Bim: a novel member of the Bcl-2 family that promotes apoptosis
- Author(s)
- O'Connor, L; Strasser, A; O'Reilly, LA; Hausmann, G; Adams, JM; Cory, S; Huang, DCS;
- Details
- Publication Year 1998-01-15,Volume 17,Issue #2,Page 384-395
- Journal Title
- EMBO JOURNAL
- Publication Type
- Journal Article
- Abstract
- Certain members of the Bcl-2 family inhibit apoptosis while others facilitate this physiological process of cell death, An expression screen for proteins that bind to Bcl-2 yielded a small novel protein, denoted Bim, whose only similarity to any known protein is the short (nine amino acid) BH3 motif shared by most Bcl-2 homologues. Bim provokes apoptosis, and the BH3 region is required for Bcl-2 binding and for most of its cytotoxicity. Like Bcl-2, Bim possesses a hydrophobic C-terminus and localizes to intracytoplasmic membranes, Three Bim isoforms, probably generated by alternative splicing, all induce apoptosis, the shortest being the most potent, Wild-type Bcl-2 associates with Bim in vivo and modulates its death function, whereas Bcl-2 mutants that lack survival function do neither, Significantly, Bcl-x(L) and Bcl-w, the two closest homologues of Bcl-2, also bind to Bim and inhibit its activity, but more distant viral homologues, adenovirus E1B19K and Epstein-Barr virus BHRF-1, can do neither, Hence, Bim appears to act as a 'death ligand' which can only neutralize certain members of the pro-survival Bcl-2 sub-family.
- Publisher
- OXFORD UNIV PRESS
- Keywords
- PROGRAMMED CELL-DEATH; CAENORHABDITIS-ELEGANS; PROTEIN IDENTIFICATION; ENDOPLASMIC-RETICULUM; SEQUENCE SIMILARITY; CONSERVED DOMAINS; NUCLEAR-ENVELOPE; HOMOLOG BAK; E1B 19K; B-CELLS
- Publisher's Version
- https://doi.org/10.1093/emboj/17.2.384
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1998-01-15 12:00:00