A Peptide Sequence from Bax That Converts Bcl-2 into an Activator of Apoptosis

摘要: Abstract Bcl-2 and Bax are members of a family cytoplasmic proteins that regulate apoptosis. The two have highly similar amino acid sequences but functionally opposed: acts to inhibit apoptosis, whereas counteracts this effect. antagonism appears depend upon dimerization between Bax, its mechanism is otherwise unknown. Here we report overexpressing induces apoptosis in mammalian fibroblast cell line, identify novel, short “suicide domain” required for Inserting domain place the corresponding, divergent sequence converts from an inhibitor into activator death. These findings imply specific region confers active propensity cells support view may block death primarily by suppressing activity.