The beta identity of class I PtdIns3K: A positive role of p110beta in autophagy revealed.
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Autophagy is critically controlled by phosphatidylinositol 3-kinases (PtdIns3Ks). The common understanding for mammalian autophagy is that class I PtdIns3Ks inhibit autophagy by activating the Akt-TOR kinase cascade, whereas the class III PtdIns3K (Vps34) promotes autophagy by generating the phospholipid PtdIns(3)P. However, direct genetic evidence for a role of class I PtdIns3Ks in autophagy has been lacking. Using mice with a conditional deletion of the class I PtdIns3K catalytic subunit isoform p110alpha or p110beta, we revealed an unexpected function of p110beta as a positive regulator of autophagy. (+info)
Cell-to-cell variability in PI3K protein level regulates PI3K-AKT pathway activity in cell populations.
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G-protein alpha-s and -12 subunits are involved in androgen-stimulated PI3K activation and androgen receptor transactivation in prostate cancer cells.
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A beta version of life: p110beta takes center stage.
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The PI3K pathway is frequently activated in tumors, most commonly through p110alpha mutation or PTEN deletion. In contrast to p110alpha, p110beta is oncogenic when over-expressed in the wild-type state, suggesting that its regulation by p85 is different than that of p110alpha. In this perspective, we summarize recent data concerning the regulation of p110beta, which shows that wild-type p110beta acts like an oncogenic mutant of p110alpha. We also discuss the significance of this altered regulation in tumor models of PTEN deletion, as well as the potential implications of the unique p110beta regulation on GPCR-driven tumorigenesis. (+info)
p85alpha regulates osteoblast differentiation by cross-talking with the MAPK pathway.
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