kinase II inhibitor; prevents the carbachol- or UTP-mediated activation
KN-62
-
calmodulin-dependent protein kinase II inhibitor; prevents the Ca2+/calmodulin-mediated activation
KN-93
-
calmodulin-dependent protein kinase II inhibitor; prevents the carbachol- or UTP-mediated activation
KN-93
-
calmodulin-dependent protein kinase II inhibitor; prevents the carbachol- or UTP-mediated activation
KN-93
-
calmodulin-dependent protein kinase II inhibitor; prevents the Ca2+/calmodulin-mediated activation
myricetin
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
myricetin
-
inhibition of isozyme A, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
myricetin
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
N-(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide
-
i.e. W-7, calmodulin-antagonist; inhibits Ca2+-activated enzyme activity
N-(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide
-
i.e. W-7, calmodulin-antagonist
N-(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide
-
i.e. W-7, calmodulin-antagonist; inhibits Ca2+-activated enzyme activity
Protein kinase C
-
phosphorylates and inactivates enzyme
-
Protein kinase C
-
phosphorylates and inactivates enzyme
-
Protein kinase C
-
negative regulatory function, phosphorylates the enzyme at a serine residue
-
Protein kinase C
-
protein kinase C alone, without CaM kinase II, inhibits in the presence of Ca2+ and calmodulin
-
Protein kinase C
-
isoforms A and B are differentially regulated via phosphorylation by protein kinase C, isoform A: phosphorylated to the extent of 2 mol/mol, 72% inhibition in the absence of Ca2+/calmodulin, isoform B: phosphorylated to the extent of 2.7 mol/mol, no effect on activity in the absence of Ca2+/calmodulin, both isoforms are inhibited by 70% in the presence of Ca2+/calmodulin
-
Protein kinase C
-
negative regulatory function, phosphorylates the enzyme at Ser175, simultaneous phosphorylation at Ser109 and Ser175 also inactivates the enzyme
-
Protein kinase C
-
negative regulatory function, phosphorylates the enzyme at a Ser residue
-
quercetin
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
quercetin
-
inhibition of isozyme A, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
quercetin
-
mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
Rose bengal
-
-
Rose bengal
-
slight inhibition of isozyme B, mixed-type versus ATP, noncompetitive versus 1D-myo-inositol 1,4,5-trisphosphate
SDS
-
complete inhibition at 0.1%, 1% Triton X-100 partially reverses
additional information
-
IC50 values, overiew, the inhibition by the synthetic or plant phenols can in some cases be partially or completely reversed by Triton X-100, no inhibition by chlorogenic acid and by Rose Bengal
-
additional information
-
All inhibitors display a mixed-type inhibition with respect to ATP and a noncompetitive inhibition with respect to 1D-myo-inositol 1,4,5-triphosphate. Mutagenesis studies reveal that both the calmodulin binding and the ATP binding domains in IP3K are involved in inhibitor binding. Most discovered potent IP3K inhibitors exert antiproliferative effects on cultured cells in vitro or in animal experiments and tumor treatment studies in vivo.; Reversal of enzyme inhibition by addition of Triton X-100 and Ca2+-calmodulin.
-
additional information
-
IC50 values, overiew, inhibitory potency of the synthetic and plant phenolics, no inhibition by chlorogenic acid
-
additional information
All inhibitors display a mixed-type inhibition with respect to ATP and a noncompetitive inhibition with respect to inositol-1,4,5-trisphosphate. Mutagenesis studies reveal that both the calmodulin binding and the ATP binding domains in IP3K are involved in inhibitor binding. Most discovered potent IP3K inhibitors exert antiproliferative effects on cultured cells in vitro or in animal experiments and tumor treatment studies in vivo.; All inhibitors display a mixed-type inhibition with respect to ATP and a noncompetitive inhibition with respect to Ins(1,4,5)P3. Mutagenesis studies reveal that both the calmodulin binding and the ATP binding domains in IP3K are involved in inhibitor binding. Most discovered potent IP3K inhibitors exert antiproliferative effects on cultured cells in vitro or in animal experiments and tumor treatment studies in vivo.
-
additional information
All inhibitors display a mixed-type inhibition with respect to ATP and a noncompetitive inhibition with respect to inositol-1,4,5-trisphosphate. Mutagenesis studies reveal that both the calmodulin binding and the ATP binding domains in IP3K are involved in inhibitor binding. Most discovered potent IP3K inhibitors exert antiproliferative effects on cultured cells in vitro or in animal experiments and tumor treatment studies in vivo.; All inhibitors display a mixed-type inhibition with respect to ATP and a noncompetitive inhibition with respect to Ins(1,4,5)P3. Mutagenesis studies reveal that both the calmodulin binding and the ATP binding domains in IP3K are involved in inhibitor binding. Most discovered potent IP3K inhibitors exert antiproliferative effects on cultured cells in vitro or in animal experiments and tumor treatment studies in vivo.
-
additional information
in order to inhibit the metastasis-promoting activity of ITPKA, both its actin bundling and its InsP3kinase activity has to be blocked, inhibitor library screening, overview
-
additional information
-
not inhibited by GTP or 5'-guanylylimidodiphosphate
-
additional information
-
enzyme contains several motifs susceptible to a variety of proteases
-
additional information
-
inhibitor binding structures and mechanism, scyllo-inositol pentakisphosphate, scyllo-inositol hexakisphosphate, scyllo-inositol monophosphate, and scyllo-inositol S-bisphosphates are poor inhibitors
-
additional information
-
poor inhibition by adenophostin analogues xylo-furanophostin and furanophostin, by L-myo-inositol 2,4,5-trisphosphate, synthetic bicyclic inositol trisphosphate R epimer, and by epi-1D-myo-inositol 1,3,6-trisphosphate
-
additional information
-
IC50 values, overiew, no inhibition by chlorogenic acid, poor inhibition by rose bengal, and ellagic acid
-
additional information
All inhibitors display a mixed-type inhibition with respect to ATP and a noncompetitive inhibition with respect to 1D-myo-inositol 1,4,5-triphosphate. Mutagenesis studies reveal that both the calmodulin binding and the ATP binding domains in IP3K are involved in inhibitor binding. Most discovered potent IP3K inhibitors exert antiproliferative effects on cultured cells in vitro or in animal experiments and tumor treatment studies in vivo.; The flavonoids myricetin, 3',4',7,8-tetrahydroxyflavone, and epigallocatechin-3-gallate have a markedly stronger effect on isoforms A and C than on isoform B
-
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Adenocarcinoma
Functional role of inositol-1,4,5-trisphosphate-3-kinase-A for motility of malignant transformed cells.
Adenocarcinoma of Lung
Functional role of inositol-1,4,5-trisphosphate-3-kinase-A for motility of malignant transformed cells.
Adenocarcinoma of Lung
Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is frequently over-expressed and functions as an oncogene in several tumor types.
Adenocarcinoma of Lung
TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma.
Alzheimer Disease
Inositol trisphosphate 3-kinase B is increased in human Alzheimer brain and exacerbates mouse Alzheimer pathology.
Alzheimer Disease
Microglia-Derived Extracellular Vesicles Carrying miR-711 Alleviate Neurodegeneration in a Murine Alzheimer's Disease Model by Binding to Itpkb.
Aneurysm
ITPKC functional polymorphism associated with Kawasaki disease susceptibility and formation of coronary artery aneurysms.
Aneurysm
ITPKC single nucleotide polymorphism associated with the Kawasaki disease in a Taiwanese population.
Aneurysm
Management of Kawasaki disease.
Aneurysm
Single-Nucleotide Polymorphism rs7251246 in ITPKC Is Associated with Susceptibility and Coronary Artery Lesions in Kawasaki Disease.
Arthritis
Inhibition of the Inositol Kinase Itpkb Augments Calcium Signaling in Lymphocytes and Reveals a Novel Strategy to Treat Autoimmune Disease.
Arthritis
Inositol 1,4,5-trisphosphate 3-kinase B promotes Ca2+ mobilization and the inflammatory activity of dendritic cells.
Autoimmune Diseases
Inhibition of the Inositol Kinase Itpkb Augments Calcium Signaling in Lymphocytes and Reveals a Novel Strategy to Treat Autoimmune Disease.
Breast Neoplasms
Expression Regulation of the Metastasis-Promoting Protein InsP3-Kinase-A in Tumor Cells.
Breast Neoplasms
Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is frequently over-expressed and functions as an oncogene in several tumor types.
Breast Neoplasms
ITPKC as a Prognostic and Predictive Biomarker of Neoadjuvant Chemotherapy for Triple Negative Breast Cancer.
Breast Neoplasms
Relationship of ITPKA expression with the prognosis of breast cancer.
Carcinogenesis
Down-regulation of 1D-myo-inositol 1,4,5-trisphosphate 3-kinase A protein expression in oral squamous cell carcinoma.
Carcinogenesis
ITPKA Gene Body Methylation Regulates Gene Expression and Serves as an Early Diagnostic Marker in Lung and Other Cancers.
Carcinogenesis
ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203.
Carcinoma
Expression Regulation of the Metastasis-Promoting Protein InsP3-Kinase-A in Tumor Cells.
Carcinoma
Genetic polymorphisms in the ITPKC gene and cervical squamous cell carcinoma risk.
Carcinoma
ITPKA Gene Body Methylation Regulates Gene Expression and Serves as an Early Diagnostic Marker in Lung and Other Cancers.
Carcinoma
The Expression of miR-375 Is Associated with Carcinogenesis in Three Subtypes of Lung Cancer.
Carcinoma
The new InsP3Kinase inhibitor BIP-4 is competitive to InsP3 and blocks proliferation and adhesion of lung cancer cells.
Carcinoma, Hepatocellular
ITPKA expression is a novel prognostic factor in hepatocellular carcinoma.
Carcinoma, Squamous Cell
Genetic polymorphisms in the ITPKC gene and cervical squamous cell carcinoma risk.
Colorectal Neoplasms
Immune-related genes STIM1, ITPKC and PELI1 polymorphisms are associated with risk of colorectal cancer.
Common Variable Immunodeficiency
Common variable immunodeficiency associated with microdeletion of chromosome 1q42.1-q42.3 and inositol 1,4,5-trisphosphate kinase B (ITPKB) deficiency.
Erythema
ITPKC and SLC11A1 Gene Polymorphisms and Gene-Gene Interactions in Korean Patients with Kawasaki Disease.
