BD Pharmingen™ Purified Mouse Anti-Human BAK
Clone G317-2 (RUO)
Preparation And Storage
Recommended Assay Procedures
Applications include western blot analysis (1-2 µg/ml). HeLa cells (ATCC CCL-2) are recommended as a positive control. HeLa cell lysate is also available as a ready-to-use positive western blot control (Cat. No. 611449).
Product Notices
- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- 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.
- Please refer to http://regdocs.bd.com to access safety data sheets (SDS).
- Sodium azide is a reversible inhibitor of oxidative metabolism; therefore, antibody preparations containing this preservative agent must not be used in cell cultures nor injected into animals. Sodium azide may be removed by washing stained cells or plate-bound antibody or dialyzing soluble antibody in sodium azide-free buffer. Since endotoxin may also affect the results of functional studies, we recommend the NA/LE (No Azide/Low Endotoxin) antibody format, if available, for in vitro and in vivo use.
- Please refer to www.bdbiosciences.com/us/s/resources for technical protocols.
Companion Products
Bak (for Bcl-2 homologous Antagonist/Killer) is a recently identified member of the Bcl-2 family. Bcl-2 family members are involved in mediating programmed cell death or apoptosis, and share two highly conserved functional regions, Bcl-2 homology 1 and 2 (BH1 and BH2). Several of the family members, including Bcl-2, act as inhibitors of apoptosis, whereas others such as Bax promote cell death. Like Bax promote cell death. Like Bax, Bak primarily promotes apoptosis. However, unlike Bax, Bak has also been shown to inhibit cell death. Bak inhibited both serum-starvation and drug induced apoptosis when overexpressed in an Epstein-Barr virus (EBV)-transformed cell line. However, Bax did not inhibit cell death under the same conditions. Bak mRNA has been identified in a wide variety of fetal and adult tissues, with the highest levels observed in heart and skeletal muscle. The apparently ubiquitous expression of Bak has lead to the suggestion that its function may be mediated by cell death inhibitory factors, particularly in cell types with a long life span. Bak migrates at a reduced molecular weight ~24 kDa. G317-2 reacts with activated human Bak. A synthetic peptide corresponding to the first 50 amino acids of human Bak, which is only accessible when activated during apoptosis, was used as immunogen.
Development References (5)
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Chittenden T, Harrington EA, O'Connor R, et al. Induction of apoptosis by the Bcl-2 homologue Bak. Nature. 1995; 374(6524):733-736. (Biology). View Reference
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Kiefer MC, Brauer MJ, Powers VC, et al. Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak. Nature. 1995; 374(6524):736-739. (Biology). View Reference
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Reed JC. Bcl-2 and the regulation of programmed cell death. J Cell Biol. 1994; 124(1-2):1-6. (Biology). View Reference
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Westphal D, Dewson G, Czabotar PE, Kluck RM. Molecular biology of Bax and Bak activation and action.. Biochim Biophys Acta. 2011; 1813(4):521-31. (Biology). View Reference
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Yin XM, Oltvai ZN, Korsmeyer SJ. BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax. Nature. 1994; 369(6478):321-323. (Biology). View Reference
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For Research Use Only. Not for use in diagnostic or therapeutic procedures.