Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling

Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling

Autor Smaili, Soraya Soubhi Autor UNIFESP Google Scholar
Hsu, Y.-t. Google Scholar
Carvalho, A.c.p. Autor UNIFESP Google Scholar
Rosenstock, T.r. Autor UNIFESP Google Scholar
Sharpe, J.c. Google Scholar
Youle, R.j. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
University of Southern Carolina Department of Biochemistry
National Institutes of Health NINDS Biochemistry Section
Resumo Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injury and programmed cell death through the regulation of a number of Ca2+-dependent enzymes such as phospholipases, proteases, and nucleases. Mitochondria along with the endoplasmic reticulum play pivotal roles in regulating intracellular Ca2+ content. Mitochondria are endowed with multiple Ca2+ transport mechanisms by which they take up and release Ca2+ across their inner membrane. During cellular Ca2+ overload, mitochondria take up cytosolic Ca2+, which in turn induces opening of permeability transition pores and disrupts the mitochondrial membrane potential (Dym). The collapse of Dym along with the release of cytochrome c from mitochondria is followed by the activation of caspases, nuclear fragmentation and cell death. Members of the Bcl-2 family are a group of proteins that play important roles in apoptosis regulation. Members of this family appear to differentially regulate intracellular Ca2+ level. Translocation of Bax, an apoptotic signaling protein, from the cytosol to the mitochondrial membrane is another step in this apoptosis signaling pathway.
Palavra-chave Ca2+
Mitochondrial Ca2+ uptake
Mitochondrial Ca2+ efflux
Permeability transition
Bcl-2 family
Bax and apoptosis
Idioma Inglês
Data de publicação 2003-02-01
Publicado em Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 36, n. 2, p. 183-190, 2003.
ISSN 0100-879X (Sherpa/Romeo, fator de impacto)
Publicador Associação Brasileira de Divulgação Científica
Extensão 183-190
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000181135700004
SciELO S0100-879X2003000200004 (estatísticas na SciELO)
Endereço permanente

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