Glioma
Mining the glioma susceptibility genes in children from gene expression profiles and a methylation database.
Graft vs Host Disease
Inhibition of inositol kinase B controls acute and chronic graft-versus-host disease.
Hirschsprung Disease
Potential association between ITPKC genetic variations and Hirschsprung disease.
Hodgkin Disease
Diagnostic utility of STAT6YE361 expression in classical Hodgkin lymphoma and related entities.
Immune System Diseases
New therapeutic targets in immune disorders: ItpkB, Orai1 and UNC93B.
Influenza, Human
Identification of Host Kinase Genes Required for Influenza Virus Replication and the Regulatory Role of MicroRNAs.
inositol-trisphosphate 3-kinase deficiency
Tonic BCR signaling represses receptor editing via Raf- and calcium-dependent signaling pathways.
Lung Neoplasms
Effect of the actin- and calcium-regulating activities of ITPKB on the metastatic potential of lung cancer cells.
Lung Neoplasms
Functional role of inositol-1,4,5-trisphosphate-3-kinase-A for motility of malignant transformed cells.
Lung Neoplasms
Identification of a new membrane-permeable inhibitor against inositol-1,4,5-trisphosphate-3-kinase A.
Lung Neoplasms
Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is frequently over-expressed and functions as an oncogene in several tumor types.
Lung Neoplasms
ITPKA Gene Body Methylation Regulates Gene Expression and Serves as an Early Diagnostic Marker in Lung and Other Cancers.
Lung Neoplasms
TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma.
Lung Neoplasms
The new InsP3Kinase inhibitor BIP-4 is competitive to InsP3 and blocks proliferation and adhesion of lung cancer cells.
Lymphatic Metastasis
Relationship of ITPKA expression with the prognosis of breast cancer.
Mucocutaneous Lymph Node Syndrome
A functional polymorphism, rs28493229, in ITPKC and risk of Kawasaki disease: an integrated meta-analysis.
Mucocutaneous Lymph Node Syndrome
A replication study for association of ITPKC and CASP3 two-locus analysis in IVIG unresponsiveness and coronary artery lesion in Kawasaki disease.
Mucocutaneous Lymph Node Syndrome
Clinical Implication of the C Allele of the ITPKC Gene SNP rs28493229 in Kawasaki Disease: Association With Disease Susceptibility and BCG Scar Reactivation.
Mucocutaneous Lymph Node Syndrome
ITPKC and CASP3 polymorphisms and risks for IVIG unresponsiveness and coronary artery lesion formation in Kawasaki disease.
Mucocutaneous Lymph Node Syndrome
ITPKC and SLC11A1 Gene Polymorphisms and Gene-Gene Interactions in Korean Patients with Kawasaki Disease.
Mucocutaneous Lymph Node Syndrome
ITPKC as a Prognostic and Predictive Biomarker of Neoadjuvant Chemotherapy for Triple Negative Breast Cancer.
Mucocutaneous Lymph Node Syndrome
ITPKC functional polymorphism associated with Kawasaki disease susceptibility and formation of coronary artery aneurysms.
Mucocutaneous Lymph Node Syndrome
ITPKC gene SNP rs28493229 and Kawasaki disease in Taiwanese children.
Mucocutaneous Lymph Node Syndrome
ITPKC single nucleotide polymorphism associated with the Kawasaki disease in a Taiwanese population.
Mucocutaneous Lymph Node Syndrome
ITPKC susceptibility in Kawasaki syndrome as a sensitizing factor for autoimmunity and coronary arterial wall relaxation induced by thimerosal's effects on calcium signaling via IP3.
Mucocutaneous Lymph Node Syndrome
Kawasaki disease: update on pathogenesis.
Mucocutaneous Lymph Node Syndrome
PPP3CC feedback regulates IP3-Ca2+ pathway through preventing ITPKC degradation.
Mucocutaneous Lymph Node Syndrome
Single-nucleotide Polymorphism rs2290692 in the 3'UTR of ITPKC Associated With Susceptibility to Kawasaki Disease in a Han Chinese Population.
Mucocutaneous Lymph Node Syndrome
Single-Nucleotide Polymorphism rs7251246 in ITPKC Is Associated with Susceptibility and Coronary Artery Lesions in Kawasaki Disease.
Mucocutaneous Lymph Node Syndrome
Superantigen involvement and susceptibility factors in Kawasaki disease: profiles of TCR V?2+ T cells and HLA-DRB1, TNF-? and ITPKC genes among Filipino patients.
Mucocutaneous Lymph Node Syndrome
[Association study of a functional SNP rs28493229 of ITPKC gene and Kawasaki disease in a Chinese population].
Neoplasm Metastasis
Inositol 1,4,5-trisphosphate 3-kinase-A is a new cell motility-promoting protein that increases the metastatic potential of tumor cells by two functional activities.
Neoplasm Metastasis
Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is frequently over-expressed and functions as an oncogene in several tumor types.
Neoplasm Metastasis
Relationship of ITPKA expression with the prognosis of breast cancer.
Neoplasms
DNA methylation profiling in nonfunctioning pituitary adenomas.
Neoplasms
Effect of the actin- and calcium-regulating activities of ITPKB on the metastatic potential of lung cancer cells.
Neoplasms
Expression Regulation of the Metastasis-Promoting Protein InsP3-Kinase-A in Tumor Cells.
Neoplasms
Functional role of inositol-1,4,5-trisphosphate-3-kinase-A for motility of malignant transformed cells.
Neoplasms
Identification of a new membrane-permeable inhibitor against inositol-1,4,5-trisphosphate-3-kinase A.
Neoplasms
Inositol 1,4,5-trisphosphate 3-kinase-A is a new cell motility-promoting protein that increases the metastatic potential of tumor cells by two functional activities.
Neoplasms
Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is frequently over-expressed and functions as an oncogene in several tumor types.
Neoplasms
Inositol-triphosphate 3-kinase B confers cisplatin resistance by regulating NOX4-dependent redox balance.
Neoplasms
ITPKA expression is a novel prognostic factor in hepatocellular carcinoma.
Neoplasms
ITPKA Gene Body Methylation Regulates Gene Expression and Serves as an Early Diagnostic Marker in Lung and Other Cancers.
Neoplasms
ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203.
Neoplasms
ITPKA1 Promotes Growth, Migration and Invasion of Renal Cell Carcinoma via Activation of mTOR Signaling Pathway.
Neoplasms
ITPKC as a Prognostic and Predictive Biomarker of Neoadjuvant Chemotherapy for Triple Negative Breast Cancer.
Neoplasms
Pervasive mutations of JAK-STAT pathway genes in classical Hodgkin lymphoma.
Neoplasms
Physiological relevance of the neuronal isoform of inositol-1,4,5-trisphosphate 3-kinases in mice.
Neoplasms
Relationship of ITPKA expression with the prognosis of breast cancer.
Neoplasms
TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma.
Neoplasms
The catalytic domain of inositol-1,4,5-trisphosphate 3-kinase-a contributes to ITPKA-induced modulation of F-actin.
Neoplasms
The new InsP3Kinase inhibitor BIP-4 is competitive to InsP3 and blocks proliferation and adhesion of lung cancer cells.
Nephrolithiasis
Study of the association between ITPKC genetic polymorphisms and calcium nephrolithiasis.
Neuroblastoma
Inositol trisphosphate 3-kinase B is increased in human Alzheimer brain and exacerbates mouse Alzheimer pathology.
Neuroblastoma
Tissue- and cell-specific expression of Ins(1,4,5)P3 3-kinase isoenzymes.
Osteosarcoma
miR-140-5p attenuates chemotherapeutic drug induced cell death by regulating autophagy through IP3k2 in human osteosarcoma cells.
Ovarian Neoplasms
ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203.
Parkinson Disease
Association of ITPKB, IL1R2 and COQ7 with Parkinson's disease in Taiwan.
Parkinson Disease
Association of ZNF184, IL1R2, LRRK2, ITPKB, and PARK16 with sporadic Parkinson's disease in Eastern China.
Parkinson Disease
ITPKB and ZNF184 are associated with Parkinson's disease risk in East Asians.
Parkinson Disease
The Parkinson's disease-associated gene ITPKB protects against ?-synuclein aggregation by regulating ER-to-mitochondria calcium release.
Severe Combined Immunodeficiency
Severe combined immunodeficiency caused by inositol-trisphosphate 3-kinase B (ITPKB) deficiency.
Small Cell Lung Carcinoma
The Expression of miR-375 Is Associated with Carcinogenesis in Three Subtypes of Lung Cancer.
Triple Negative Breast Neoplasms
ITPKC as a Prognostic and Predictive Biomarker of Neoadjuvant Chemotherapy for Triple Negative Breast Cancer.
Uterine Cervical Neoplasms
Genetic polymorphisms in the ITPKC gene and cervical squamous cell carcinoma risk.
