Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling
Braz. j. med. biol. res
;
36(2): 183-190, Feb. 2003. ilus
Artículo
en Inglés
| 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:
Disponible
Índice:
LILACS (Américas)
Asunto principal:
Linfocinas
/
Apoptosis
/
Proteínas Proto-Oncogénicas c-bcl-2
/
Señalización del Calcio
/
Mitocondrias
Límite:
Animales
Idioma:
Inglés
Revista:
Braz. j. med. biol. res
Asunto de la revista:
Biologia
/
Medicina
Año:
2003
Tipo del documento:
Artículo
País de afiliación:
Brasil
/
Estados Unidos
Institución/País de afiliación:
National Institutes of Health/US
/
Universidade Federal de São Paulo/BR
/
University of Southern Carolina/US
Similares
MEDLINE
...
LILACS
LIS