EC Number   |
General Information |
Reference |
|---|
   2.7.1.127 | evolution |
a member of the inositol 1,4,5-trisphosphate 3-kinases family |
737403 |
| 2.7.1.127 | evolution |
enzyme IP3 3-kinase 2 (IP3K2) is a member of the inositol polyphosphate kinase gene family |
761191 |
| 2.7.1.127 | 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 |
760316 |
| 2.7.1.127 | 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 |
737402 |
| 2.7.1.127 | malfunction |
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 |
700975 |
| 2.7.1.127 | 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 |
760540 |
| 2.7.1.127 | malfunction |
enzyme knock-out mice show deficits of synaptic plasticity in perforant path and in hippocampal-dependent memory performances |
699694 |
| 2.7.1.127 | 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 |
-, 762412 |
| 2.7.1.127 | 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 |
-, 739679 |
| 2.7.1.127 | malfunction |
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 |
699348 |
