p85beta deficiency does not alter NK cell differentiation and maturation in spleen or bone marrow. NK cells from p85beta(-/-) mice nonetheless produced more IFN-gamma and degranulated more effectively when stimulated with anti-NKG2D antibody. p85beta deficiency impaired NKG2D internalization which could contribute to the activated phenotype.
Activation of PI3K (p110beta and p85beta) and phospho-AKT (Ser473) participated in the regulation of activating macrophages by wear particles ultimately resulting in the secretion of TNF-alpha.
miR-126-mediated phosphoinositide-3-kinase regulation not only fine-tunes VEGF-signaling but it strongly enhances the activities of Ang-1 on vessel stabilization and maturation.
study shows that p110beta nuclear localization signal and p85beta nuclear export sequence regulate p85beta/p110beta nuclear localization supporting the idea that nuclear but not cytoplasmic p110beta controls cell survival
These results indicate that the p85beta regulatory isoform has partially overlapping functions with p85alpha in B cells as well as a unique role in opposing BCR responses.
Data show that mesothelin is a potential target in reducing resistance to cytotoxic drugs and mesothelin-treated cells revealed rapid tyrosine phosphorylation of the p85 subunit of PI3K.
Complete loss of all PI3K regulatory subunits caused acute embryonic lethality at E11.5 due to hemorrhaging whereas retention of a single p85alpha allele yielded viable mice that survived to adulthood
PI3K activity is required for PMA-induced colocalization between AFAP-110 and cSrc and subsequent cSrc activation and this signaling pathway promotes cell migration.
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