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Titolo:
Proapoptotic BAX and BAK: A requisite gateway to mitochondrial dysfunctionand death
Autore:
Wei, MC; Zong, WX; Cheng, EHY; Lindsten, T; Panoutsakopoulou, V; Ross, AJ; Roth, KA; MacCregor, GR; Thompson, CB; Korsmeyer, SJ;
Indirizzi:
Univ Penn, Abramson Family Canc Res Inst, Dept Med, Philadelphia, PA 19104USA Univ Penn Philadelphia PA USA 19104 , Dept Med, Philadelphia, PA 19104USA Univ Penn, Abramson Family Canc Res Inst, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 & Lab Med, Philadelphia, PA 19104 USA Harvard Univ, Brigham & Womens Hosp, Sch Med,Dana Farber Canc Inst, Dept Pathol,Howard Huges Med Inst, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 ard Huges Med Inst, Boston, MA 02115 USA Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Dana Farber Canc Inst, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 a Farber Canc Inst, Boston, MA 02115 USA Washington Univ, Sch Med, Div Biol & Biomed Sci, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Biomed Sci, St Louis, MO 63110 USA Emory Univ, Sch Med, Ctr Mol Med, Atlanta, GA 30322 USA Emory Univ Atlanta GA USA 30322 h Med, Ctr Mol Med, Atlanta, GA 30322 USA Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Pathol, St Louis, MO 63110 USA
Titolo Testata:
SCIENCE
fascicolo: 5517, volume: 292, anno: 2001,
pagine: 727 - 730
SICI:
0036-8075(20010427)292:5517<727:PBABAR>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
BCL-2 FAMILY MEMBERS; CYTOCHROME-C RELEASE; ENDOPLASMIC-RETICULUM; CELL-DEATH; APOPTOTIC PATHWAYS; PROTEIN; ACTIVATION; MEMBRANE; CASPASE-9; SURVIVAL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Physical, Chemical & Earth Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Thompson, CB Univ Penn, Abramson Family Canc Res Inst, Dept Med, Philadelphia, PA 19104USA Univ Penn Philadelphia PA USA 19104 hiladelphia, PA 19104USA
Citazione:
M.C. Wei et al., "Proapoptotic BAX and BAK: A requisite gateway to mitochondrial dysfunctionand death", SCIENCE, 292(5517), 2001, pp. 727-730

Abstract

Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. We find that cells lacking both Bax and Bak, but not cellslacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis. Moreover, doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin. Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 21:24:09