Anti-PI3K (p85 beta)

0.5mg/ml if reconstituted with 0.2ml sterile DI water. Phosphatidylinositol 3-kinase regulatory subunit 2, also called p85-Beta, PIK3R2 and PIK3, is an enzyme that in humans is encoded by the PIK3R2 gene. The NS1 protein from various influenza strains bind p85-beta, but not p85-alpha. Binding of p85-beta and activation of PI3K required tyr89 of NS1, and mutant viruses expressing NS1 with a tyr89-to-phe substitution grew more slowly in cell culture than wildtype viruses. Using mouse embryonic fibroblasts, Park et al. showed that, in addition to regulating PI3K function, p85-alpha/beta regulated the function of Xbp1s, a transcription factor that orchestrates the unfolded protein response (UPR) following endoplasmic reticulum (ER) stress. Overexpression of the protein in livers of ob/ob mice increased glucose tolerance and reduced blood glucose concentrations. Protein function: Regulatory subunit of phosphoinositide-3-kinase (PI3K), a kinase that phosphorylates PtdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5- trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Binds to activated (phosphorylated) protein-tyrosine kinases, through its SH2 domain, and acts as an adapter, mediating the association of the p110 catalytic unit to the plasma membrane. Indirectly regulates autophagy (PubMed:23604317). Promotes nuclear translocation of XBP1 isoform 2 in a ER stress- and/or insulin- dependent manner during metabolic overloading in the liver and hence plays a role in glucose tolerance improvement. [The UniProt Consortium]