Publication Date:
1998-08-28
Description:
A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins. The different signals that converge on mitochondria to trigger or inhibit these events and their downstream effects delineate several major pathways in physiological cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, D R -- Reed, J C -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1309-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9721092" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
*Apoptosis
;
Cysteine Endopeptidases/metabolism
;
Cytochrome c Group/metabolism
;
Electron Transport
;
Humans
;
Intracellular Membranes/metabolism
;
Ion Channels/metabolism
;
Membrane Potentials
;
Mitochondria/*metabolism
;
Oxidation-Reduction
;
Permeability
;
Proto-Oncogene Proteins c-bcl-2/metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
