Mouse Bcl2 Associated X Protein (Bax) ELISA Kit-Sandwich

Apoptosis regulator BAX facilitates programmed cell death by binding to and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress, BAX undergoes a conformational change, translocating to the mitochondrial membrane and causing the release of cytochrome c, which initiates apoptosis. It promotes CASP3 activation, thereby inducing apoptosis. BAX deficiency results in lymphoid hyperplasia and male sterility due to the halt in sperm production. BAX is vital in apoptosis by enhancing mitochondrial outer membrane permeability (MOMP) through its interaction with the mitochondrial outer membrane, leading to cytochrome c release and activation of downstream apoptotic pathways. In mice, BAX deficiency reduces apoptosis in specific cell types. For instance, in Bax-/- mice, neuron and immune cell (including T and B cells) apoptosis is significantly diminished.