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Titolo:
p70S6 kinase signals cell survival as well as growth, inactivating the pro-apoptotic molecule BAD
Autore:
Harada, H; Andersen, JS; Mann, M; Terada, N; Korsmeyer, SJ;
Indirizzi:
Harvard Univ, Sch Med, Howard Hughes Med Inst, Dana Farber Canc Inst,Dept Pathol, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 c Inst,Dept Pathol, Boston, MA 02115 USA Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA Harvard Univ BostonMA USA 02115 Sch Med, Dept Med, Boston, MA 02115 USA Univ Florida, Dept Pathol, Gainesville, FL 32610 USA Univ Florida Gainesville FL USA 32610 t Pathol, Gainesville, FL 32610 USA Univ So Denmark, Dept Biochem & Mol Biol, DK-5230 Odense, Denmark Univ So Denmark Odense Denmark DK-5230 Mol Biol, DK-5230 Odense, Denmark
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 17, volume: 98, anno: 2001,
pagine: 9666 - 9670
SICI:
0027-8424(20010814)98:17<9666:PKSCSA>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT PROTEIN-KINASE; DEATH AGONIST BAD; BCL-X-L; BH3 DOMAIN; S6 KINASE; PHOSPHORYLATION; RAPAMYCIN; MITOCHONDRIA; RIBOSOME; BINDING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Korsmeyer, SJ Harvard Univ, Sch Med, Howard Hughes Med Inst, Dana Farber Canc Inst,Dept Pathol, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 thol, Boston, MA 02115 USA
Citazione:
H. Harada et al., "p70S6 kinase signals cell survival as well as growth, inactivating the pro-apoptotic molecule BAD", P NAS US, 98(17), 2001, pp. 9666-9670

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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 00:07:51