|Other Names||Apoptosis regulator Bcl-2, BCL2|
|Target/Specificity||The synthetic peptide sequence is selected from aa 63-74 of HUMAN BCL2|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI 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||Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release (PubMed:17418785).|
|Cellular Location||Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein|
|Tissue Location||Expressed in a variety of tissues.|
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Provided below are standard protocols that you may find useful for product applications.
This gene encodes an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants, produced by alternate splicing, differ in their C-terminal ends. [provided by RefSeq].
Feng, H., et al. Cancer Cell 18(4):353-366(2010)
Azad, N., et al. Ann. N. Y. Acad. Sci. 1203, 1-6 (2010) :
Dubikov, A.I., et al. Scand. J. Rheumatol. 39(5):368-372(2010)
Yu, B., et al. J. Exp. Clin. Cancer Res. 29, 107 (2010) :
Trisciuoglio, D., et al. PLoS ONE 5 (7), E11772 (2010) :
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