BCL2-Associated Agonist of Cell Death (BAD) (AA 39-198) antibody
|Synonyms||BBC2, BCL2L8, wu:fa01b12, wu:fa96d04, MGC72439, BAD, MGC127164|
Alternatives Western Blotting (WB), Immunofluorescence (IF), Immunohistochemistry (IHC)
|5 references available|
|Price||Product not available in this region.|
|Cross-Reactivity||Human, Rat (Rattus)|
|Description||Isolated by screening for Bcl-2 interacting proteins, Bad shows significant homology to Bcl-2 within the Bcl-2 homology domains 1 and 2 (BH1 and BH2). In addition, several other proteins involved in cell death such as Bax, Bcl-X[L], Mcl-1, and A1 share similar homology with Bcl-2. Bcl-2 is known to oppose several apoptotic signals and is considered to be a central downstream cell death repressor. Bcl-X[L] represses apoptosis, but its short form, Bcl-X[S], promotes cell death. Bax is known to homodimerize as well as heterodimerize with Bcl-2. An excess concentration of Bax opposes the ability of Bcl-2 to repress cell death. Bad can selectively dimerize with Bcl-X[L] and Bcl-2, but not with Bax, Bcl-X[S], Mcl-1, A1, or itself. In mammalian cells, Bad binds more strongly to Bcl-X[L] than Bcl-2. This may explain why Bad reverses the death repressor activity of Bcl-X[L], but not that of Bcl-2. The formation of the Bad-Bcl-X[L] heterodimer displaces Bax and restores favorable conditions for apoptosis. This antibody is tested by western blot analysis.|
1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
4. Source of all serum proteins is from USDA inspected abattoirs located in the United States.
|Molecular Weight||23 kDa|
Related Products: ABIN968533, ABIN967389
|Purification||Purified from tissue culture supernatant or ascites by affinity chromatography.|
|Buffer||Aqueous buffered solution containing BSA, glycerol.|
|Preservative||0.09% Sodium azide.|
|Storage||Store undiluted at -20°C.|
|Research Area||Cancer, Apoptosis/Necrosis|
|Restrictions||For Research Use only|
Yang, Zha, Jockel et al.: "Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death." in: Cell, Vol. 80, Issue 2, pp. 285-91, 1995 (PubMed).
Graff, Konicek, McNulty et al.: "Increased AKT activity contributes to prostate cancer progression by dramatically accelerating prostate tumor growth and diminishing p27Kip1 expression." in: The Journal of biological chemistry, Vol. 275, Issue 32, pp. 24500-5, 2000 (PubMed).
Ayllón, Cayla, García et al.: "Bcl-2 targets protein phosphatase 1 alpha to Bad." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 166, Issue 12, pp. 7345-52, 2001 (PubMed).
Tomicic, Thust, Kaina: "Ganciclovir-induced apoptosis in HSV-1 thymidine kinase expressing cells: critical role of DNA breaks, Bcl-2 decline and caspase-9 activation." in: Oncogene, Vol. 21, Issue 14, pp. 2141-53, 2002 (PubMed).
Walsh, Lutz, Cotter et al.: "Erythrocyte survival is promoted by plasma and suppressed by a Bak-derived BH3 peptide that interacts with membrane-associated Bcl-X(L)." in: Blood, Vol. 99, Issue 9, pp. 3439-48, 2002 (PubMed).