Mitochondria, calcium and pro-apoptotic proteins as mediators in cell death signaling
Braz. j. med. biol. res
;
36(2): 183-190, Feb. 2003. ilus
Article
in English
| 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
Full text:
Available
Index:
LILACS (Americas)
Main subject:
Lymphokines
/
Apoptosis
/
Proto-Oncogene Proteins c-bcl-2
/
Calcium Signaling
/
Mitochondria
Limits:
Animals
Language:
English
Journal:
Braz. j. med. biol. res
Journal subject:
Biology
/
Medicine
Year:
2003
Type:
Article
Affiliation country:
Brazil
/
United States
Institution/Affiliation country:
National Institutes of Health/US
/
Universidade Federal de São Paulo/BR
/
University of Southern Carolina/US
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