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Titolo:
The protein kinase PKB/Akt regulates cell survival and apoptosis by inhibiting Bax conformational change
Autore:
Yamaguchi, H; Wang, HG;
Indirizzi:
Univ S Florida, Coll Med, H Lee Moffit Canc Ctr & Res Inst, Drug DiscoveryProgram,Dept Interdisciplinary Onc, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 erdisciplinary Onc, Tampa, FL 33612 USA Univ S Florida, Coll Med, Dept Pharmacol & Therapeut, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 rmacol & Therapeut, Tampa, FL 33612 USA
Titolo Testata:
ONCOGENE
fascicolo: 53, volume: 20, anno: 2001,
pagine: 7779 - 7786
SICI:
0950-9232(20011122)20:53<7779:TPKPRC>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYTOCHROME-C RELEASE; BCL-2 FAMILY PROTEINS; NF-KAPPA-B; DEATH; MITOCHONDRIA; AKT; ACTIVATION; TRANSLOCATION; PHOSPHORYLATION; MEMBERS;
Keywords:
IL-3; Akt; Bax conformational change; apoptosis; mitochondria;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, HG Univ S Florida, Coll Med, H Lee Moffit Canc Ctr & Res Inst, Drug DiscoveryProgram,Dept Interdisciplinary Onc, 12902 Magnolia Dr, Tampa, FL 33612 USA Univ S Florida 12902 Magnolia Dr Tampa FL USA 33612 FL 33612 USA
Citazione:
H. Yamaguchi e H.G. Wang, "The protein kinase PKB/Akt regulates cell survival and apoptosis by inhibiting Bax conformational change", ONCOGENE, 20(53), 2001, pp. 7779-7786

Abstract

The serine-threonine kinase Akt exerts its anti-apoptotic effects through several downstream targets, including the pro-apoptotic Bcl-2 family memberBad, Forkhead transcription factors, and the cyclic AMT response element-binding protein (CREB). In this report we demonstrate that Akt inhibits a conformational change in the pro-apoptotic Bax protein and its translocation to mitochondria, thus preventing the disruption of the mitochondrial inner membrane potential (Delta psi (m)), caspase-3 activation, and apoptosis in pre-B hematopoietic cells FL5.12 following interleukin-3 (IL-3) withdrawal. Inhibition of PI-3 kinase, but not MAPK kinase, promotes this conformational change in Bax. Moreover, overexpression of Akt suppresses the relocalization of GFP-Bax to mitochondria and apoptosis in Hela cells induced by the DNA-damaging agent methyl methanesulphonate. However, Akt does not abolish the ability of a conformationally changed Bax mutant, GFP-Bax (Delta S184),to translocate to mitochondria and to induce apoptosis. These findings indicate that Akt exerts its anti-apoptotic effects in cells at a premitochondrial stage, at least in part, by inhibiting Bax conformational change and its redistribution to the mitochondrial membranes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 20:50:42