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0.156
(2'S)-1D-1,2-O-[(2'-phosphoryloxy)propane-1',3'-diyl]-myo-inositol 4,5-bisphosphate
Rattus norvegicus
-
synthetic bicyclic inositol trisphosphate S epimer, IC50 is 0.156 mM
0.013
1D-myo-inositol 1,3,4,5-tetrakisphosphate
Rattus norvegicus
-
product inhibition, IC50 is 0.013 mM
0.000157
2-[3,5-dimethyl-1-(4-nitrophenyl)-1H-pyrazol-4-yl]-5,8-dinitro-1H-benzo[de]isoquinoline-1,3(2H)-dione
Homo sapiens
pH and temperature not specified in the publication
-
0.00018 - 0.0843
3',4',7,8-tetrahydroxyflavone
0.036
7-methylsulfanyl-3-phenyl-[1,3,4]thiadiazolo[2,3-c][1,2,4]triazin-4-one
Homo sapiens
pH 7.5, 30°C, recombinant enzyme
0.000062 - 0.00015
aurintricarboxylic acid
0.0054
D-2-deoxyinositol 1,3,4,5-tetrakisphosphate
Rattus norvegicus
-
strong inhibition of isozyme A, IC50 is 0.0054 mM
0.0017
D-2-deoxyinositol 1,4,5-trisphosphate
Rattus norvegicus
-
strong inhibition of isozyme A, IC50 is 0.0017 mM
0.0014
D-3-deoxyinositol 1,4,6-trisphosphate
Rattus norvegicus
-
strong inhibition of isozyme A, IC50 is 0.0014 mM
0.0051
D-6-deoxyinositol 1,3,4,5-tetrakisphosphate
Rattus norvegicus
-
strong inhibition of isozyme A, IC50 is 0.0051 mM
0.003
D-myo-inositol 1,4,5-trisphosphate
Rattus norvegicus
-
strong inhibition, purified recombinant enzyme, IC50 value is 0.003 mM in absence of Ca2+
0.117
D-myo-inositol 2,4,5-trisphosphate
Rattus norvegicus
-
IC50 is 0.117 mM
0.1
D-scyllo-inositol 1,2,3,4-tetrakisphosphate
Rattus norvegicus
-
purified recombinant enzyme, IC50 value is above 0.1 mM in absence of Ca2+
0.044
D-scyllo-inositol 1,2,4-trisphosphate
Rattus norvegicus
-
purified recombinant enzyme, IC50 value is 0.044 mM in absence of Ca2+
0.000036 - 0.00069
ellagic acid
0.000094 - 0.00056
epicatechin-3-gallate
0.00012 - 0.00278
epigallocatechin-3-gallate
0.000058 - 0.00034
gossypol
0.00017 - 0.00021
hypericin
0.1
L-scyllo-inositol 1,2,3,4-tetrakisphosphate
Rattus norvegicus
-
purified recombinant enzyme, IC50 value is above 0.1 mM in absence of Ca2+
0.006
L-scyllo-inositol 1,2,4-trisphosphate
Rattus norvegicus
-
purified recombinant enzyme, IC50 value is 0.006 mM in absence of Ca2+
0.00015 - 0.0042
myricetin
0.037
N-(1,2-benzoxazol-3-yl)-4-methylbenzamide
Homo sapiens
pH 7.5, 30°C, recombinant enzyme
0.017
N-(4-ethoxyphenyl)pyrazolo[1,5-a]pyridine-3-carboxamide
Homo sapiens
pH 7.5, 30°C, recombinant enzyme
0.00018 - 0.00125
quercetin
0.00017 - 0.00312
Rose bengal
0.028
scyllo-inositol 1,2,3,5-tetrakisphosphate
Rattus norvegicus
-
weak inhibition, purified recombinant enzyme, IC50 value is 0.028 mM in absence of Ca2+
0.027
scyllo-inositol 1,2,3-trisphosphate
Rattus norvegicus
-
purified recombinant enzyme, IC50 value is 0.027 mM in absence of Ca2+
0.039
scyllo-inositol 1,2,4,5-tetrakisphosphate
Rattus norvegicus
-
weak inhibition, purified recombinant enzyme, IC50 value is 0.039 mM in absence of Ca2+
0.09
scyllo-inositol 1,3,5-trisphosphate
Rattus norvegicus
-
purified recombinant enzyme, IC50 value is 0.090 mM in absence of Ca2+
additional information
chlorogenic acid
0.00018
3',4',7,8-tetrahydroxyflavone
Homo sapiens
-
0.00019
3',4',7,8-tetrahydroxyflavone
Rattus norvegicus
IP3K-C, maximal inhibition 75%
0.00019
3',4',7,8-tetrahydroxyflavone
Rattus norvegicus
recombinant enzyme IP3K-C fragment comprising calmodulin binding and catalytic domain
0.00029
3',4',7,8-tetrahydroxyflavone
Gallus gallus
-
IP3K-A, maximal inhibition 97%
0.00029
3',4',7,8-tetrahydroxyflavone
Gallus gallus
-
recombinant enzyme fragment comprising calmodulin binding domain
0.00061
3',4',7,8-tetrahydroxyflavone
Rattus norvegicus
recombinant enzyme IP3K-C fragment comprising catalytic domain
0.0034
3',4',7,8-tetrahydroxyflavone
Homo sapiens
-
0.0843
3',4',7,8-tetrahydroxyflavone
Gallus gallus
-
IP3K-A, K336Q mutant
0.000062
aurintricarboxylic acid
Rattus norvegicus
IP3K-C, maximal inhibition 100%
0.00011
aurintricarboxylic acid
Homo sapiens
-
0.000138
aurintricarboxylic acid
Homo sapiens
-
0.00015
aurintricarboxylic acid
Gallus gallus
-
IP3K-A, maximal inhibition 100%
0.000036
ellagic acid
Gallus gallus
-
IP3K-A, maximal inhibition 75%
0.00022
ellagic acid
Homo sapiens
-
0.00055
ellagic acid
Homo sapiens
-
0.00069
ellagic acid
Rattus norvegicus
IP3K-C, maximal inhibition 85%
0.000094
epicatechin-3-gallate
Gallus gallus
-
IP3K-A, maximal inhibition 100%
0.000385
epicatechin-3-gallate
Rattus norvegicus
IP3K-C, maximal inhibition 100%
0.0004
epicatechin-3-gallate
Homo sapiens
-
0.00056
epicatechin-3-gallate
Homo sapiens
-
0.00012
epigallocatechin-3-gallate
Gallus gallus
-
IP3K-A, maximal inhibition 100%
0.00015
epigallocatechin-3-gallate
Homo sapiens
-
0.00021
epigallocatechin-3-gallate
Rattus norvegicus
IP3K-C, maximal inhibition 100%
0.00278
epigallocatechin-3-gallate
Homo sapiens
-
0.000058
gossypol
Gallus gallus
-
IP3K-A, maximal inhibition 100%
0.000115
gossypol
Homo sapiens
-
0.000175
gossypol
Rattus norvegicus
IP3K-C, maximal inhibition 100%
0.00034
gossypol
Homo sapiens
-
0.00017
hypericin
Gallus gallus
-
IP3K-A, maximal inhibition 100%
0.00017
hypericin
Rattus norvegicus
IP3K-C, maximal inhibition 100%
0.00018
hypericin
Homo sapiens
-
0.00021
hypericin
Homo sapiens
-
0.00015
myricetin
Homo sapiens
-
0.00029
myricetin
Rattus norvegicus
IP3K-C, maximal inhibition 62%
0.00054
myricetin
Gallus gallus
-
IP3K-A, maximal inhibition 85%
0.0042
myricetin
Homo sapiens
-
0.00018
quercetin
Gallus gallus
-
IP3K-A, maximal inhibition 80%
0.0003
quercetin
Homo sapiens
-
0.00039
quercetin
Rattus norvegicus
IP3K-C, maximal inhibition 71%
0.00125
quercetin
Homo sapiens
-
0.00017
Rose bengal
Rattus norvegicus
IP3K-C, maximal inhibition 100%
0.00052
Rose bengal
Homo sapiens
-
0.00219
Rose bengal
Homo sapiens
-
0.00312
Rose bengal
Gallus gallus
-
IP3K-A, maximal inhibition 100%
additional information
chlorogenic acid
Homo sapiens
IC > 0.1
additional information
chlorogenic acid
Homo sapiens
IC > 0.1
additional information
chlorogenic acid
Gallus gallus
-
IP3K-A, IC > 0.1
additional information
chlorogenic acid
Rattus norvegicus
IP3K-C, IC > 0.1
additional information
F-actin
Homo sapiens
the full length form of inositol 1,4,5-trisphosphate-3-kinase-A bundles F-actin in a concentration dependent manner, inhibition of the initial rate of gelsolin induces F-actin severing and the degree of bundling are half maximal at an similar concentration of about 300 nM, whereas inhibition of the rate of actin depolymerization after dilution to 100 nM actin is half maximal at about 30 nM, the much lower EC 50 for the latter effect may reflect the high affinity of enzyme for binding to F actin
-
additional information
F-actin
Homo sapiens
-
the full length form of inositol 1,4,5-trisphosphate-3-kinase-A bundles F-actin in a concentration dependent manner, inhibition of the initial rate of gelsolin induces F-actin severing and the degree of bundling are half maximal at an similar concentration of about 300 nM, whereas inhibition of the rate of actin depolymerization after dilution to 100 nM actin is half maximal at about 30 nM, the much lower EC 50 for the latter effect may reflect the high affinity of enzyme for binding to F actin
-
additional information
additional information
Rattus norvegicus
RnIP3K-C including the calmodulin binding and the catalytic domain shows a 3-fold lower IC50 value for 3',4',7,8-tetrahydroxyflavone than RnIP3K including only the calmodulin binding domain. The maximum degree of inhibition is unchanged. Together with the finding that Ca2+-calmodulin partly reverses IP3K inhibition indicates a facilitating but not essential involvement of the calmodulin binding domain in inhibitor binding.
