Proper development and maintenance of homeostasis within tissues is achieved through cell proliferation, differentiation, and apoptosis. Members of the Bcl-2 protein family function to either inhibit (Bcl-2 and Bcl-XL) or promote (Bax and Bak) apoptosis. Similar to other family members, Bax contains the conserved Bcl-2 homology 1 (BH1) and 2 (BH2) domains which allow for its homodimerization or heterodimerization with Bcl-2. Although Bax alone does not induce cell death, elevated levels of Bax accelerate apoptosis following a death signal such as cytokine deprivation or Fas/Fas ligand interaction. The ratio of Bax homodimers to Bax/Bcl-2 heterodimers is an apoptotic checkpoint. When Bcl-2 is in excess, apoptosis is inhibited. However, if Bax levels increase in response to a death signal, the cell is pushed toward death. Bax function is also affected by Bax Inhibitor-1 (BI-1). Although it interacts directly with Bcl-2 and not Bax, BI-1 can suppress Bax-induced apoptosis. Alternative splicing of Bax mRNA produces Bax-α, the integral membrane form, and the two cytosolic forms β and γ. These isoforms are thought to allow for differential regulation of Bax activity and localization.
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注意事项:
1.Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2.Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.