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Bad (A17) Antibody DB003 0.200 mg/ml $190.00

Datasheet 
Datasheet 

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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.) C Clybouw, B E L Mchichi, A Hadji, A Portier, M T Auffredou, D Arnoult, G Leca and A Vazquez. 2008. TGFbeta-mediated apoptosis of Burkitt's lymphoma BL41 cells is associated with the relocation of mitochondrial BimEL. Oncogene advance online publication 14 January 2008. 
Origin Bad is provided as an affinity purified rabbit polyclonal antibody, raised against a peptide mapping to the amino terminus of mouse Bad. 
Product Details Each vial contains 200 g/ml of affinity purified rabbit IgG, Bad DB003 (A17), in 1 ml PBS containing 0.1 % sodium azide and 0.2% gelatin. 
Competition Studies A blocking peptide is also available, DB003P, 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 mouse Bad 
Specificity Mouse and rat Bad 
Use Western blotting 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
 

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