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smooth muscle
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brenda
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brenda
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brenda
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-
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brenda
Itpkb protein level is increased upon differentiation of human embryonic stem cells
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brain
brenda
low expression level
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thyroid cells
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human glioma cell line HTB-138, InsP3 3-kinase B mRNA
brenda
-
brenda
-
brenda
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inositol trisphosphate 3-kinase B gene is expressed in all hematopoietic stem/progenitor cell populations
brenda
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brenda
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non-differentiated promyelocytic-leukaemia cell line, InsP3 3-kinase B mRNA
brenda
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brenda
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brenda
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brenda
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brenda
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human cell line SH-SY5Y, InsP3 3-kinase B mRNA
brenda
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brenda
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brenda
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brenda
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brenda
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brenda
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brenda
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brenda
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brenda
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brenda
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brenda
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brenda
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mast cell
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insulin-secreting
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brenda
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brenda
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brenda
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-
brenda
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brenda
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brenda
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aortic
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MTEC
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IP3K-A expression is highly enriched in the central nucleus of the amygdala (CeA), which plays a pivotal role in the processing and expression of emotional phenotypes in mammals. P3K-A is primarily expressed in neurons rather than glia in the amygdala. In the CeA, IP3K-A primarily colocalizes with GAD67-positive GABAergic interneurons, whereas most IP3K-A in the BLA is in CAMKIIalpha-positive excitatory pyramidal neurons
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IP3K-A expression is highly enriched in the central nucleus of the amygdala (CeA), which plays a pivotal role in the processing and expression of emotional phenotypes in mammals. P3K-A is primarily expressed in neurons rather than glia in the amygdala. In the CeA, IP3K-A primarily colocalizes with GAD67-positive GABAergic interneurons, whereas most IP3K-A in the BLA is in CAMKIIalpha-positive excitatory pyramidal neurons
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brenda
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cerebral cortex astrocytes, isoform B
brenda
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highest expression of recombinant isoenzyme A in astrocytes of hippocampal cultures transfected with isoenzyme A
brenda
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brenda
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1321N1 cells, isoform B
brenda
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-
brenda
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brenda
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brenda
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-
brenda
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distribution in different anatomic regions of brain
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brenda
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isoenzyme A is the major isoform present in neuronal cells
brenda
IP3K-A
brenda
Itpka is particularly active in neurons of the hippocampus and cerebellum
brenda
Itpkb protein level is increased in the cerebral cortex of most patients with Alzheimer's disease compared with control subjects
brenda
high expression level in pyramidal neurons of the CA1 region and the dentate gyrus of the hippocampus
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-
brenda
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brenda
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brenda
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brenda
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-
brenda
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higher expression of isozyme IP3-3KB
brenda
Itpka is particularly active in neurons of the hippocampus and cerebellum
brenda
ITPKA is mainly expressed in pyramidal cells of the hippocampal CA1 region and granule cells of the dentate gyrus
brenda
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brenda
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-
brenda
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brenda
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brenda
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cortex
brenda
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isoform A
brenda
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cortical astrocytes, isoform B
brenda
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InsP3 3-kinase A and B mRNA
brenda
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isoenzyme A is the major isoform present in neuronal cells
brenda
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isoform C
brenda
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isozymes IP33K-A, IP33K-B, and IP33K-C
brenda
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primary hippocampal and corical cultures
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Itpka is particularly active in neurons of the hippocampus and cerebellum
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brenda
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brenda
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brenda
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brenda
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brenda
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brenda
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Enzymes expressed in Escherichia coli
brenda
cloning and expression in Escherichia coli
brenda
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-
brenda
Enzymes and their fragments expressed in Escherichia coli.
brenda
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brenda
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brenda
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brenda
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-
brenda
tracheal and bronchial, multiciliated tracheal epithelial cells
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isozyme IP33K-C
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-
brenda
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-
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brenda
enzyme expression is highly enriched in the central nucleus of the amygdala
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brenda
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enzyme expression is highly enriched in the central nucleus of the amygdala
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brenda
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isoform C
brenda
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InsP3 3-kinase B mRNA
brenda
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isozymes IP33K-B, and IP33K-C
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primary
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vasopressin-stimulated cells
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brenda
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brenda
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-
brenda
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-
-
brenda
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brenda
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endogenous isoenzyme A is localized to the dentritic spines of pyramidal neurons in primary hippocampal cultures from neonatal rats, highest expression of recombinant isoenzyme A in astrocytes
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dendritic spines
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isoform C, low expression
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high expression level
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isoform C, low expression
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brenda
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higher expression of isozyme IP3-3KB
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isoform C, low expression
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predominant expression of InsP3 3-kinase B mRNA in lung
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isozyme IP33K-B
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high expression
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hippocampal neuron
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localized to the post-dendritic spines of neurons. Itpka is particularly active in neurons of the hippocampus and cerebellum
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neuron-specific isozyme
brenda
pyramidal, in neurons, ITPKA is concentrated at postsynaptic densities (PSD) of hippocampal dendritic spines
brenda
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brenda
isozyme inositol-1,4,5-trisphosphate-3-kinase-A is a neuron-specific, actin bundling protein concentrated at dendritic spines
brenda
isozyme IP3K-A is enriched in dendritic spines of mature neurons
brenda
localized to the post-dendritic spines of neurons. Itpka is particularly active in neurons of the hippocampus and cerebellum
brenda
in mature neurons, ITPKA accumulates at postsynaptic densities (PSDs), where the protein is bound to F-actin
brenda
in the CeA, IP3K-A primarily colocalizes with GAD67-positive GABAergic interneurons, whereas most IP3K-A in the BLA is in CAMKIIalpha-positive excitatory pyramidal neurons
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isozyme inositol-1,4,5-trisphosphate-3-kinase-A is a neuron-specific, actin bundling protein concentrated at dendritic spines
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brenda
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in the CeA, IP3K-A primarily colocalizes with GAD67-positive GABAergic interneurons, whereas most IP3K-A in the BLA is in CAMKIIalpha-positive excitatory pyramidal neurons
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isozyme IP3K-A is enriched in dendritic spines of mature neurons
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endogenous isoenzyme A is localized to the dentritic spines of pyramidal neurons in primary hippocampal cultures
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aberrantly sustained neuronal activity down-regulates the expression of IP3K A in vivo and in cultured neurons
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localized to the post-dendritic spines of neurons. Itpka is particularly active in neurons of the hippocampus and cerebellum
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epididymal spermatozoa
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IP3K-A is identified mainly in brain and testis and shows an exclusive F-actin localization
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high expression level
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high expression level
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InsP3 3-kinase A and B mRNA
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isoform C
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isozymes IP33K-A, IP33K-B, and IP33K-C
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higher expression of isozyme IP3-3KB
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isolation of a cDNA clone encoding InsP3 3-kinase B from a thymus cDNA library
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isozyme IP33K-B
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strongest expression of isoform C in tongue epithelium
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isozyme IP33K-C
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low expression level
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additional information
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isoenzymes A and B are specifically expressed in different tissues and cells, expression pattern
brenda
additional information
-
isoenzyme C is not found in brain
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
-
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
-
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
ITPKA is expressed in a broad range of tumor types but shows limited expression in normal cells. ITPKA enzyme expression analysis, overview
