特異性：Mouse Bax (Mr 21 kDa) Apoptosis, or programmed cell death, is a well-documented phenomenon in many cellular systems.2 It plays a key role in tissue and organ development as well as in adult tissues during cell turnover. Apoptosis can be induced by a variety of internal and external stimuli including growth factor deprivation, cytokine treatment, antigen-receptor engagement, cell-cell interactions, irradiation and glucocorticoid treatment.3 Bax is a member of the Bcl-2 family of apoptosis-associated proteins and, although it is similar in structure to Bcl-2, Bax exerts a pro-apoptotic rather than an anti-apoptotic effect on cells. Bax targets mitochondrial membranes, inducing mitochondrial damage and subsequent cell death in a caspase-independent manner, presumably via their ion channel-forming activity. These channels may then function to promote a mitochondrial permeability transition or to puncture the outer mitochondrial membrane. In addition to forming homodimer, Bax can heterodimerize with Bcl-2 and Bcl-XL proteins. This heterodimerization between pro- and anti-apoptotic family members may serve a titration function and act as a sensor for the programmed cell death program.4-13 Mab 5B7 is specific for mouse Bax.1
