Ontology highlight
ABSTRACT:
SUBMITTER: Zhang HH
PROVIDER: S-EPMC1880887 | biostudies-literature | 2006 Oct
REPOSITORIES: biostudies-literature
Zhang Hui H HH Lipovsky Alex I AI Dibble Christian C CC Sahin Mustafa M Manning Brendan D BD
Molecular cell 20061001 2
Feedback inhibition of the PI3K-Akt pathway by the mammalian target of rapamycin complex 1 (mTORC1) has emerged as an important signaling event in tumor syndromes, cancer, and insulin resistance. Cells lacking the tuberous sclerosis complex (TSC) gene products are a model for this feedback regulation. We find that, despite Akt attenuation, the Akt substrate GSK3 is constitutively phosphorylated in cells and tumors lacking TSC1 or TSC2. In these settings, GSK3 phosphorylation is sensitive to mTOR ...[more]