Bax translocation to mitochondria subsequent to a rapid loss of mitochondrial membrane potential

Bax translocation to mitochondria subsequent to a rapid loss of mitochondrial membrane potential

Autor Smaili, Soraya Soubhi Autor UNIFESP Google Scholar
Hsu, Y. T. Google Scholar
Sanders, K. M. Google Scholar
Russel, J. T. Google Scholar
Youle, R. J. Google Scholar
Instituição NINDS
Universidade Federal de São Paulo (UNIFESP)
Med Univ S Carolina
Resumo Bax, a pro-apoptotic member of the Bcl-2 family, is a cytosolic protein that inserts into mitochondrial membranes upon induction of cell death. Using the 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-Bax translocation 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 by Bax association with mitochondria. the mitochondria uncoupler FCCP, in the presence 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.
Assunto mitochondria
mitochondrial membrane potential
mitochondrial inhibitors
Idioma Inglês
Data 2001-09-01
Publicado em Cell Death and Differentiation. Basingstoke: Nature Publishing Group, v. 8, n. 9, p. 909-920, 2001.
ISSN 1350-9047 (Sherpa/Romeo, fator de impacto)
Editor Nature Publishing Group
Extensão 909-920
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000170472300005

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