2.7.1.127: inositol-trisphosphate 3-kinase
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For detailed information about inositol-trisphosphate 3-kinase, go to the full flat file.
Word Map on EC 2.7.1.127
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2.7.1.127
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1,3,4,5-tetrakisphosphate
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kawasaki
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vasculitis
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5-phosphatase
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tetrakisphosphate
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diagnostics
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medicine
- 2.7.1.127
- 1,3,4,5-tetrakisphosphate
- kawasaki
-
vasculitis
-
5-phosphatase
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tetrakisphosphate
- diagnostics
- medicine
Reaction
Synonyms
1D-myo-inositol-trisphosphate 3-kinase, Arg82, ArgRIII, D-myo-inositol 1,4,5-trisphosphate 3-kinase, GsIP3K-A, HsIP3K-A, inositol (1,4,5) trisphosphate 3 kinase B, inositol (1,4,5) trisphosphate 3-kinase, inositol 1,4,5-trisphosphate 3-kinase, inositol 1,4,5-trisphosphate 3-kinase A, inositol 1,4,5-trisphosphate 3-kinase B, inositol 1,4,5-trisphosphate 3-kinase C, inositol 1,4,5-trisphosphate 3-kinases, inositol 1,4,5-trisphosphate kinase, inositol 1,4,5-trisphosphate kinase 2, inositol 1,4,5-trisphosphate-3-kinase-A, inositol polyphosphate multikinase, inositol trisphosphate 3-kinase B, inositol(1,4,5)P3 3-kinase, inositol(1,4,5)trisphosphate 3-kinase, inositol(1,4,5)trisphosphate 3-kinases, inositol-1,4,5-trisphosphate 3-kinase, inositol-1,4,5-trisphosphate 3-kinase A, inositol-1,4,5-trisphosphate 3-kinase-A, inositol-1,4,5-trisphosphate-3-kinase, inositol-1,4,5-trisphosphate-3-kinase A, inositol-1,4,5-trisphosphate-3-kinase-A, inositol-trisphosphate 3-kinase B, Ins(1,4,5)P(3) 3-kinase B, Ins(1,4,5)P3 3-kinase, Ins(1,4,5)P3 3-kinase isoform B, Ins(1,4,5)P3 kinase, InsP3 3-kinase, InsP3 3-kinase A, InsP3 3-kinase B, InsP3 3-kinase C, InsP3K, InsP3KB, InsP3Kinase, IP3 3-kinase, IP3 3-kinase 2, IP3-3K, IP3K, IP3K-A, IP3K-B, IP3K-C, IP3K1, IP3K2, IP3KA, IP3KB, IP3KC, IP3kin, Ipk2, IPMK, ITPKA, Itpkb, Itpkc, kinase (phosphorylating), inositol 1,4,5-trisphosphate 3-, More, RnIP3K-C, wavy
ECTree
2.7.1.127 inositol-trisphosphate 3-kinaseAdvanced search results
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results (Engineering
Engineering on EC 2.7.1.127 - inositol-trisphosphate 3-kinase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
K268E
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site-directed mutagenesis, activity is similar to the wild-type enzyme, the sensitivity to inhibitor 3',4',7,8-tetrahydroxyflavone is highly reduced compared to the wild-type enzyme
K272D
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site-directed mutagenesis, activity is similar to the wild-type enzyme, the sensitivity to inhibitor 3',4',7,8-tetrahydroxyflavone is highly reduced compared to the wild-type enzyme
K336Q
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By substituting lysine 336, involving in ATP binding and located in the C-lobe, an inhibitor-resistant IP3K-A with full enzymatic activity and normal substrate affinity is created.
