Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Bax translocation to mitochondria subsequent to a rapid loss of mitochondrial membrane potential
Autore:
Smaili, SS; Hsu, YT; Sanders, KM; Russel, JT; Youle, RJ;
Indirizzi:
NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA NINDS Bethesda MD USA 20892 rg Neurol Branch, NIH, Bethesda, MD 20892 USA Univ Fed Sao Paulo, Dept Farmacol, Sao Paulo, Brazil Univ Fed Sao Paulo Sao Paulo Brazil o, Dept Farmacol, Sao Paulo, Brazil NICHHD, Lab Cellular & Mol Neurophysiol, NIH, Bethesda, MD 20892 USA NICHHD Bethesda MD USA 20892 ol Neurophysiol, NIH, Bethesda, MD 20892 USA Med Univ S Carolina, Charleston, SC 29425 USA Med Univ S Carolina Charleston SC USA 29425 ina, Charleston, SC 29425 USA
Titolo Testata:
CELL DEATH AND DIFFERENTIATION
fascicolo: 9, volume: 8, anno: 2001,
pagine: 909 - 920
SICI:
1350-9047(200109)8:9<909:BTTMST>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
CYTOCHROME-C RELEASE; PERMEABILITY TRANSITION PORE; PROGRAMMED CELL-DEATH; BCL-X-L; INDUCED CASPASE ACTIVATION; PROAPOPTOTIC PROTEIN BAX; CHANNEL-FORMING ACTIVITY; IN-VIVO; MAMMALIAN-CELLS; DEFICIENT MICE;
Keywords:
mitochondria; Bax; mitochondrial membrane potential; mitochondrial inhibitors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Youle, RJ NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892USA NINDS Bethesda MD USA 20892 Branch, NIH, Bethesda, MD 20892 USA
Citazione:
S.S. Smaili et al., "Bax translocation to mitochondria subsequent to a rapid loss of mitochondrial membrane potential", CELL DEAT D, 8(9), 2001, pp. 909-920

Abstract

Bax, a pro-apoptotic member of the Bcl-2 family, is a cytosolic protein that inserts into mitochondrial membranes upon induction of cell death. Usingthe green fluorescent protein fused to Bax (GFP-Bax) to quantitate mitochondrial binding in living cells we have investigated the cause of Bax association with mitochondria and the time course relative to endogenous and induced changes in mitochondrial membrane potential (Delta Psi (m)). We have found that staurosporine (STS) induces a loss in Delta Psi (m) before GFP-Baxtranslocation can be measured. The onset of the Delta Psi (m) loss is followed by a rapid and complete collapse of Delta Psi (m) which is followed byBax association with mitochondria. The mitochondria uncoupler FCCP, in thepresence of the F-1-F-0 ATPase inhibitor oligomycin, can trigger Bax translocation to mitochondria suggesting that when ATP levels are maintained a collapse of Delta Psi (m) induces Bax translocation. Neither FCCP nor oligomycin alone alters Bax location. Bax association with mitochondria is also triggered by inhibitors of the electron transport chain, antimycin and rotenone, compounds that collapse Delta Psi (m) without inducing rapid ATP hydrolysis that typically occurs with uncouplers such as FCCP. Taken together, our results suggest that alterations in mitochondrial energization associated with apoptosis can initiate Bax docking to mitochondria.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 01:34:59