特異性：Human Bcl-xL (Mr 29 kDa) Apoptosis, or programmed cell death, is a well-documented phenomenon in many cellular systems.1 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.2 Bcl- 2 and one of its homologues, Bcl-xL, protect cells from apoptosis3,4, while other homologues of Bcl-2 such as Bax, Bad and Bak have been shown to enhance apoptosis.5-8 Bcl-xL has been shown to block apoptosis which is induced by a variety of stimuli and, under certain conditions, offers greater protection against apoptosis than Bcl-2.9-13 In contrast, Bad and Bax inhibit the protective functions of Bcl-xL and Bcl-2, respectively. Although heterodimerization between Bcl-xL/Bad and Bcl-2/Bax was originally thought to be essential for the differential anti-apoptotic activity of Bcl-xL and Bcl-2,5,14 other results suggest that the formation of heterodimers may not be necessary for this death-repressing activity.15,16 Mab 7B2.5 recognizes both human and rodent Bcl-xL.17
