Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling
Braz. j. med. biol. res
;
36(2): 183-190, Feb. 2003. ilus
Artigo
em Inglês
| LILACS
| ID: lil-326426
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 (FACE="Symbol">Dym). The collapse of FACE="Symbol">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
Texto completo:
DisponíveL
Índice:
LILACS (Américas)
Assunto principal:
Linfocinas
/
Apoptose
/
Proteínas Proto-Oncogênicas c-bcl-2
/
Sinalização do Cálcio
/
Mitocôndrias
Limite:
Animais
Idioma:
Inglês
Revista:
Braz. j. med. biol. res
Assunto da revista:
Biologia
/
Medicina
Ano de publicação:
2003
Tipo de documento:
Artigo
País de afiliação:
Brasil
/
Estados Unidos
Instituição/País de afiliação:
National Institutes of Health/US
/
Universidade Federal de São Paulo/BR
/
University of Southern Carolina/US
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