brenda
additional information
-
ITPKA is expressed in a broad range of tumor types but shows limited expression in normal cells. ITPKA enzyme expression analysis, overview
brenda
additional information
-
tissue-dependent expression of isozyme IP3-3KB
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
-
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
-
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
enzyme tissue expression analysis by immunohistochemic analysis and situ hybridization. Cells positive for ITPKC express either a multicilium (tracheal and bronchial epithelia, brain ependymal cells), microvilli forming a brush border (small and large intestine, and kidney proximal tubule cells) or a flagellum (spermatozoa)
brenda
additional information
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enzyme tissue expression analysis by immunohistochemic analysis and situ hybridization. Cells positive for ITPKC express either a multicilium (tracheal and bronchial epithelia, brain ependymal cells), microvilli forming a brush border (small and large intestine, and kidney proximal tubule cells) or a flagellum (spermatozoa)
brenda
additional information
ubiquitous tissue expression of isozyme Itpkb, the Itpkb protein contributes mainly to the majority of the Ins(1,4,5)P3 3-kinase activity in resting T and B lymphocytes as well as in neutrophils and mast cells
brenda
additional information
cells positive for ITPKC in the studied tissues express either a multicilium (tracheal and bronchial epithelia, brain ependymal cells), microvilli forming a brush border (small and large intestine, and kidney proximal tubule cells) or a flagellum (spermatozoa), suggesting a role for ITPKC either in the development or the function of these specialized cellular structures. Tissue expression and localization study, overview
brenda
additional information
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cells positive for ITPKC in the studied tissues express either a multicilium (tracheal and bronchial epithelia, brain ependymal cells), microvilli forming a brush border (small and large intestine, and kidney proximal tubule cells) or a flagellum (spermatozoa), suggesting a role for ITPKC either in the development or the function of these specialized cellular structures. Tissue expression and localization study, overview
brenda
additional information
isozyme ITPKA is mainly expressed in neurons of the central nervous system and is also overexpressed in tumor cells
brenda
additional information
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isoenzymes A and B are specifically expressed in different tissues and cells, expression pattern
brenda
additional information
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widespread tissue distribution of isoform B
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
additional information
enzyme activity determined in cell homogenates with Ins(1,4,5)P3 and ATP as substrate is generally very low compared to Ins(1,4,5)P3 5-phosphatase, EC 3.1.3.56, except in a few tissues such as brain, testis, thymus or intestine. Itpkb and Itpkc are widespread expressed in many different tissues and cell lines
brenda
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evolution
a member of the inositol 1,4,5-trisphosphate 3-kinases family
evolution
inositol(1,4,5)trisphosphate 3-kinases (Itpks) occur in three isoenzyme forms, Itpka/b and c, in human, rat and mouse. They share a catalytic domain relatively well conserved at the C-terminal end and a quite isoenzyme specific regulatory domain at the N-terminal end of the protein
evolution
inositol(1,4,5)trisphosphate 3-kinases (Itpks) occur in three isoenzyme forms, Itpka/b and c, in human, rat and mouse. They share a catalytic domain relatively well conserved at the C-terminal end and a quite isoenzyme specific regulatory domain at the N-terminal end of the protein
evolution
inositol(1,4,5)trisphosphate 3-kinases (Itpks) occur in three isoenzyme forms, Itpka/b and c, in human, rat and mouse. They share a catalytic domain relatively well conserved at the C-terminal end and a quite isoenzyme specific regulatory domain at the N-terminal end of the protein
evolution
enzyme IP3 3-kinase 2 (IP3K2) is a member of the inositol polyphosphate kinase gene family
evolution
inositol 1,4,5-trisphosphate 3-kinase C (ITPKC) is the last identified member of the inositol 1,4,5-trisphosphate 3-kinases family which phosphorylates inositol 1,4,5-trisphosphate into inositol 1,3,4,5-tetrakisphosphate
malfunction
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disruption of InsP3KB leads to impaired T cell and B cell development as well as hyperactivation of neutrophils, in InsP3KB null mice, the bone marrow granulocyte monocyte progenitor (GMP) population is expanded, and GMP cells proliferated significantly faster, neutrophil production in the bone marrow is enhanced, and the peripheral blood neutrophil count is also substantially elevated, neutrophil apoptotic death is enhanced in enzyme knock-out mice, disruption of enzyme promotes myeloid differentiation
malfunction
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enzyme knock-out mice show deficits of synaptic plasticity in perforant path and in hippocampal-dependent memory performances
malfunction
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In transgenic mice that also express soluble hen egg lysozyme, lack of inositol 1,4,5-trisphosphate 3-kinase B converts anergy induction to deletion, mice lacking inositol 1,4,5-trisphosphate 3-kinase B have normal B cell development in the bone marrow, but reduced numbers of all splenic B cell subsets and a shift in the developmental fate toward compartments that are normally selected by strong B cell receptor signals, mature B cells lacking the enzyme fail to proliferate in response to B cell receptor stimulation but show normal responses to the TLR4 ligand LPS or agonistic Abs to CD40. At the immature stage, inositol 1,4,5-trisphosphate 3-kinase B-deficient mice possess a 60% increase in the numbers of immature B cells compared with wild type mice. Examination of splenic B cell populations in inositol 1,4,5-trisphosphate 3-kinase B-deficient/IgHEL tg mice reveals that while the total numbers of B220+ cells are relatively normal, the numbers of follicular mature B cells are increased 2.2fold, while the number of T2 and marginal zone cells are reduced 3- and 3.8fold
malfunction
genetic abrogation of IP3K-A alters amygdala gene expression, particularly in genes involved in key intracellular signaling pathways and genes mediating fear- and anxiety-related behaviors. In agreement with the changes in amygdala gene expression profiles, IP3K-A knockout mice display more robust responses to aversive stimuli and spend less time in the open arms of the elevated plus maze, indicating high levels of innate fear and anxiety. IP3K-A KO mice show decreased excitatory and inhibitory postsynaptic current and reduced c-Fos immunoreactivity in the central nucleus of the amygdala. Overexpression of inositol 1,4,5-trisphosphate 3-kinases isozymes consistently suppresses inositol 1,4,5-trisphosphate-evoked increases in intracellular calcium in response to an agonist, whereas deletion or inactivation of different genes elicits diverse phenotypes depending on cell type. Genetic deletion of IP3K-A produces deficits in long-term potentiation in the dentate gyrus and impairs memory performance. Deletion does not affect spatial learning in the Morris water maze. Phenotypes, overview
malfunction
isozyme Itpka-deficient mice exhibit increased LTP in the CA1 region of the hippocampus
malfunction
ITPKA depletion in mice increases the number of hippocampal spine-synapses while reducing average spine length, depletion of ITPKA reduces the length of dendritic spines of hippocampal pyramidal cells
malfunction
mice deficient for Itpkb have a severe defect in thymocytes differentiation and thus lack peripheral T cells
malfunction
mice genetically-deficient for the B isoform of the inositol 1,4,5-trisphosphate 3-kinase have a severe defect in thymocytes differentiation and thus lack peripheral T cells. Mutant T cells show an increased activated/memory phenotype as well as a decreased proliferative capacity and survival, Itpkb-deficient peripheral T cells have also an increased capacity to secrete cytokines upon stimulation
malfunction
neurite length is significantly decreased in cells overexpressing isozymes Itpka and Itpkb but not Itpkc or IPMK. This result does not depend on the overexpression level of any of the kinases. PC-12 cells overexpressing GFP-tagged kinase-dead mutants Itpka/b have shorter neurites than GFP control cells
malfunction
neurite length is significantly decreased in cells overexpressing isozymes Itpka and Itpkb but not Itpkc or IPMK. This result does not depend on the overexpression level of any of the kinases. PC12 cells overexpressing GFP-tagged kinase-dead mutants Itpka/b have shorter neurites than GFP control cells
malfunction
downregulation of ITPKA in lung adenocarcinoma cancers reduced both, tumor growth and metastasis. Re-expression of wild-type ITPKA completely restores reduced transmigration of ITPKA-depleted cells. Combined inhibition of F-actin bundling and InsP3Kinase activity should inhibit metastasis at early (adhesion, invasion) and late steps (colonization at secondary sites) of metastasis. Inhibition of cellular InsP3Kinase by BIP-4 reduces important steps in the metastatic cascade
malfunction
genetic abrogation of IP3K-A alters amygdala gene expression, particularly in genes involved in key intracellular signaling pathways and genes mediating fear- and anxiety-related behaviors. In agreement with the changes in amygdala gene expression profiles, IP3K-A knockout (KO) mice display more robust responses to aversive stimuli and spent less time in the open arms of the elevated plus maze, indicating high levels of innate fear and anxiety. Decreased excitatory and inhibitory postsynaptic current and reduced c-Fos immunoreactivity are found in the CeA of IP3K-A KO mice
malfunction
IP3K-A knockout mice exhibit deficits in some forms of hippocampus-dependent learning and synaptic plasticity, such as long-term potentiation in the dentate gyrus synapses of the hippocampus. Enzyme overexpressing mutant Tg mice show an increase in both presynaptic release probability of evoked responses, along with bigger synaptic vesicle pools, and miniature excitatory postsynaptic current amplitude, although the spine density or the expression levels of the postsynaptic density-related proteins NR2B, synaptotagmin 1, and PSD-95 are not affected. Hippocampal-dependent learning and memory tasks, including novel object recognition and radial arm maze tasks, are partially impaired in Tg mice. (R,S)-3,5-dihydroxyphenylglycine-induced metabotropic glutamate receptor long-term depression is inhibited in Tg mice and this inhibition is dependent on protein kinase C but not on the IP3 receptor. Long-term potentiation and depression dependent on N-methyl-D-aspartate receptor are marginally affected in Tg mice. The CA1 synapse of Tg mouse have greater evoked synaptic transmission efficacy in mutant mice compared too wild-type
malfunction
ITPKA depletion in mice results in altered synaptic plasticity and thus in impaired learning and memory. Stable knockdown of ITPKA in high expressing tumor cells results in decreased cell growth, colony formation and suppression of xenograft growth in immunosuppressed mice. Stable knockdown of ITPKA suppresses xenograft growth in immunosuppressed mice
malfunction
Itpka-deficient mice exhibit a weak metabolic phenotype, in keeping with functional studies revealing no clear role of ITPKA in metabolic organs. Broad phenotypic screening of itpka-deficient mice, Effects of itpka deficiency on brain function, overview. Among the neurobehavioral tests analyzed, itpka-deficient mice reacted faster to a hot plate, prepulse inhibition is impaired and the accelerating rotarod test shows decreased latency of itpka deficient mice to fall. Analysis of extracerebral functions in control and itpka deficient mice reveals significantly reduced glucose, lactate, and triglyceride plasma concentrations in itpka-deficient mice. Itpka deficiency affects energy metabolism, phenotype. Reduced glucose level is measured in plasma of itpka-deficient mice
malfunction
mutant alleles of wavy (wy), a classic locus of the fruit fly Drosophila melanogaster, map to IP3 3-kinase 2 (IP3K2). Mutations in wy disrupt wing structure in a highly specific pattern. RNAi experiments using GAL4 and GAL80ts. Gradations in the severity of the wy phenotype provide high-resolution readouts of IP3K2 function and of overall IP3 signaling are analyzed. A dominant modifier screen reveals that mutations in IP3R strongly suppress the wy phenotype, suggesting that the wy phenotype results from reduced IP4 levels, and/or excessive IP3R signaling. Potential models for how IP3K2 affects wing morphology and how mutations in IP3R dominantly suppress the wy phenotype, modeling the interactions between wavy and IP3R, overview
malfunction
the expression of microRNA-140, termed miR-140-5p, is highly induced during chemotherapy of osteosarcoma cells accompanied by upregulated autophagy. The increased miR-140-5p expression levels upregulate anticancer drug-induced autophagy in osteosarcoma cells and ameliorate the anticancer drug-induced cell proliferation and viability decrease. miR-140-5p regulates this context-specific autophagy through its target, inositol 1,4,5-trisphosphate kinase 2 (IP3k2). miR-140-5p mediated drug-resistance in osteosarcoma cells occurs by inducing autophagy, and miRNA regulation of autophagy through modulation of IP3 signalling. IP3K2 expression and Ca2+ entry are upregulated in osteosarcoma cells following treatment with chemotherapeutic drugs
