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

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 (<FONT FACE=Symbol>Dy</FONT>m). The collapse of <FONT FACE=Symbol>Dy</FONT>m 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.

Bibliographic Details

Main Authors:	Smaili,S.S., Hsu,Y.-T., Carvalho,A.C.P., Rosenstock,T.R., Sharpe,J.C., Youle,R.J.
Format:	Digital revista
Language:	English
Published:	Associação Brasileira de Divulgação Científica 2003
Online Access:	http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003000200004
Tags:	Add Tag No Tags, Be the first to tag this record!