The role of calcium in the regulation of apoptosis

Research output: Contribution to journalArticle

Abstract

The recognition that apoptosis is regulated by an evolutionarily conserved set of polypeptides from the nematode Caenorhabditis elegans to humans suggests that a conserved set of biochemical mechanism(s) may also be involved in the response. Early evidence suggested that the endogenous endonuclease implicated in apoptosis in most model systems is Ca2+- dependent, and subsequent work from a number of independent laboratories suggests that alterations in cytosolic Ca2+ homeostasis are one of the conserved biochemical pathways regulating the response. Molecular targets for Ca2+ are now being identified and include signal transduction intermediates, endonuclease(s) and proteases, and the enzymes involved in the maintenance of phospholipid asymmetry in the plasma membrane. Furthermore, interesting preliminary work suggests that BCL-2 suppresses apoptosis via a mechanism that is linked to intracellular Ca2+ compartmentalization, and it appears that Ca2+ alterations in some examples of apoptosis occur as the result of changes within the mitochondria. This review will summarize what is known about the role of Ca2+ in the regulation of apoptosis and discuss how Ca2+ might interact with some of the other biochemical signals implicated in cell death.

Original languageEnglish (US)
Pages (from-to)777-794
Number of pages18
JournalScanning Microscopy
Volume10
Issue number3
StatePublished - 1996
Externally publishedYes

Fingerprint

apoptosis
Cell death
calcium
Calcium
homeostasis
protease
mitochondria
polypeptides
Signal transduction
Mitochondria
death
Polypeptides
Phospholipids
maintenance
Cell membranes
enzymes
asymmetry
membranes
Enzymes

Keywords

  • Apoptosis
  • BCL-2
  • Calcium
  • Endonuclease
  • Oxidative stress

ASJC Scopus subject areas

  • Instrumentation

Cite this

The role of calcium in the regulation of apoptosis. / McConkey, David.

In: Scanning Microscopy, Vol. 10, No. 3, 1996, p. 777-794.

Research output: Contribution to journalArticle

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