malfunction
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ITPKA depletion in mice increases the number of hippocampal spine-synapses while reducing average spine length, depletion of ITPKA reduces the length of dendritic spines of hippocampal pyramidal cells
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malfunction
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genetic abrogation of IP3K-A alters amygdala gene expression, particularly in genes involved in key intracellular signaling pathways and genes mediating fear- and anxiety-related behaviors. In agreement with the changes in amygdala gene expression profiles, IP3K-A knockout (KO) mice display more robust responses to aversive stimuli and spent less time in the open arms of the elevated plus maze, indicating high levels of innate fear and anxiety. Decreased excitatory and inhibitory postsynaptic current and reduced c-Fos immunoreactivity are found in the CeA of IP3K-A KO mice
-
malfunction
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genetic abrogation of IP3K-A alters amygdala gene expression, particularly in genes involved in key intracellular signaling pathways and genes mediating fear- and anxiety-related behaviors. In agreement with the changes in amygdala gene expression profiles, IP3K-A knockout mice display more robust responses to aversive stimuli and spend less time in the open arms of the elevated plus maze, indicating high levels of innate fear and anxiety. IP3K-A KO mice show decreased excitatory and inhibitory postsynaptic current and reduced c-Fos immunoreactivity in the central nucleus of the amygdala. Overexpression of inositol 1,4,5-trisphosphate 3-kinases isozymes consistently suppresses inositol 1,4,5-trisphosphate-evoked increases in intracellular calcium in response to an agonist, whereas deletion or inactivation of different genes elicits diverse phenotypes depending on cell type. Genetic deletion of IP3K-A produces deficits in long-term potentiation in the dentate gyrus and impairs memory performance. Deletion does not affect spatial learning in the Morris water maze. Phenotypes, overview
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metabolism
1D-myo-inositol 1,3,4,5-tetrakisphosphate, Ins(1,3,4,5)P4 can interact with a relatively specific Ins(1,3,4,5)P4 binding protein Rasa3, alternatively, Ins(1,3,4,5)P4 can also compete with phosphoinositides to the binding of PH domain containing proteins such as Akt, protein kinase B. In neutrophils and hematopoietic progenitors, elevated levels of Ins(1,3,4,5)P4 inhibit the recruitment of Akt at the plasma membrane, and its activation, acting as a competitor of PtdIns(3,4,5)P3 binding to its PH domain
metabolism
1D-myo-inositol 1,3,4,5-tetrakisphosphate, Ins(1,3,4,5)P4 can interact with a relatively specific Ins(1,3,4,5)P4 binding protein Rasa3, alternatively, Ins(1,3,4,5)P4 can also compete with phosphoinositides to the binding of PH domain containing proteins such as Akt, protein kinase B. In neutrophils and hematopoietic progenitors, elevated levels of Ins(1,3,4,5)P4 inhibit the recruitment of Akt at the plasma membrane, and its activation, acting as a competitor of PtdIns(3,4,5)P3 binding to its PH domain
metabolism
1D-myo-inositol 1,3,4,5-tetrakisphosphate, Ins(1,3,4,5)P4 can interact with a relatively specific Ins(1,3,4,5)P4 binding protein Rasa3, alternatively, Ins(1,3,4,5)P4 can also compete with phosphoinositides to the binding of PH domain containing proteins such as Akt, protein kinase B. In neutrophils and hematopoietic progenitors, elevated levels of Ins(1,3,4,5)P4 inhibit the recruitment of Akt at the plasma membrane, and its activation, acting as a competitor of PtdIns(3,4,5)P3 binding to its PH domain
metabolism
isozyme IP3K-A expression is highly enriched in the central nucleus of the amygdala, which plays a pivotal role in the processing and expression of emotional phenotypes in mammals
metabolism
inositol 1,4,5-trisphosphate (IP3) regulates a host of biological processes from egg activation to cell death. When IP3-specific receptors (IP3Rs) bind to IP3, they release calcium from the ER into the cytoplasm, triggering a variety of cell type- and developmental stage-specific responses. Alternatively, inositol polyphosphate kinases can phosphorylate IP3. This limits IP3R activation by reducing IP3 levels, and also generates new signaling molecules altogether. The divergent pathways draw from the same IP3 pool yet cause very different cellular responses. Controlling the relative rates of IP3R activation vs. phosphorylation of IP3 is essential for proper cell functioning. Modeling the interactions between wavy and IP3R
metabolism
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main mechanisms of platelet calcium signaling implemented in the model. The model includes two main compartments: cytosol and dense tubular system (DTS). Thrombin binding to PAR1 receptor leads to phospholipase C (PLC) activation and inositol-3-phosphate (IP3) release into cytosol. IP3 binding to its receptors (IP3R) in the DTS membrane opens this channels for release of calcium that is normally contained in the DTS because of the SERCA pump action. Cytosolic IP3 is being phosphorylated by inositol triphosphate-kinase (IP3K) into IP4 that might be included in the phosphoinositide turnover. Two feedback loops: a PLC-dependent positive feedback loop and the IP3K-dependent negative loop. System modeling, overview
metabolism
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isozyme IP3K-A expression is highly enriched in the central nucleus of the amygdala, which plays a pivotal role in the processing and expression of emotional phenotypes in mammals
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physiological function
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inositol 1,4,5-trisphosphate 3-kinase B converts inositol 1,4,5-trisphosphate to inositol 1,3,4,5-tetrakisphosphate upon Ag receptor activation and controls the fate and function of lymphocytes
physiological function
inositol-1,4,5-trisphosphate-3-kinase-A is a cell motility-promoting protein that increases the metastatic potential of tumour cells by 2 functional activities: it promotes migration of tumour cells by 2 different mechanisms: growth factor independently, high levels of inositol-1,4,5-trisphosphate-3-kinase-A induce the formation of large cellular protrusions by directly modulating the actin cytoskeleton, the F-actin binding activity of inositol-1,4,5-trisphosphate-3-kinase-A stabilizes and bundles actin filaments and thus increases the levels of cellular F-actin, in growth factor stimulated cells, the catalytically active domain enhances basal inositol-1,4,5-trisphosphate-3-kinase-A induced migration by activating store-operated calcium entry through production of inositol-1,3,4,5-tetrakisphosphate and subsequent inhibition of inositol-phosphate-5-phosphatase
physiological function
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on neural activation, inositol 1,4,5-trisphosphate 3-kinase A binds directly to activated Rac1 and recruits it to the actin cytoskeleton in the postsynaptic area, enzyme is critical for the spatial and temporal regulation of spine actin remodeling, synaptic plasticity, and learning and memory via an activity-dependent Rac scaffolding mechanism, inositol 1,4,5-trisphosphate 3-kinase A catalytic activity regulates calcium levels by modulating the metabolism of 1D-myo-inositol 1,4,5-trisphosphate
physiological function
on neural activation, inositol 1,4,5-trisphosphate 3-kinase A binds directly to activated Rac1 and recruits it to the actin cytoskeleton in the postsynaptic area, enzyme is critical for the spatial and temporal regulation of spine actin remodeling, synaptic plasticity, and learning and memory via an activity-dependent Rac scaffolding mechanism, inositol 1,4,5-trisphosphate 3-kinase A catalytic activity regulates calcium levels by modulating the metabolism of 1D-myo-inositol 1,4,5-trisphosphate
physiological function
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physiological modulator of myelopoiesis, enzyme plays a crucial role in hematopoiesis
physiological function
cell-specific inositol phosphate signalling specifically via inositol 1,4,5-trisphosphate 3-kinase, negatively regulates organismal responses to oxidative stress. The Drosophila malpighian tubule is a key epithelial sensor for organismal oxidative stress responses, precise targeting of either gain-of-function constructs of isoforms IP3K-1 and IP3K-2, or loss-of-function constructs to only one cell type in tubule reversibly modulates survival of stress-challenged adult flies
physiological function
cell-specific inositol phosphate signalling specifically via inositol 1,4,5-trisphosphate 3-kinase, negatively regulates organismal responses to oxidative stress. The Drosophila malpighian tubule is a key epithelial sensor for organismal oxidative stress responses, precise targeting of either gain-of-function constructs of isoforms IP3K-1 and IP3K-2, or loss-of-function constructs to only one cell type in tubule reversibly modulates survival of stress-challenged adult flies. In vivo, targeted isoform IP3K-1 directly increases H2O2 production, pro-apoptotic caspase-9 activity and mitochondrial membrane potential. The mitochondrial calcium load in tubule principal cells is significantly increased by isoform IP3K-1 under oxidative stress conditions, leading to apoptosis
physiological function
isoform inositol 1,4,5-trisphosphate 3-kinase A is ectopically expressed in different human tumor cell lines and during tumor progression in the metastatic tumor model Balb-neuT. High expression of isoform 1,4,5-trisphosphate 3-kinase A increases invasive migration in vitro and metastasis in a xenograft SCID mouse model. 1,4,5-Trisphosphate 3-kinase A promotes migration of tumor cells by two different mechanisms: growth factor independently high levels of enzyme induce the formation of large cellular protrusions by directly modulating the actin cytoskeleton. The F-actin binding activity of 1,4,5-trisphosphate 3-kinase A stabilizes and bundles actin filaments and thus increases the levels of cellular F-actin. In growth factor-stimulated cells, the catalytically active domain enhances basal 1,4,5-trisphosphate 3-kinase A-induced migration by activating store-operated calcium entry through production of inositol 1,3,4,5-tetrakisphosphate and subsequent inhibition of inositol phosphate 5-phosphatase
physiological function
isoform inositol 1,4,5-trisphosphate 3-kinase B is important for the control of Bim protein expression and B cell survival rather than for the control of B cell development from one stage to another. B cell receptor transgenic inositol 1,4,5-trisphosphate 3-kinase B-/- B cells exhibit an anergic phenotype with the notable exception of their enhanced antigen-induced calcium signalling. On a deleting H2-Kb genetic background, inositol 1,4,5-trisphosphate 3-kinase B is not essential for B cell receptor editing or negative selection
physiological function
overexpression of isoform inositol-1,4,5-trisphosphate 3-kinase A increases the number of dendritic protrusions by 71% in immature primary neurons. In mature neurons, the effect of inositol-1,4,5-trisphosphate 3-kinase A overexpression on formation of dendritic spines is weaker and depletion of the enzyme does not alter spine density and synaptic contacts. In synaptosomes of mature neurons, enzyme loss results in decreased duration of Ins(1,4,5)P3 signals and shorter Ins(1,4,5)P3-dependent Ca2+ transients. At synapses of inositol-1,4,5-trisphosphate 3-kinase A deficient neurons the levels of Ins(1,4,5)P3-5-phosphatase and sarcoplasmic/endoplasmic reticulum calcium ATPase pump-2b are increased
physiological function
1D-myo-inositol 1,4,5-trisphosphate is a key point in Ca2+ metabolism that promotes Ca2+ release from intracellular stores and together with 1D-myo-inositol 1,3,4,5-tetrakisphosphate regulates Ca2+ homoeostasis. In addition, 1D-myo-inositol 1,3,4,5-tetrakisphosphate is involved in immune cell development. Ca2+ and calmodulin regulate the activity of inositol(1,4,5)trisphosphate 3-kinases via direct interaction
physiological function
ectopic expression of the neuron-specific inositol-1,4,5-trisphosphate-3-kinase A in lung cancer cells increases their metastatic potential because the protein exhibits two actin regulating activities. The isozyme ITPKA bundles actin filaments and regulates inositol-1,4,5-trisphosphate (InsP3)-mediated calcium signals by phosphorylating InsP3
physiological function
functional role of isozyme Itpkb in peripheral T cells, potential role for Itpkb in autoimmunity
physiological function
in addition to cross-linking actin filaments, ITPKA strongly inhibits Arp2/3-complex induced actin filament branching by displacing the complex from F-actin. n vivo ITPKA negatively regulates formation and/or maintenance of synaptic contacts in the mammalian brain. On the molecular level this effect appears to result from the ITPKA-mediated inhibition of Arp2/3-complex F-actin branching activity. ITPKA does not affect the F-actin bundling activity of drebrin A
physiological function
in natural killer (NK) cells, isozyme Itpkb promotes NK-cell terminal maturation but limits NK-cell effector functions
physiological function
in natural killer (NK) cells, isozyme Itpkb promotes NK-cell terminal maturation but limits NK-cell effector functions. Itpka and Itpkb isoforms inhibit neurite outgrowth in PC12 cells, while isozyme Itpkc does not
physiological function
in natural killer (NK) cells, isozyme Itpkb promotes NK-cell terminal maturation but limits NK-cell effector functions. Itpkb controls hematopoietic stem cell homeostasis and prevents lethal hematopoietic failure in mice
