MODULATION OF APOPTOSIS BY THE WIDELY DISTRIBUTED BCL-2 HOMOLOG BAK

Citation
Mc. Kiefer et al., MODULATION OF APOPTOSIS BY THE WIDELY DISTRIBUTED BCL-2 HOMOLOG BAK, Nature, 374(6524), 1995, pp. 736-739
Citations number
19
Categorie Soggetti
Multidisciplinary Sciences
Journal title
NatureACNP
ISSN journal
00280836
Volume
374
Issue
6524
Year of publication
1995
Pages
736 - 739
Database
ISI
SICI code
0028-0836(1995)374:6524<736:MOABTW>2.0.ZU;2-O
Abstract
MEMBERS Of the Bcl-2 family of proteins are characterized by their abi lity to modulate cell death, Bcl-2 and some of its homologues inhibit apoptosis(1-4), whereas other family members, such as Bax, will accele rate apoptosis under certain conditions(5). Here we describe the ident ification and characterization of a complementary DNA that encodes a p reviously unknown Bcl-2 homologue designated Bak, Like Bax, the bak ge ne product primarily enhances apoptotic cell death following an approp riate stimulus, Unlike Bar, however, Bak can inhibit cell death in an Epstein-Barr-virus-transformed cell line. The widespread tissue distri bution of Bak messenger RNA, including those containing long-lived, te rminally differentiated cell types, suggests that cell-death-inducing activity is broadly distributed, and that tissue-specific modulation o f apoptosis is controlled primarily by regulation of molecules that in hibit apoptosis.