BAD antibody (AA 39-198)

Catalog No. ABIN967940

The Mouse Monoclonal anti-BAD antibody has been validated for WB, IHC, IF and IP. It is suitable to detect BAD in samples from Human, Mouse and Rat. There are 4+ publications available.

Quick Overview for BAD antibody (AA 39-198) (ABIN967940)

Target: BAD (BCL2-Associated Agonist of Cell Death (BAD))

Reactivity: Human, Mouse, Rat

Host: Mouse

Clonality: Monoclonal

Conjugate: This BAD antibody is un-conjugated

Application: Western Blotting (WB), Immunohistochemistry (IHC), Immunofluorescence (IF), Immunoprecipitation (IP)

Clone: 48-Bad

Product Details anti-BAD Antibody

Binding Specificity: AA 39-198

Cross-Reactivity: Human, Rat (Rattus)

Characteristics: 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

Isotype: IgG2b

Application Details

Comment:

Related Products: ABIN968533, ABIN967389

Restrictions: For Research Use only

Handling

Format: Liquid

Concentration: 250 μg/mL

Buffer: Aqueous buffered solution containing BSA, glycerol, and ≤0.09 % sodium azide.

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Storage: -20 °C

Storage Comment: Store undiluted at -20° C.

References for anti-BAD antibody (ABIN967940)

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, 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) (PubMed).

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) (PubMed).

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) (PubMed).

Target Details for BAD

Target: BAD (BCL2-Associated Agonist of Cell Death (BAD))

Alternative Name: Bad

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

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