L34P
a point mutant that blocks actin-binding is overexpressed in H1299 cells, the morphology of cells expressing the mutant and those of cells expressing green fluorescent protein do not show visible differences
K262A
the green fluorescent protein-inositol 1,4,5-trisphosphate 3-kinase A point mutant is generated by site-directed mutagenesis, point mutant lacks kinase activity
additional information
additional information
mutant alleles of wavy (wy), a classic locus of the fruit fly Drosophila melanogaster, map to IP3 3-kinase 2 (IP3K2), mapping of the wy locus. Mutations in wy disrupt wing structure in a highly specific pattern, wy alleles, mapping, complementation tests, RNAi experiments of IP3K2 (using VDRC v19159: P(GD8778)v19159/TM3 Sb), phenotype analysis, overview. All three mutant alleles of wy are dominantly suppressed by both mutant alleles of IP3R
additional information
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mutant alleles of wavy (wy), a classic locus of the fruit fly Drosophila melanogaster, map to IP3 3-kinase 2 (IP3K2), mapping of the wy locus. Mutations in wy disrupt wing structure in a highly specific pattern, wy alleles, mapping, complementation tests, RNAi experiments of IP3K2 (using VDRC v19159: P(GD8778)v19159/TM3 Sb), phenotype analysis, overview. All three mutant alleles of wy are dominantly suppressed by both mutant alleles of IP3R
additional information
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InsP3 3-kinase dead mutant cells with much lower or undetectable enzyme activities, the N-terminal deletion mutant of InsP3 3-kinase A starting at Leu-133 and the N-terminal deletion mutant of InsP3 3-kinase B starting at Asp-483 are cytoplasmic
additional information
generation of isozyme ITPKA mutant DELTA1-54 or DELTA1-134. Insertion of the enzyme's catalytic domain inbetween actin filaments increases its inositol-1,4,5-trisphosphate 3-kinase-a activity
additional information
construction of Itpkb-/- mice transgenically expressing Itpkb in thymocytes, tese mutant mice have some peripheral T cells left. The mutant mice shows partial rescue of T cell lineage development through recombinant expression of HA-tagged isozyme Itpkb in thymocytes
additional information
generation of a transgenic (Tg) mouse line in which IP3K-A is conditionally overexpressed approximately 3fold in the excitatory neurons of forebrain regions, including the hippocampus. The 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 (mGluR-dependent DHPG-LTD) 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
additional information
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generation of a transgenic (Tg) mouse line in which IP3K-A is conditionally overexpressed approximately 3fold in the excitatory neurons of forebrain regions, including the hippocampus. The 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 (mGluR-dependent DHPG-LTD) 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
additional information
generation of IP3K-A KO mice and electrophysiological properties of IP3K-A KO mice, overview. No significant differences in basic electrophysiological properties between groups, such as resting membrane potential and input resistance is found. But the input-output functions of CeL neurons are significantly attenuated along with a longer latency to the first spike in KO mice
additional information
generation of ITPKA knock-out mice that exhibit increased synaptic plasticity and slight impairments of learning and memory
additional information
generation of Itpkc-/- mice, a Itpkc knockout mouse model
additional information
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generation of Itpkc-/- mice, a Itpkc knockout mouse model
additional information
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generation of IP3K-A KO mice and electrophysiological properties of IP3K-A KO mice, overview. No significant differences in basic electrophysiological properties between groups, such as resting membrane potential and input resistance is found. But the input-output functions of CeL neurons are significantly attenuated along with a longer latency to the first spike in KO mice
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additional information
construction of a mutant isozyme B by helix-breaking mutations in the actin binding domain and deletion of the actin binding domain in full-length isozyme B resulting in loss of actin binding ability
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKA, generation of Itpka N-terminal F-actin binding domain (N66-GFP) and the N66(L34P)-GFP mutants. N-terminal deletion mutants are fully active
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKA, generation of Itpka N-terminal F-actin binding domain (N66-GFP) and the N66(L34P)-GFP mutants. N-terminal deletion mutants are fully active
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKA, generation of Itpka N-terminal F-actin binding domain (N66-GFP) and the N66(L34P)-GFP mutants. N-terminal deletion mutants are fully active
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKB. N-terminal deletion mutants are fully active
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKB. N-terminal deletion mutants are fully active
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKB. N-terminal deletion mutants are fully active
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKC
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKC
additional information
construction of a kinase-dead mutant and a DELTAN-terminal deletion mutant of isozyme ITPKC
