期刊
CELL CYCLE
卷 4, 期 10, 页码 1309-1312出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.4.10.2062
关键词
phosphoinositide 3-kinase; p85; p110; PTEN; intestinal polyps
类别
资金
- NCI NIH HHS [P01-CA089021] Funding Source: Medline
- NIGMS NIH HHS [R01 GM041890] Funding Source: Medline
The phosphoinositide 3-kinase (PI3K) signaling pathway critically regulates cell growth and cell survival. Mutations that lead to aberrant activation of this pathway are frequent events in human cancers. Here we discuss some recent studies identifying the mechanisms by which p85, the regulatory subunit of PI3K, negatively regulates PI3K signaling. While necessary for the stability and membrane recruitment of the p110 catalytic subunit of PI3K. p85 represses the basal activity of p110 in the absence of growth factor stimulation. In its unbound, free form, p85 sequesters the adaptor protein IRS-1 and therefore limits the extent of PI3K signaling downstream of the insulin and IGF-1 receptors. These findings lend new insight to how changes in p85 gene dosage or mutations in p85 could lead to the hyper-activation of PI3K and thus contribute towards tumorigenesis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据