- Western blotting
Human, mouse and rat
The S472 antibody was generated using Ac-CRNLARAL(pS)TD-amide as the antigen.
150-200 mL at 1.5-3 mg/mL
PIKE-A is a ubiquitously expressed GTPase, which binds and enhances Akt kinase activity in a guanine nucleotide-dependent manner. PIKE-A is one of the components of CDK4 amplicon, which is amplified in numerous human cancers. PIKE-A itself overexpression alone can mediate cell transformation, proliferation and migration remain. PIKE-A is overexpressed in various human cancer samples, provokes NIH3T3 cell transformation and escalates U87MG glioblastoma invasion. Overexpression of wild-type PIKE-A enhances NIH3T3 and U87MG cell growth. Moreover, PIKE-A and its mutants also exhibit similar activities on U87MG cell survival and invasion, coupling to their catalytic effects on Akt activation. Interestingly, Akt feeds back and phosphorylates PIKE on S472 and further enhances its catalytic effect on Akt kinase activity. PIKE-A directly binds to UNC5B tumor suppressor and inhibits its pro-apoptotic activity. In addition, it strongly activates Akt, leading to p53 downregulation. UNC5B is also called p53RDL. UNC5B is tightly controlled by p53. Overexpression of PIKE-A substantially diminishes p53, resulting in UNC5B transcription suppression. Therefore, PIKE-A amplification might upregulate cancer cell survival by inhibiting UNC5B transciptionally and physical interaction.
Publication: PIKE-A phosphorylation by Akt enhances its cell survival function by interaction with UNC5B and suppression of UNC5B transcription. Submitted to PNAS.