| Literature DB >> 31211243 |
Yanqiong Zhang1,2, H Shelton Earp1,3, Pengda Liu1,2.
Abstract
Canonically the oncogenic kinase AKT is activated by growth signals. Our work suggests apoptotic materials, abundant in tumors, also contribute to AKT activation by stimulating MERTK that in turn phosphorylates Y26 in the AKT PH domain. pY26 reverses binding of an AKT endogenous, WW-domain containing inhibitor, SAV1, allowing AKT responsiveness to classic growth signals. This novel mechanism may contribute to drug resistance.Entities:
Keywords: Akt; Kidney cancer; MERTK; SAV1; drug resistance
Year: 2019 PMID: 31211243 PMCID: PMC6548477 DOI: 10.1080/23723556.2019.1611161
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556