anti-Inositol-Trisphosphate 3-Kinase A (ITPKA) Antibodies

Mouse (Murine) Inositol-Trisphosphate 3-Kinase A (ITPKA) interaction partners

1. Thisstudy shows that overexpressed IP3-kinase 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.

2. 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.

3. At synapses of Inositol-1,4,5-trisphosphate 3-kinase-A deficient neurons the levels of Ins(1,4,5)P3-5-phosphatase (inpp5a) and sarcoplasmic/endoplasmic reticulum calcium ATPase pump-2b (serca2b) were increased.

4. 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.

5. These data show that the absence of expression of the three isoenzymes of Itpk does not prevent the formation of IP5 and IP6, at least in mouse embryonic fibroblasts.[Itpka, Itpkb, Itpkc]

6. 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 scaffolding mechanism.

Human Inositol-Trisphosphate 3-Kinase A (ITPKA) interaction partners

1. IP3K-A binds to EB3 and their binding affinity is precisely regulated by protein kinase A (PKA)-dependent phosphorylation of IP3K-A at Ser119 (pSer119). The complex of IP3K-A and EB3 dissociates and reassociates rapidly during chemically induced LTP.

2. ITPKA is a potential oncogene that it is overexpressed in most tumors, and its overexpression promotes tumorigenesis; ITPKA gene body methylation regulates its expression and serves as a novel and potential biomarker for early cancer detection

3. Our data indicated that ITPKA expression was significantly up-regulated in hepatocellular carcinoma and could serve as a potential novel prognostic biomarker

4. describe the crystal structure of the complex between human Ca2+/CaM and the CaM-binding region of human IP3-3K isoform A (residues 158-183)

5. we conclude that the observed expression of ITPKA early in tumor development increases the metastatic potential of lung adenocarcinoma cells.

6. 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.

7. results highlight the potential role of the three isoforms of InsP3 3-kinase as direct InsP3 metabolizing enzymes and direct regulators of Ca2+ responses to extracellular signals

8. We report the structure of an IPK, the human Ins(1,4,5)P3 3-kinase-A, both free and in complexes with substrates and products.

9. 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.

10. the morphological changes induced by IP3K-A are mediated by non-enzymatic activities of the protein.