Cloned (Comment) | Organism |
---|---|
gene Itpka, quantitative real-time PCR expression analysis | Mus musculus |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
endoplasmic reticulum | - |
Mus musculus | 5783 | - |
Metals/Ions | Comment | Organism | Structure |
---|---|---|---|
Ca2+ | activates | Mus musculus | |
Mg2+ | required | Mus musculus |
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 | - |
? | |
ATP + 1D-myo-inositol 1,4,5-trisphosphate | Mus musculus C57BL/6N | - |
ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | Q8R071 | gene Itpka | - |
Mus musculus C57BL/6N | Q8R071 | gene Itpka | - |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
forebrain | enzyme expression is highly enriched in the central nucleus of the amygdala | Mus musculus | - |
hippocampus | - |
Mus musculus | - |
neuron | isozyme IP3K-A is enriched in dendritic spines of mature neurons | Mus musculus | - |
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 | - |
? | |
ATP + 1D-myo-inositol 1,4,5-trisphosphate | - |
Mus musculus C57BL/6N | ADP + 1D-myo-inositol 1,3,4,5-tetrakisphosphate | - |
? |
Synonyms | Comment | Organism |
---|---|---|
inositol 1,4,5-trisphosphate 3-kinase A | - |
Mus musculus |
IP3K-A | - |
Mus musculus |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
ATP | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
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 | Mus musculus |
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 | Mus musculus |
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 | Mus musculus |