Critical roles of Rictor/Sin1complexes in IFN-dependent Stat activation and generation of antiproliferative responses
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ABSTRACT: We provide evidence that IFN-induced Stat-activation is defective in cells with targeted disruption of the Rictor gene, whose protein product is a key element of mTOR complex 2 (mTORC2). Our studies show that transient or stable knockdown of Rictor leads to decreased expression of several IFN-inducible genes that mediate important biological functions, including antiproliferative and pro-apoptotic responses. Rictor+/+ and Rictor-/- MEFs were treated with 2500 U/ml of mouse IFNα for 24 hours
ORGANISM(S): Mus musculus
SUBMITTER: Raffaele Calogero
PROVIDER: E-GEOD-47896 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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