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Details for Product No. ABIN968294

BCL2-Associated X Protein (BAX) (AA 55-178) antibody

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Synonyms BCL2L4, BAX-ALPHA, bax, fj16e01, wu:fc50b10, wu:fj16e01, bax-A, xBax, xlbax, BAX
»Alternatives AA 55-178
»Alternatives Human
»Alternatives Mouse
Clonality (Clone) Monoclonal ()
»Alternatives Un-conjugated
»Alternatives Western Blotting (WB), Immunoprecipitation (IP), Immunofluorescence (IF)
Pubmed 5 references available
Catalog no. ABIN968294
Quantity 50 µg
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Immunogen Human Bax-alpha
Clone 3
Isotype IgG1
Cross-Reactivity Dog (Canine)
Characteristics 1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Source of all serum proteins is from USDA inspected abattoirs located in the United States.
4. 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.
Purification Purified from tissue culture supernatant or ascites by affinity chromatography.
Purity Purified
Alternative Name Bax
Background Proper development and maintenance of homeostasis within tissues is achieved through cell proliferation, differentiation, and apoptosis. Members of the Bcl-2 protein family function to either inhibit (Bcl-2 and Bcl-XL) or promote (Bax and Bak) apoptosis. Similar to other family members, Bax contains the conserved Bcl-2 homology 1 (BH1) and 2 (BH2) domains which allow for its homodimerization or heterodimerization with Bcl-2. Although Bax alone does not induce cell death, elevated levels of Bax accelerate apoptosis following a death signal such as cytokine deprivation or Fas/Fas ligand interaction. The ratio of Bax homodimers to Bax/Bcl-2 heterodimers is an apoptotic checkpoint. When Bcl-2 is in excess, apoptosis is inhibited. However, if Bax levels increase in response to a death signal, the cell is pushed toward death. Bax function is also affected by Bax Inhibitor-1 (BI-1). Although it interacts directly with Bcl-2 and not Bax, BI-1 can suppress Bax-induced apoptosis. Alternative splicing of Bax mRNA produces Bax-alpha, the integral membrane form, and the two cytosolic forms beta and gamma. These isoforms are thought to allow for differential regulation of Bax activity and localization. This antibody is routinely tested by western blot analysis.
Molecular Weight 21 kDa
Research Area Cancer, Apoptosis/Necrosis

Related Products: ABIN968587, ABIN967389

Restrictions For Research Use only
Format Liquid
Concentration 250 µg/ml
Buffer Aqueous buffered solution containing BSA, glycerol.
Preservative Sodium azide
Storage -20 °C
Product cited in: Oltvai, Milliman, Korsmeyer: "Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death." in: Cell, Vol. 74, Issue 4, pp. 609-19, 1993 (PubMed).

Xu, Reed: "Bax inhibitor-1, a mammalian apoptosis suppressor identified by functional screening in yeast." in: Molecular cell, Vol. 1, Issue 3, pp. 337-46, 1998 (PubMed).

Rytömaa, Lehmann, Downward: "Matrix detachment induces caspase-dependent cytochrome c release from mitochondria: inhibition by PKB/Akt but not Raf signalling." in: Oncogene, Vol. 19, Issue 39, pp. 4461-8, 2000 (PubMed).

Aoudjit, Vuori: "Integrin signaling inhibits paclitaxel-induced apoptosis in breast cancer cells." in: Oncogene, Vol. 20, Issue 36, pp. 4995-5004, 2001 (PubMed).

Kartasheva, Contente, Lenz-Stöppler et al.: "p53 induces the expression of its antagonist p73 Delta N, establishing an autoregulatory feedback loop." in: Oncogene, Vol. 21, Issue 31, pp. 4715-27, 2002 (PubMed).

Alternatives for antigen "BCL2-Associated X Protein (BAX)", type "Antibodies"
Hosts (206), (112), (5)
Reactivities (287), (147), (143), (53), (52), (50), (12), (6), (2), (2), (1), (1), (1), (1), (1), (1), (1)
Applications (222), (103), (91), (83), (61), (60), (40), (18), (9), (9), (7), (2), (2), (2), (2), (2), (1), (1)
Conjugates (10), (5), (4), (4), (4), (4), (4), (4), (4), (4), (4), (1), (1)
Epitopes (55), (17), (17), (13), (10), (7), (6), (4), (2), (2), (2), (2), (2), (2), (2), (2), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1), (1)