Non-phosphorylatable mutants of Ser184 lead to incomplete activation of Bax.

The S184 residue of Bax is the target of several protein kinases regulating cell fate, including AKT. It is well-established that, , the substitution of S184 by a non-phosphorylatable residue stimulates both the mitochondrial localization of Bax, cytochrome c release, and apoptosis. However, in experiments, substituted mutants did not exhibit any increase in their binding capacity to isolated mitochondria or liposomes.