| Literature DB >> 19962665 |
Bijay S Jaiswal1, Vasantharajan Janakiraman, Noelyn M Kljavin, Subhra Chaudhuri, Howard M Stern, Weiru Wang, Zhengyan Kan, Hashem A Dbouk, Brock A Peters, Paul Waring, Trisha Dela Vega, Denise M Kenski, Krista K Bowman, Maria Lorenzo, Hong Li, Jiansheng Wu, Zora Modrusan, Jeremy Stinson, Michael Eby, Peng Yue, Josh S Kaminker, Frederic J de Sauvage, Jonathan M Backer, Somasekar Seshagiri.
Abstract
Members of the mammalian phosphoinositide-3-OH kinase (PI3K) family of proteins are critical regulators of various cellular process including cell survival, growth, proliferation, and motility. Oncogenic activating mutations in the p110alpha catalytic subunit of the heterodimeric p110/p85 PI3K enzyme are frequent in human cancers. Here we show the presence of frequent mutations in p85alpha in colon cancer, a majority of which occurs in the inter-Src homology-2 (iSH2) domain. These mutations uncouple and retain p85alpha's p110-stabilizing activity, while abrogating its p110-inhibitory activity. The p85alpha mutants promote cell survival, AKT activation, anchorage-independent cell growth, and oncogenesis in a p110-dependent manner.Entities:
Mesh：
Substances：
Year: 2009 PMID： 19962665 PMCID： PMC2804903 DOI： 10.1016/j.ccr.2009.10.016
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743