Article
A common binding site mediates heterodimerization and homodimerization of Bcl-2 family members.
The Journal of biological chemistry - 25 Apr 1997
Diaz J L, Oltersdorf T, Horne W, McConnell M, Wilson G, Weeks S, Garcia T, Fritz L C
Abstract excerpt
Bcl-2 inhibits apoptosis induced by a wide variety of stimuli. In contrast, the Bcl-2 homologue, Bax, antagonizes Bcl-2's death protecting function. Bcl-2 forms protein-protein homodimers with itself and heterodimers with Bax, and previous experiments have shown that point mutations in Bcl-2 can abrogate Bax binding while leaving homodimerization intact. These mutagenesis results can be interpreted to suggest...
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