- CITATIONS: 1
|Application ||WB, IHC, FC|
|Calculated MW||26266 Da|
|Other Names||Apoptosis regulator Bcl-2, BCL2|
|Target/Specificity||A synthetic peptide corresponding to residues between BH3 and BH4 of human Bcl-2 was used as immunogen. The antibody does not cross-react with other Bcl-2 family members|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Bcl-2 Antibody is for research use only and 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.|
Provided below are standard protocols that you may find useful for product applications.
The Bcl-2 family of proteins regulate apoptosis by controlling mitochondrial permeability and release of cytochrome c. Bcl-2 is an anti-apoptotic protein that resides in the outer mitochondrial wall and inhibits release of cytochrome c (1). Over-expression of Bcl-2 has been shown to promote cell survival by suppressing apoptosis. It has been documented that bcl-2 becomes deregulated in tumor cells as a result of translocation into the immunoglobulin heavy-chain locus and is therefore activated in B cell malignancies (2). It has also been shown that post-translational modification of Bcl-2, phosphorylation at serine 70, may be required to render its full and/or enhanced anti-apoptotic effect (3, 4).
1. Hockenbery, D. et al. Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death. Nature 348: 334
2. Cleary, M.L. et al. Cloning and structural analysis of cDNAs for bcl-2 and a hybrid bcl-2/immunoglobulin transcript resulting from the t(14;18) translocation. Cell 47: 19
3. Ruvolo, P.P et al. Phosphorylation of Bcl2 and regulation of apoptosis. Leukemia 15: 515
4. Deng, X. et al. Novel Role for JNK as a Stress-activated Bcl2 Kinase. J. Biol. Chem. 276: 23681
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