Article
Bax activation by engagement with, then release from, the BH3 binding site of Bcl-xL.
Molecular and cellular biology - 1 Feb 2011
Gautier F, Guillemin Y, Cartron P F, Gallenne T, Cauquil N, Le Diguarher T, Casara P, Vallette F M, Manon S, Hickman J A, Geneste O, Juin P
Abstract excerpt
Bcl-2 homologues (such as Bcl-x(L)) promote survival in part through sequestration of "activator" BH3-only proteins (such as Puma), preventing them from directly activating Bax. It is thus assumed that inhibition of interactions between activators and Bcl-x(L) is a prerequisite for small molecules to antagonize Bcl-x(L) and induce cell death. The biological properties, described here of a terphenyl-based...
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