Literature summary for 2.7.1.127 extracted from

Windhorst, S.; Minge, D.; Baehring, R.; Hueser, S.; Schob, C.; Blechner, C.; Lin, H.Y.; Mayr, G.W.; Kindler, S.
Inositol-1,4,5-trisphosphate 3-kinase A regulates dendritic morphology and shapes synaptic Ca2+ transients (2012), Cell. Signal., 24, 750-757.

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Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	P23677	isoform inositol-1,4,5-trisphosphate 3-kinase A	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
neuron	hippocampal neuron	Homo sapiens	-

Synonyms

Synonyms	Comment	Organism
inositol-1,4,5-trisphosphate 3-kinase A	-	Homo sapiens
inositol-1,4,5-trisphosphate 3-kinase-A	-	Homo sapiens
ITPKA	-	Homo sapiens

General Information

General Information	Comment	Organism
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	Homo sapiens

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Release 2023.1 (January 2023)