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BAD antibody (BCL2-Associated Agonist of Cell Death) (AA 39-198)

Details for Product anti-BAD Antibody No. ABIN967940, Supplier: Log in to see
Antigen
  • AI325008
  • bad
  • BAD
  • Bbc2
  • BBC2
  • BCL2L8
  • fa01b12
  • wu:fa01b12
  • wu:fa96d04
Alternatives
anti-Mouse (Murine) BAD antibody for Immunohistochemistry (Frozen Sections)
Epitope
AA 39-198
51
47
41
38
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34
27
27
24
20
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Reactivity
Human, Mouse (Murine), Rat (Rattus)
726
376
216
9
5
4
2
2
1
1
Host
Mouse
920
49
2
1
Clonality (Clone)
Monoclonal ()
Conjugate
This BAD antibody is un-conjugated
66
65
65
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59
6
6
6
6
6
6
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6
Application
Immunofluorescence (IF), Immunoprecipitation (IP), Immunohistochemistry (IHC), Western Blotting (WB)
511
432
418
292
75
67
53
26
10
8
4
3
2
2
1
1
1
Supplier
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Immunogen Mouse Bad aa. 39-198
Clone 48-Bad
Isotype IgG2b
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.
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
Comment

Related Products: ABIN968533, ABIN967389

Restrictions For Research Use only
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.
Supplier Images
Western Blotting (WB) image for anti-BAD antibody (BCL2-Associated Agonist of Cell Death) (AA 39-198) (ABIN967940) Western blot analysis of Bad on an A431 cell lysate (Human epithelial carcinoma, ATCC...
Immunofluorescence (IF) image for anti-BAD antibody (BCL2-Associated Agonist of Cell Death) (AA 39-198) (ABIN967940) Immunofluorescence staining of WI-38 cells (Human lung fibroblasts, ATCC CCL-75).
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 (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).

Background publications 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 (PubMed).