|Other Names||Bcl-2-interacting killer, Apoptosis inducer NBK, BIP1, BP4, BIK, NBK|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP1319a was selected from the region of human Bik BH3 Domain. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Accelerates programmed cell death. Association to the apoptosis repressors Bcl-X(L), BHRF1, Bcl-2 or its adenovirus homolog E1B 19k protein suppresses this death-promoting activity. Does not interact with BAX.|
|Cellular Location||Endomembrane system; Single-pass membrane protein. Mitochondrion membrane; Single-pass membrane protein. Note=Around the nuclear envelope, and in cytoplasmic membranes|
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Provided below are standard protocols that you may find useful for product applications.
The Bik protein is known to interact with cellular and viral survival-promoting proteins, such as BCL2 and the Epstein-Barr virus in order to enhance programmed cell death. Because its activity is suppressed in the presence of survival-promoting proteins, this protein is suggested as a likely target for antiapoptotic proteins. This protein shares a critical BH3 domain with other death-promoting proteins, BAX and BAK.
Arena, V., et al., Genes Chromosomes Cancer 38(1):91-96 (2003).Gillissen, B., et al., EMBO J. 22(14):3580-3590 (2003).Germain, M., et al., J. Biol. Chem. 277(20):18053-18060 (2002).Zou, Y., et al., Cancer Res. 62(1):8-12 (2002).Castells, A., et al., Gastroenterology 117(4):831-837 (1999).
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