Article
Structural and functional complementation of an inactive Bcl-2 mutant by Bax truncation.
The Journal of biological chemistry - 4 Jul 1997
Ottilie S, Diaz J L, Chang J, Wilson G, Tuffo K M, Weeks S, McConnell M, Wang Y, Oltersdorf T, Fritz L C
Abstract excerpt
Interactions among proteins in the Bcl-2 family regulate the onset of programmed cell death. Previous work has shown that the death-inhibiting family members Bcl-2 and Bcl-xL form heterodimers with the death-promoting homologue Bax and that certain site-directed mutants of Bcl-2 and Bcl-xL lose both biological activity and the ability to bind Bax. To better understand the structural basis of heterodimer...
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