catalog number :
MBS440005
products full name :
Bax (A20) Antibody
products short name :
Bax
other names :
bax, partial; Apoptosis regulator BAX; apoptosis regulator BAX; Bcl2-associated X protein
other gene names :
Bax; Bax
uniprot entry name :
BAX_RAT
reactivity :
Mouse, rat, human
specificity :
Mouse, rat and human Bax
form :
200 ug/ml rabbit polyclonal IgG in 1 ml PBS containing 0.1 % sodium azide and 0.2% gelatin.
concentration :
0.200 mg/ml
storage stability :
Store this product at 4 degree C, do not freeze. The product is stable for one year from the date of shipment.
tested application :
Western Blot (WB), Immunoprecipitation (IP), Immunohistochemistry (IHC)
other info1 :
Origin: Bax is provided as an affinity purified rabbit polyclonal antibody, raised against a peptide mapping to the amino terminus of human Bax.
other info2 :
Immunogen: Synthetic peptide mapping to the amino terminal domain of human Bax
products description :
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).
products references :
1.) You WK, Seo HJ, Chung KH, Kim DS. 2003. A novel metalloprotease from Gloydius halys venom induces endothelial cell apoptosis through its protease and disintegrin-like domains. J Biochem (Tokyo) Nov;134(5):739-49. 2.) Kim J, Seong J, and Kim SH. 2004. Enhancement of Tumor Response by Farnesyltransferase Inhibitor in C3H/HeJ Hepatocarcinoma. Ann N Y Acad Sci. Dec;1030:95-102. 3.) Ma D, Hossain M, Chow A, Arshad M, Battson RM, Sanders RD, Mehmet H, Edwards AD, Franks NP, Maze M. 2005. Xenon and hypothermia combine to provide neuroprotection from neonatal asphyxia. Ann Neurol. Aug;58(2):182-93.4.) 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. 1. Huang Z. 2000. Bcl-2 family proteins as targets for anticancer drug design. Oncogene 19(56): 6627-66312. Reed JC. 1997. Double identity for proteins of the Bcl-2 family. Nature 387(6635): 773-7763. 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): 1953-19614. 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): 4095-41005. 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): 319-3306. 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): 624-6267. 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): 285-2918. Fridman JS, Parsels J, Rehemtulla A, Maybaum J. 2001. Cytochrome c depletion upon expression of Bcl-XS. J Biol Chem 276(6): 4205-109. Lindenboim L, Yuan J, Stein R. 2000. Bcl-xS and Bax induce different apoptotic pathways in PC12 cells. Oncogene 19(14): 1783-1793
ncbi acc num :
AAA75200.1
ncbi pathways :
ATM Pathway 198524!!Activation, Translocation And Oligomerization Of BAX Pathway 1178315!!Amyotrophic Lateral Sclerosis (ALS) Pathway 83491!!Amyotrophic Lateral Sclerosis (ALS) Pathway 511!!Apoptosis Pathway 219785!!Apoptosis Pathway 83452!!Apoptosis Pathway 470!!Apoptosis Pathway 1178301!!B Cell Receptor Signaling Pathway 198486!!Colorectal Cancer Pathway 83494
ncbi summary :
Bcl2-related gene; involved in the regulation of apoptotic cell death [RGD, Feb 2006]