physiological function
isozyme IP3K-A has a profound influence on the basal activities of fear- and anxiety-mediating amygdala circuitry and plays an important role in regulating affective states by modulating metabotropic receptor signaling pathways and neural activity in the amygdala. Inositol 1,4,5-trisphosphate 3-kinases modulate intracellular calcium signaling induced by the activation of G-protein coupled receptors associated with phospholipase C. Isozyme IP3K-A is enriched in dendritic spines of mature neurons and modulates actin dynamics in the hippocampus
physiological function
isozyme Itpka contains an F-actin binding site at the N-terminal part that confers to Itpka the properties of an F-actin bundling protein with two major consequences: it can reorganize the cytoskeletal network, particularly in dendritic spines, and it can provide an opportunity for Ins(1,3,4,5)P4 to act very locally as second messenger. Isozyme Itpka is an F-actin bundling protein regulating dendritic spines structural plasticity and a scaffold protein for synaptic rac signaling, Itpka overexpression induces cytoskeletal reorganization, high expression of Itpka in cancer cells increases invasion and migration in vitro
physiological function
isozyme Itpka contains an F-actin binding site at the N-terminal part that confers to Itpka the properties of an F-actin bundling protein with two major consequences: it can reorganize the cytoskeletal network, particularly in dendritic spines, and it can provide an opportunity for Ins(1,3,4,5)P4 to act very locally as second messenger. Isozyme Itpka is an F-actin bundling protein regulating dendritic spines structural plasticity and a scaffold protein for synaptic rac signaling, Itpka overexpression induces cytoskeletal reorganization, high expression of Itpka in cancer cells increases invasion and migration in vitro
physiological function
isozyme Itpka contains an F-actin binding site at the N-terminal part that confers to Itpka the properties of an F-actin bundling protein with two major consequences: it can reorganize the cytoskeletal network, particularly in dendritic spines, and it can provide an opportunity for Ins(1,3,4,5)P4 to act very locally as second messenger. Isozyme Itpka is an F-actin bundling protein regulating dendritic spines structural plasticity and a scaffold protein for synaptic rac signaling, Itpka overexpression induces cytoskeletal reorganization, high expression of Itpka in cancer cells increases invasion and migration in vitro. Itpka and Itpkb isoforms inhibit neurite outgrowth in PC12 cells, while isozyme Itpkc does not
physiological function
isozyme ITPKA induces formation of complex actin networks, but exibits only one N-terminal actin binding domain, the C-terminus of ITPKA acts as spacer between actin filaments, overview. ITPKA induces the formation of a dense network of branched actin filaments, not of linear filaments. Overexpression of ITPKA induces the formation of lamellipodia-like protrusions which consist of cross-linked actin filaments. 1D-myo-inositol 1,3,4,5-tetrakisphosphate inhibits actin polymerization, but does not show a significant effect on bundling activity of ITPKA, while binding of ITPKA to actin stimulates inositol-1,4,5-trisphosphate 3-kinase-a activity
physiological function
isozyme Itpka inhibits neurite outgrowth through both F-actin binding
physiological function
isozyme Itpkb inhibits neurite outgrowth through both F-actin binding
physiological function
isozyme Itpkc does not influence neurite length and neuron growth or F-actin binding
physiological function
Itpka and Itpkb isoforms inhibit neurite outgrowth in PC12 cells, while isozyme Itpkc does not
physiological function
role for ITPKC either in the development or the function of these specialized cellular structures
physiological function
among the ITPK-isoforms ITPKA is the most specialized one. In cells it is exclusively bound to F-actin resulting in cross-linking of actin filaments. ITPKA has two very distinct functions, regulating both, calcium signaling and actin dynamics. Isoform A of ITPK is an oncogene, it is involved in cancer progression, tumor growth is stimulated by the InsP3Kinase activity of ITPKA and metastasis by its actin bundling activity. ITPKA regulates actin dynamics by binding with its homodimeric N-terminal actin binding domain (ABD) to F-actin
physiological function
among the ITPK-isoforms ITPKA is the most specialized one. In cells it is exclusively bound to F-actin resulting in cross-linking of actin filaments. ITPKA has two very distinct functions, regulating both, calcium signaling and actin dynamics. Isoform A of ITPK is an oncogene, it is involved in cancer progression, tumor growth is stimulated by the InsP3Kinase activity of ITPKA and metastasis by its actin bundling activity. ITPKA regulates actin dynamics by binding with its homodimeric N-terminal actin binding domain (ABD) to F-actin. The bulky C-terminus, which includes the InsP3Kinase-domain, acts as spacer between actin filaments resulting in formation of loose networks of F-actin bundles. Cellular calcium signals are regulated by the InsP3Kinase activity of ITPKA. Calcium is an ubiquitous second messenger that is involved in many signal transduction pathways, including protein kinase C and CAMKII signaling. ITPKA phosphorylates the calcium-mobilizing second messenger Ins(1,4,5)P3 at 3'-position, thereby producing Ins(1,3,4,5)P4. Since the Ins(1,4,5)P3 loop binds Ins(1,4,5)P3 with high affinity, but no other InsP-isomers or phosphatidylinositol phosphates, ITPKA is a highly specialized enzyme. Ins(1,3,4,5)P4 is substantially involved in the control of Ins(1,4,5)P3-mediated calcium release. The (1,4,5)P3 phosphatase INPP5A binds Ins(1,3,4,5)P4 with tenfold higher affinity than Ins(1,4,5)P3, resulting in decreased (1,4,5)P3 dephosphorylation. Therefore, production of Ins (1,3,4,5)P4 increases half-life of Ins(1,4,5)P3, thus Ins(1,4,5)P3-mediated calcium release from the endoplasmic reticulum. Based on this property, in the absence of ITPKA calcium release is shortened and calcium-induced calcium entry abrogated. ITPKA is involved in both, the control of calcium signals and the control of dendritic spine morphology. ITPKA belongs to the invasive signature of p130Cas/ErbB2 transformed breast cancer cells showing that in different tumor entities expression of ITPKA is associated with malignancy of tumor cells. Regulation of ITPKA expression in tumor cells, overview
physiological function
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analysis of the roles of feedbacks through phospholipase C and inositol 1,4,5-trisphosphate 3-kinase (IP3K) by means of a computer model of calcium signal transduction in platelets
physiological function
cells positive for ITPKC in the studied tissues express either a multicilium (tracheal and bronchial epithelia, brain ependymal cells), microvilli forming a brush border (small and large intestine, and kidney proximal tubule cells) or a flagellum (spermatozoa), suggesting a role for ITPKC either in the development or the function of these specialized cellular structures
physiological function
inositol 1,4,5-trisphosphate 3-kinase A (IP3K-A) is enriched in the brain and neurons that regulates intracellular calcium levels via signaling through the inositol trisphosphate receptor. IP3K-A expression is highly enriched in the central nucleus of the amygdala (CeA), which plays a pivotal role in the processing and expression of emotional phenotypes in mammals. IP3K-A has a profound influence on the basal activities of fear- and anxiety-mediating amygdala circuitry. IP3K-A plays an important role in regulating affective states by modulating metabotropic receptor signaling pathways and neural activity in the amygdala
physiological function
inositol 1,4,5-trisphosphate 3-kinase A (IP3K-A) regulates the level of the inositol polyphosphates, inositol trisphosphate (IP3) and inositol tetrakisphosphate to modulate cellular signaling and intracellular calcium homeostasis in the central nervous system. IP3K-A binds to F-actin in an activity-dependent manner and accumulates in dendritic spines, where it is involved in the regulation of synaptic plasticity. Overexpressed IP3K-A plays a role in some forms of hippocampus-dependent learning and memory tasks as well as in synaptic transmission and plasticity by regulating both presynaptic and postsynaptic functions
physiological function
IP3K2 function is required in the wing discs of early pupae for normal wing development. Controlling the relative rates of IP3R activation vs. phosphorylation of IP3 is essential for proper cell functioning. IP3K2 function is required in the developing wing blade during early pupal life
physiological function
isozyme ITPKA is involved in the regulation of nociceptive pathways, sensorimotor gating, and motor learning. Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is the neuronal isoform of ITPKs and exhibits both actin bundling and InsP3 kinase activity. In addition to neurons, ITPKA is ectopically expressed in tumor cells, where its oncogenic activity increases tumor cell malignancy. ITPKA is involved in the regulation of nociceptive pathways, sensorimotor gating and motor learning. ITPKA plays a functional role in calcium signaling of CaCo-2 cells
physiological function
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in addition to cross-linking actin filaments, ITPKA strongly inhibits Arp2/3-complex induced actin filament branching by displacing the complex from F-actin. n vivo ITPKA negatively regulates formation and/or maintenance of synaptic contacts in the mammalian brain. On the molecular level this effect appears to result from the ITPKA-mediated inhibition of Arp2/3-complex F-actin branching activity. ITPKA does not affect the F-actin bundling activity of drebrin A
-
physiological function
-
inositol 1,4,5-trisphosphate 3-kinase A (IP3K-A) is enriched in the brain and neurons that regulates intracellular calcium levels via signaling through the inositol trisphosphate receptor. IP3K-A expression is highly enriched in the central nucleus of the amygdala (CeA), which plays a pivotal role in the processing and expression of emotional phenotypes in mammals. IP3K-A has a profound influence on the basal activities of fear- and anxiety-mediating amygdala circuitry. IP3K-A plays an important role in regulating affective states by modulating metabotropic receptor signaling pathways and neural activity in the amygdala
-
physiological function
-
isozyme IP3K-A has a profound influence on the basal activities of fear- and anxiety-mediating amygdala circuitry and plays an important role in regulating affective states by modulating metabotropic receptor signaling pathways and neural activity in the amygdala. Inositol 1,4,5-trisphosphate 3-kinases modulate intracellular calcium signaling induced by the activation of G-protein coupled receptors associated with phospholipase C. Isozyme IP3K-A is enriched in dendritic spines of mature neurons and modulates actin dynamics in the hippocampus
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additional information
an F-actin binding site is located in the N-terminal part of isozyme Itpka. The catalytic activity is located at the C-terminal end, N-terminal deletion mutants are fully active
additional information
an F-actin binding site is located in the N-terminal part of isozyme Itpka. The catalytic activity is located at the C-terminal end, N-terminal deletion mutants are fully active
additional information
an F-actin binding site is located in the N-terminal part of isozyme Itpka. The catalytic activity is located at the C-terminal end, N-terminal deletion mutants are fully active
additional information
an F-actin binding site is located in the N-terminal part of isozyme Itpkb. The catalytic activity is located at the C-terminal end, N-terminal deletion mutants are fully active
additional information
an F-actin binding site is located in the N-terminal part of isozyme Itpkb. The catalytic activity is located at the C-terminal end, N-terminal deletion mutants are fully active
additional information
an F-actin binding site is located in the N-terminal part of isozyme Itpkb. The catalytic activity is located at the C-terminal end, N-terminal deletion mutants are fully active
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
-
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
-
isozyme Itpkb contains an F-actin binding site at the N-terminal part
additional information
ITPKC functional polymorphism associates with Kawasaki disease susceptibility
additional information
ITPKC functional polymorphism associates with Kawasaki disease susceptibility
additional information
ITPKC functional polymorphism associates with Kawasaki disease susceptibility
additional information
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ITPKC functional polymorphism associates with Kawasaki disease susceptibility
additional information
neurite length is significantly decreased in cells overexpressing isozymes Itpka and Itpkb but not Itpkc or IPMK. This result does not depend on the overexpression level of any of the kinases
additional information
neurite length is significantly decreased in cells overexpressing isozymes Itpka and Itpkb but not Itpkc or IPMK. This result does not depend on the overexpression level of any of the kinases
additional information
neurite length is significantly decreased in cells overexpressing isozymes Itpka and Itpkb but not Itpkc or IPMK. This result does not depend on the overexpression level of any of the kinases
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Homo sapiens (P23677)
brenda
Marechal, Y.; Queant, S.; Polizzi, S.; Pouillon, V.; Schurmans, S.
