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Bcl-2 (A18) Antibody DB001 0.200 mg/ml $190.00


For technical service please call (800) 595 1994
Product Info
Background Bcl-2 family of proteins is a key regulator of apoptosis that function to either inhibit or promote cell death. The over expression of members such as Bcl-2 and Bcl-xL inhibit the apoptotic process (1,2). The Bcl-2 family members are also characterized by dimerizing to further modulate apoptosis. Bag-1, for example, has been found to form a heterodimer with Bcl-2 resulting in the enhancement of the anti-apoptotic effect of Bcl-2 (3,4). Other anti-apoptotic Bcl-2 family members include A1, Bcl-xg, Bcl-xb, Mcl-1, BAR, BI-1 and Bcl-w (5). The pro-apoptotic family members include Bax, Bcl-xS, Bad, Bak, NBK, BID, Hrk, Bok, Bim, Noxa and Diva. Bax and Bak have been shown to play a critical role in cytochrome c release from mitochondria and thus initiate apoptosis (6). Bad plays a critical role in the Bax-mediated apoptosis pathway by dimerizing with Bcl-xL, causing the displacment of Bax. The displacement of Bax allows apoptosis to proceed (7). Bcl-xS, a shorter version of Bcl-xL (lacking amino acids 126-188), apparently utilizes a different pathway than Bax to induce cell death. Some research suggests that Bcl-xS uses a novel mechanism for regulating caspase or it may use an alternate cell death effector pathway (8,9). 
*Product Citations* 1.) Kim BE, Lee JH, Kim HS, Kwon OJ, Jeong SW, and Kim IK. 2004. Involvement of Sox-4 in the cytochrome c-dependent AIF-independent apoptotic pathway in HeLa cells induced by Delta12-prostaglandin J2. Exp Mol Med. 36(5): 444-453.
2.) Sohn WJ, Lee KW, Choi SY, Chung E, Lee Y, Kim TY, Lee SK, Choe YK, Lee JH, Kim DS, Kwon HJ. 2006. CpG-oligodeoxynucleotide protects immune cells from gamma-irradiation-induced cell death. Mol Immunol. Mar;43(8):1163-71.
3.)Yaiw KC, Ong KC, Chua KB, Bingham J, Wang L, Shamala D, Wong KT. 2007. Tioman virus infection in experimentally infected mouse brain and its association with apoptosis. J Virol Methods Aug;143(2):140-6.
4.) Wan Y, Xu J, Ma D, Zeng Y, Cibelli M, Maze M. 2007. Postoperative impairment of cognitive function in rats: a possible role for cytokine-mediated inflammation in the hippocampus. Anesthesiology. Mar;106(3):436-43. 
Origin Bcl-2 is provided as an affinity purified rabbit polyclonal antibody, raised against a peptide mapping to the amino terminus of Human Bcl-2. 
Product Details Each vial contains 200 g/ml of affinity purified rabbit IgG, Bcl-2 DB001 (A18), in 1 ml PBS containing 0.1 % sodium azide and 0.2% gelatin. 
Competition Studies A blocking peptide is also available, DB001P, for use in competition studies. Each vial contains 0.100 mg of peptide in 0.5 ml PBS with 0.1% sodium azide and 100 mg BSA. 
Form 200 g/ml rabbit polyclonal IgG in 1 ml PBS containing 0.1 % sodium azide and 0.2% gelatin. 
Immunogen Synthetic peptide mapping to the amino terminal domain of human Bcl-2 
Specificity Mouse, rat and human Bcl-2 
Use Western blotting, immunoprecipitation, and immunohistochemistry 
Storage Store this product at 4 C, do not freeze. The product is stable for one year from the date of shipment. 
References 1. Huang Z. 2000. Bcl-2 family proteins as targets for anticancer drug design. Oncogene 19(56): 6627-6631
2. Reed JC. 1997. Double identity for proteins of the Bcl-2 family. Nature 387(6635): 773-776
3. Eversole-Cire P, Concepcion FA, Simon MI, Takayama S, Reed JC, Chen J. 2000. Synergistic effect of Bcl-2 and BAG-1 on the prevention of photoreceptor cell death. Invest Ophthalmol Vis Sci 41(7): 1953-1961
4. Coldwell MJ, deSchoolmeester ML, Fraser GA, Pickering BM, Packham G, Willis AE. 2001. The p36 isoform of BAG-1 is translated by internal ribosome entry following heat shock. Oncogene 20(30): 4095-4100
5. Bae j, Hsu SY, Leo CP, Zell K, Hsueh AJ. 2001. Underphosphorylated BAD interacts with diverse antiapoptotic Bcl-2 family proteins to regulate apoptosis. Apoptosis 6(5): 319-330
6. >Wei MC, Zong WX, Cheng EH, Lindsten T, Panoutsakopoulou V, Ross AJ, Roth KA, MacGregor GR, Thompson CB, Korsmeyer SJ. 2001. Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death. Science 292(5517): 624-626
7. Yang E, Zha J, Jockel J, Boise LH, Thompson CB, Korsmeyer SJ. 1995. Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death. Cell 80(2): 285-291
8. Fridman JS, Parsels J, Rehemtulla A, Maybaum J. 2001. Cytochrome c depletion upon expression of Bcl-XS. J Biol Chem 276(6): 4205-10
9. Lindenboim L, Yuan J, Stein R. 2000. Bcl-xS and Bax induce different apoptotic pathways in PC12 cells. Oncogene 19(14): 1783-1793

For Technical service please call +1-800-595-1994
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