Phosphoinositide 3-Kinase beta, p110 beta, p85 alpha, Recombinant, Human (PI3K)

The PI3K isoform can be activated by insulin via the insulin receptor to initiate a cascade of events that control cell growth and metabolism. The activation of PI3K is mediated by the p85 regulatory subunit binding to tyrosine phosphorylated insulin receptor substrate (IRS) proteins (e.g. IRS-1 and IRS-2). It was also shown that PI3K is involved in apoptosis in human colon carcinoma cells. Injection of neutralizing antibodies specific to p110 in WiDr, HCT116 and CO\n115 adenocarcinoma cells inhibited de novo DNA synthesis PI3K is the major PI3K isoform required for apoptotic cell and Fc-receptor mediated phagocytosis shown for primary mouse macrophages and the Jurkat human leukemia T cell line. It was shown by several research groups that the catalytic subunit of PI3K can be activated by G subunits of G-protein coupled receptors.\n\nPhosphoinositide 3-kinases (PI3Ks) phosphorylate phosphatidylinositols (PIs) at their 3

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SPECIFICATIONS

Catalog Number

P4073-33D

Size

10ug

Form

Supplied as a liquid in 10mM Hepes, pH 8.0, 100mM sodium chloride, 0.5mM MgCl2, and 10% glycerol.

Purity

(same/more than) 90% by SDS-PAGE

References

1.Foster et al. . J. Cell Science 116:3037. (2003).2. Yin et al.Nature 391:707. (1998).3. Shepherd et al. Journal of Molecular Endocrinolgy 17:175.(1996).4. Sayama et al. J. Biol. Chem. 277:40390.(2002).5. Cantrell, D.A.. J. Cell Sci. 114:1439.(2001).6. Yart et al. J. Biol. Chem. 277:21167.(2002).7.Benistant et al. Oncogene 19:5083.(2000)8.Leverrier et al. J. Biol. Chem. 278:38437.(2003).9. Murga et al. Akt. J. Biol. Chem. 275:12069.(2000).10. Maier et al. J.Biol. Chem. 274:29311.(1999).