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Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9666-70. Epub 2001 Aug 7.

p70S6 kinase signals cell survival as well as growth, inactivating the pro-apoptotic molecule BAD.

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  • 1Howard Hughes Medical Institute, Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.

Abstract

Cytokines often deliver simultaneous, yet distinct, cell growth and cell survival signals. The 70-kDa ribosomal protein S6 kinase (p70S6K) is known to regulate cell growth by inducing protein synthesis components. We purified membrane-based p70S6K as a kinase responsible for site-specific phosphorylation of BAD, which inactivates this proapoptotic molecule. Rapamycin inhibited mitochondrial-based p70S6K, which prevented phosphorylation of Ser-136 on BAD and blocked cell survival induced by insulin-like growth factor 1 (IGF-1). Moreover, IGF-1-induced phosphorylation of BAD Ser-136 was abolished in p70S6K-deficient cells. Thus, p70S6K is itself a dual pathway kinase, signaling cell survival as well as growth through differential substrates which include mitochondrial BAD and the ribosomal subunit S6, respectively.

PMID:
11493700
[PubMed - indexed for MEDLINE]
PMCID:
PMC55509
Free PMC Article
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