Publication Date:
1998-09-12
Description:
Bcl-2 and related cytoplasmic proteins are key regulators of apoptosis, the cell suicide program critical for development, tissue homeostasis, and protection against pathogens. Those most similar to Bcl-2 promote cell survival by inhibiting adapters needed for activation of the proteases (caspases) that dismantle the cell. More distant relatives instead promote apoptosis, apparently through mechanisms that include displacing the adapters from the pro-survival proteins. Thus, for many but not all apoptotic signals, the balance between these competing activities determines cell fate. Bcl-2 family members are essential for maintenance of major organ systems, and mutations affecting them are implicated in cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adams, J M -- Cory, S -- CA43540/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1322-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735050" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
*Apoptosis
;
Cell Cycle
;
*Cell Survival
;
Cysteine Endopeptidases/metabolism
;
Cytokines/physiology
;
Genes, bcl-2
;
Humans
;
Neoplasms/etiology/pathology/therapy
;
Organelles/physiology
;
Proto-Oncogene Proteins c-bcl-2/chemistry/*physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
