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|Antigen||BCL2-Associated Agonist of Cell Death (BAD) Antibodies|
|Epitope||AA 39-198 Alternatives|
|Reactivity||Human, Mouse (Murine), Rat (Rattus) Alternatives|
|Conjugate||This BAD antibody is un-conjugated Alternatives|
Immunofluorescence (IF), Immunoprecipitation (IP), Immunohistochemistry (IHC), Western Blotting (WB)
|5 references available|
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Product Details anti-BAD AntibodyTarget Details BAD Application Details Handling References for anti-BAD antibody (ABIN967941) Images
|Cross-Reactivity||Human, Rat (Rattus)|
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.
|Purification||The monoclonal antibody was purified from tissue culture supernatant or ascites by affinity chromatography.|
|Immunogen||Mouse Bad aa. 39-198|
Target Details BADProduct Details anti-BAD Antibody Application Details Handling References for anti-BAD antibody (ABIN967941) Images back to top
|Alternative Name||Bad (BAD Antibody Abstract)|
|Background||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.|
|Molecular Weight||23 kDa|
|Research Area||Cancer, Apoptosis/Necrosis|
|Pathways||MAPK Signaling, PI3K-Akt Signaling, RTK Signaling, Apoptosis, Fc-epsilon Receptor Signaling Pathway, Positive Regulation of Peptide Hormone Secretion, Carbohydrate Homeostasis, Positive Regulation of Endopeptidase Activity, Regulation of Carbohydrate Metabolic Process, Hepatitis C, CXCR4-mediated Signaling Events|
Application DetailsProduct Details anti-BAD Antibody Target Details BAD Handling References for anti-BAD antibody (ABIN967941) Images back to top
Related Products: ABIN968533, ABIN967389
|Restrictions||For Research Use only|
HandlingProduct Details anti-BAD Antibody Target Details BAD Application Details References for anti-BAD antibody (ABIN967941) Images back to top
|Buffer||Aqueous buffered solution containing BSA, glycerol, and ≤0.09 % sodium azide.|
|Precaution of Use||This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.|
|Storage Comment||Store undiluted at -20° C.|
References for anti-BAD antibody (ABIN967941)Product Details anti-BAD Antibody Target Details BAD Application Details Handling Images back to top
|Product cited in:||
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
Walsh, Lutz, Cotter, OConnor: "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
Ayllón, Cayla, García, Roncal, Fernández, Albar, Martínez, Rebollo: "Bcl-2 targets protein phosphatase 1 alpha to Bad." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 166, Issue 12, pp. 7345-52, 2001
Graff, Konicek, McNulty, Wang, Houck, Allen, Paul, Hbaiu, Goode, Sandusky, Vessella, Neubauer: "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
Yang, Zha, Jockel, Boise, Thompson, Korsmeyer: "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
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