Oncogenic activity of the regulatory subunit p85β of phosphatidylinositol 3-kinase (PI3K).
Expression of the regulatory subunit p85β of PI3K induces oncogenic transformation of primary avian fibroblasts. The transformed cells proliferate at an increased rate compared with nontransformed controls and show elevated levels of PI3K signaling. The oncogenic activity of p85β requires an active PI3K-TOR signaling cascade and is mediated by the p110α and p110β isoforms of the PI3K catalytic subunit. The data suggest that p85β is a less effective inhibitor of the PI3K catalytic subunit than p85α and that this reduced level of p110 inhibition accounts for the oncogenic activity of p85β.
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037.
Yoshihiro
Y
Ito
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037.
Jonathan R
JR
Hart
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037.
Lynn
L
Ueno
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037 pkvogt@scripps.edu.
Peter K
PK
Vogt
D000818:Animals; D002471:Cell Transformation, Neoplastic; D002642:Chick Embryo; D009857:Oncogenes; D058539:Phosphatidylinositol 3-Kinase / Q000737:chemistry / Q000378:metabolism*; D015398:Signal Transduction
D058539:Phosphatidylinositol 3-Kinase
SH2 domain; inter-SH2 domain; protein–protein interaction