| First Author | O'Connor L | Year | 1998 |
| Journal | EMBO J | Volume | 17 |
| Issue | 2 | Pages | 384-95 |
| PubMed ID | 9430630 | Mgi Jnum | J:45671 |
| Mgi Id | MGI:1195826 | Doi | 10.1093/emboj/17.2.384 |
| Citation | O'Connor L, et al. (1998) Bim: a novel member of the Bcl-2 family that promotes apoptosis. EMBO J 17(2):384-95 |
| abstractText | 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-xL 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. |
