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Regulates inositol phosphate metabolism by phosphorylation of second messenger inositol 1,4,5-trisphosphate to Ins(1,3,4,5)P4. Zusätzlich bieten wir Ihnen ITPKA Proteine (4) und ITPKA Kits (1) und viele weitere Produktgruppen zu diesem Protein an.
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Findings demonstrate that IP3K-A plays an important role in regulating affective states by modulating metabotropic receptor signaling pathways and neural activity in the amygdala.
At synapses of Inositol-1,4,5-trisphosphate 3-kinase-A deficient neurons the levels of Ins (zeige INS Antikörper)(1,4,5)P3-5-phosphatase (inpp5a (zeige INPP5A Antikörper)) and sarcoplasmic/endoplasmic reticulum calcium ATPase (zeige CA-P60A Antikörper) pump-2b (serca2b (zeige ATP2A2 Antikörper)) were increased.
Inositol 1,4,5-trisphosphate 3-kinase-A is a new cell motility-promoting protein that increases the metastatic potential of tumor cells by two functional activities.
These data show that the absence of expression of the three isoenzymes of Itpk does not prevent the formation of IP5 and IP6 (zeige GPRIN2 Antikörper), at least in mouse embryonic fibroblasts.[Itpka, Itpkb (zeige ITPKB Antikörper), Itpkc (zeige ITPKC Antikörper)]
Inositol 1,4,5-trisphosphate 3-kinase A is critical for spatial and temporal regulation of spine actin remodeling, synaptic plasticity, and learning and memory via an activity-dependent Rac (zeige AKT1 Antikörper) scaffolding mechanism.
Our data indicated that ITPKA expression was significantly up-regulated in hepatocellular carcinoma and could serve as a potential novel prognostic biomarker
describe the crystal structure of the complex between human Ca2 (zeige CA2 Antikörper)+/CaM (zeige CALM1 Antikörper) and the CaM (zeige CALM1 Antikörper)-binding region of human IP3-3K isoform A (residues 158-183)
we conclude that the observed expression of ITPKA early in tumor development increases the metastatic potential of lung adenocarcinoma cells.
results highlight the potential role of the three isoforms of InsP3 3-kinase as direct InsP3 metabolizing enzymes and direct regulators of Ca2 (zeige CA2 Antikörper)+ responses to extracellular signals
We report the structure of an IPK, the human Ins (zeige INS Antikörper)(1,4,5)P3 3-kinase-A, both free and in complexes with substrates and products.
Data suggest that ITPKA may be related to carcinogenesis by the modulation of inositol polyphosphates and Ca2+ homeostasis and that ITPKA may be a potential novel molecular target and biomarker.
the morphological changes induced by IP3K-A are mediated by non-enzymatic activities of the protein.
Regulates inositol phosphate metabolism by phosphorylation of second messenger inositol 1,4,5-trisphosphate to Ins(1,3,4,5)P4. The activity of the inositol 1,4,5-trisphosphate 3-kinase is responsible for regulating the levels of a large number of inositol polyphosphates that are important in cellular signaling. Both calcium/calmodulin and protein phosphorylation mechanisms control its activity. It is also a substrate for the cyclic AMP-dependent protein kinase, calcium/calmodulin- dependent protein kinase II, and protein kinase C in vitro.
1D-myo-inositol-trisphosphate 3-kinase A
, Inositol-trisphosphate 3-kinase A
, IP3 3-kinase A
, IP3-kinase A
, IP3K A
, inositol-trisphosphate 3-kinase A
, insP 3-kinase A
, inositol 1,4,5-trisphosphate 3-kinase A
, inositol 1,4,5-triphosphate 3-kinase
, inositol 145-triphosphate 3-kinase