Inositol 1,4,5-trisphosphate 3-kinase B controls survival and prevents anergy in B cells
Immunobiology
216
103-109
2010
Mus musculus (B2RXC2), Mus musculus
brenda
Nalaskowski, M.M.; Fliegert, R.; Ernst, O.; Brehm, M.A.; Fanick, W.; Windhorst, S.; Lin, H.; Giehler, S.; Hein, J.; Lin, Y.N.; Mayr, G.W.
Human inositol 1,4,5-trisphosphate 3-kinase isoform B (IP3KB) is a nucleocytoplasmic shuttling protein specifically enriched at cortical actin filaments and at invaginations of the nuclear envelope
J. Biol. Chem.
286
4500-4510
2011
Homo sapiens (P27987), Homo sapiens
brenda
Lee, D.; Lee, H.W.; Hong, S.; Choi, B.I.; Kim, H.W.; Han, S.B.; Kim, I.H.; Bae, J.Y.; Bae, Y.C.; Rhyu, I.J.; Sun, W.; Kim, H.
Inositol 1,4,5-trisphosphate 3-kinase A is a novel microtubule-associated protein: PKA-dependent phosphoregulation of microtubule binding affinity
J. Biol. Chem.
287
15981-15995
2012
Rattus norvegicus (P17105)
brenda
Pouillon, V.; Maréchal, Y.; Frippiat, C.; Erneux, C.; Schurmans, S.
Inositol 1,4,5-trisphosphate 3-kinase B (Itpkb) controls survival, proliferation and cytokine production in mouse peripheral T cells
Adv. Biol. Regul.
53
39-50
2013
Mus musculus (B2RXC2)
-
brenda
Erneux, C.; Ghosh, S.; Koenig, S.
Inositol(1,4,5)P3 3-kinase isoenzymes: catalytic properties and importance of targeting to F-actin to understand function
Adv. Biol. Regul.
60
135-143
2016
Mus musculus (B2RXC2), Mus musculus (Q7TS72), Mus musculus (Q8R071), Mus musculus, Rattus norvegicus (P17105), Rattus norvegicus (P42335), Rattus norvegicus (Q80ZG2), Homo sapiens (P23677), Homo sapiens (P27987), Homo sapiens (Q96DU7), Homo sapiens
brenda
Scoumanne, A.; Molina-Ortiz, P.; Monteyne, D.; Perez-Morga, D.; Erneux, C.; Schurmans, S.
Specific expression and function of inositol 1,4,5-trisphosphate 3-kinase C (ITPKC) in wild type and knock-out mice
Adv. Biol. Regul.
62
1-10
2016
Mus musculus (Q7TS72), Mus musculus
brenda
Schroeder, D.; Rehbach, C.; Seyffarth, C.; Neuenschwander, M.; Kries, J.V.; Windhorst, S.
Identification of a new membrane-permeable inhibitor against inositol-1,4,5-trisphosphate-3-kinase A
Biochem. Biophys. Res. Commun.
439
228-234
2013
Homo sapiens (P23677)
brenda
Franco-Echevarria, E.; Banos-Sanz, J.I.; Monterroso, B.; Round, A.; Sanz-Aparicio, J.; Gonzalez, B.
A new calmodulin-binding motif for inositol 1,4,5-trisphosphate 3-kinase regulation
Biochem. J.
463
319-328
2014
Homo sapiens (P23677), Homo sapiens
brenda
Stygelbout, V.; Leroy, K.; Pouillon, V.; Ando, K.; DAmico, E.; Jia, Y.; Luo, H.R.; Duyckaerts, C.; Erneux, C.; Schurmans, S.; Brion, J.P.
Inositol trisphosphate 3-kinase B is increased in human Alzheimer brain and exacerbates mouse Alzheimer pathology
Brain
137
537-552
2014
Mus musculus (B2RXC2), Mus musculus, Homo sapiens (P27987), Homo sapiens
brenda
Koester, J.D.; Leggewie, B.; Blechner, C.; Brandt, N.; Fester, L.; Rune, G.; Schweizer, M.; Kindler, S.; Windhorst, S.
Inositol-1,4,5-trisphosphate-3-kinase-A controls morphology of hippocampal dendritic spines
Cell. Signal.
28
83-90
2016
Mus musculus (Q8R071), Mus musculus C57BL/6 (Q8R071)
brenda
Ashour, D.J.; Pelka, B.; Jaaks, P.; Wundenberg, T.; Blechner, C.; Zobiak, B.; Failla, A.V.; Windhorst, S.
The catalytic domain of inositol-1,4,5-trisphosphate 3-kinase-a contributes to ITPKA-induced modulation of F-actin
Cytoskeleton (Hoboken)
72
93-100
2015
Homo sapiens (P23677)
brenda
Koenig, S.; Moreau, C.; Dupont, G.; Scoumanne, A.; Erneux, C.
Regulation of NGF-driven neurite outgrowth by Ins(1,4,5)P3 kinase is specifically associated with the two isoenzymes Itpka and Itpkb in a model of PC12 cells
FEBS J.
282
2553-2569
2015
Rattus norvegicus (P17105), Rattus norvegicus (P42335), Rattus norvegicus (Q80ZG2)
brenda
Chung, S.; Kim, I.H.; Lee, D.; Park, K.; Kim, J.Y.; Lee, Y.K.; Kim, E.J.; Lee, H.W.; Choi, J.S.; Son, G.H.; Sun, W.; Shin, K.S.; Kim, H.
The role of inositol 1,4,5-trisphosphate 3-kinase A in regulating emotional behavior and amygdala function
Sci. Rep.
6
23757
2016
Mus musculus (Q8R071), Mus musculus C57BL/6N (Q8R071)
brenda
Scoumanne, A.; Molina-Ortiz, P.; Monteyne, D.; Perez-Morga, D.; Erneux, C.; Schurmans, S.
Specific expression and function of inositol 1,4,5-trisphosphate 3-kinase C (ITPKC) in wild type and knock-out mice
Adv. Biol. Regul.
62
1-10
2016
Mus musculus (Q7TS72), Mus musculus
brenda
Windhorst, S.; Song, K.; Gazdar, A.F.
Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is frequently over-expressed and functions as an oncogene in several tumor types
Biochem. Pharmacol.
137
1-9
2017
Homo sapiens (P23677), Homo sapiens, Mus musculus (Q8R071)
brenda
Wei, R.; Cao, G.; Deng, Z.; Su, J.; Cai, L.
miR-140-5p attenuates chemotherapeutic drug-induced cell death by regulating autophagy through inositol 1,4,5-trisphosphate kinase 2 (IP3k2) in human osteosarcoma cells
Biosci. Rep.
36
art:e00392
2016
Homo sapiens (P27987), Homo sapiens
brenda
Dean, D.; Maroja, L.; Cottrill, S.; Bomkamp, B.; Westervelt, K.; Deitcher, D.
The wavy mutation maps to the inositol 1,4,5-Trisphosphate 3-Kinase 2 (IP3K2) gene of drosophila and interacts with IP3R to affect wing development
G3 (Bethesda)
6
299-310
2016
Drosophila melanogaster (A0A0U2TSJ5), Drosophila melanogaster
brenda
Balabin, F.A.; Sveshnikova, A.N.
Computational biology analysis of platelet signaling reveals roles of feedbacks through phospholipase C and inositol 1,4,5-trisphosphate 3-kinase in controlling amplitude and duration of calcium oscillations
Mathr. Biosci.
276
67-74
2016
Homo sapiens
brenda
Blechner, C.; Becker, L.; Fuchs, H.; Rathkolb, B.; Prehn, C.; Adler, T.; Calzada-Wack, J.; Garrett, L.; Gailus-Durner, V.; Morellini, F.; Conrad, S.; Hoelter, S.M.; Wolf, E.; Klopstock, T.; Adamski, J.; Busch, D.; de Angelis, M.H.; Schmeisser, M.J.; Windhorst, S.
Physiological relevance of the neuronal isoform of inositol-1,4,5-trisphosphate 3-kinases in mice
Neurosci. Lett.
735
135206
2020
Mus musculus (Q8R071)
brenda
Choi, B.; Lee, H.W.; Mo, S.; Kim, J.Y.; Kim, H.W.; Rhyu, I.J.; Hong, E.; Lee, Y.K.; Choi, J.S.; Kim, C.H.; Kim, H.
Inositol 1,4,5-trisphosphate 3-kinase A overexpressed in mouse forebrain modulates synaptic transmission and mGluR-LTD of CA1 pyramidal neurons
PLoS ONE
13
e0193859
2018
Mus musculus (Q8R071), Mus musculus
brenda
Chung, S.; Kim, I.H.; Lee, D.; Park, K.; Kim, J.Y.; Lee, Y.K.; Kim, E.J.; Lee, H.W.; Choi, J.S.; Son, G.H.; Sun, W.; Shin, K.S.; Kim, H.
The role of inositol 1,4,5-trisphosphate 3-kinase A in regulating emotional behavior and amygdala function
Sci. Rep.
6
23757
2016
Mus musculus (Q8R071), Mus musculus C57BL/6N (Q8R071)
brenda