4.8 Article

Small GTPases and tyrosine kinases coregulate a molecular switch in the phosphoinositide 3-kinase regulatory subunit

Journal

CANCER CELL
Volume 1, Issue 2, Pages 181-191

Publisher

CELL PRESS
DOI: 10.1016/S1535-6108(02)00033-8

Keywords

-

Funding

  1. NATIONAL CANCER INSTITUTE [R01CA081008, T32CA078207, R01CA057436] Funding Source: NIH RePORTER
  2. NCI NIH HHS [R01CA57436, T32CA078207, R01CA81008] Funding Source: Medline

Ask authors/readers for more resources

Phosphoinositide 3-kinase (PI3K) type IA is a heterodimer of a catalytic subunit, p110, and a regulatory subunit, p85. Here we show that p85 contains a GTPase-responsive domain and an inhibitory domain, which together form a molecular switch that regulates PI3K. H-Ras and Rac1 activate PI3K by targeting the GTPase-responsive domain. The stimulatory effect of these molecules, however, is blocked by the inhibitory domain, which functions by binding to tyrosine-phosphorylated molecules and is neutralized by tyrosine phosphorylation. The complementary effects of tyrosine kinases and small GTPases on the p85 molecular switch result in synergy between these two classes of molecules toward the activation of the PI3K/Akt pathway.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.8
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available