Literature summary for 2.7.1.127 extracted from

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 (2018), PLoS ONE, 13, e0193859 .

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Protein Variants

Protein Variants	Comment	Organism
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	Mus musculus

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining
actin filament	-	Mus musculus	5884	-

Metals/Ions

Metals/Ions	Comment	Organism	Structure
Mg2+	required	Mus musculus

Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
ATP + 1D-myo-inositol 1,4,5-trisphosphate	Mus musculus	-	ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate	-	?

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q8R071	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
brain	-	Mus musculus	-
forebrain	-	Mus musculus	-
hippocampus	-	Mus musculus	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
ATP + 1D-myo-inositol 1,4,5-trisphosphate	-	Mus musculus	ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate	-	?

Synonyms

Synonyms	Comment	Organism
inositol 1,4,5-trisphosphate 3-kinase A	-	Mus musculus
IP3K-A	-	Mus musculus

Cofactor

Cofactor	Comment	Organism	Structure
ATP	-	Mus musculus

General Information

General Information	Comment	Organism
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	Mus musculus
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	Mus musculus

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Release 2023.1 (January 2023)