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BID antibody (BH3 Interacting Domain Death Agonist) (AA 46-168)

Details for Product anti-BID Antibody No. ABIN968686, Supplier: Log in to see
Antigen
  • 2700049M22Rik
  • AI875481
  • AU022477
  • BID
  • bid
  • DKFZp469E066
  • FP497
  • fp497
  • si:ch211-238n5.6
  • xbid
Alternatives
anti-Human BID antibody for Immunohistochemistry (Paraffin-embedded Sections)
Epitope
AA 46-168
43
34
32
17
16
14
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11
9
8
6
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4
4
4
3
3
3
3
3
3
3
2
2
2
2
1
1
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1
1
1
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1
Reactivity
Human, Mouse (Murine)
274
128
56
2
1
Host
Mouse
268
68
21
10
Clonality (Clone)
Monoclonal ()
Conjugate
This BID antibody is un-conjugated
20
18
13
8
7
7
3
3
3
3
3
3
3
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3
Application
Immunofluorescence (IF), Western Blotting (WB)
280
166
108
63
34
34
25
18
12
11
9
3
2
1
1
1
1
1
Supplier
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Immunogen Mouse Bid aa. 46-168
Clone 40-Bid
Isotype IgG1
No Cross-Reactivity Human
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 Bid (BID Antibody Abstract)
Background Members of the Bcl-2 protein family function to inhibit (Bcl-2, Bcl-XL, Mcl-1, A1) or promote (Bax, Bak, Bcl-Ls, Bad) apoptosis. Bid is a Bcl-2 family death agonist that heterodimerizes with either agonists (Bax) or antagonists (Bcl-2). Bid contains a centrally located BH3 domain that allows interaction with the BH1 domain of Bax and Bcl-2, as well as two caspase cleavage sites (CCS). However, Bid does not contain other domains commonly found in Bcl-2 family members, such as BH1, BH2, or BH4. In addition, Bid does not contain a C-terminal hydrophobic region that is characteristic of membrane-bound Bcl-2 family members. Singlet oxygen-induced apoptosis in human leukemia cells and Fas-induced apoptosis involve caspase-8 cleavage of Bid, which produces a 15 kDa C-terminal fragment and a 6.5 kDa N-terminal fragment. The C-terminal fragment translocates to the mitochondria and promotes the release of cytochrome C through a mechanism that might involve destabilization of the mitochondrial membrane. Thus, the proapoptotic role of Bid may involve mitochondrial membrane destabilization, as well as multiple protein-protein interactions.
Molecular Weight 23 kDa
Research Area Cancer, Apoptosis/Necrosis
Pathways Apoptosis, Caspase Cascade in Apoptosis
Comment

Related Products: ABIN967389, ABIN968550

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-BID antibody (BH3 Interacting Domain Death Agonist) (AA 46-168) (ABIN968686) Western blot analysis of Bid on Mouse Macrophage + IFNgamma/LPS. Lane 1: 1:1000, lane...
Product cited in: Kudla, Montessuit, Eskes, Berrier, Martinou, Ghazi, Antonsson: "The destabilization of lipid membranes induced by the C-terminal fragment of caspase 8-cleaved bid is inhibited by the N-terminal fragment." in: The Journal of biological chemistry, Vol. 275, Issue 30, pp. 22713-8, 2000

Zhuang, Demirs, Kochevar: "p38 mitogen-activated protein kinase mediates bid cleavage, mitochondrial dysfunction, and caspase-3 activation during apoptosis induced by singlet oxygen but not by hydrogen peroxide." in: The Journal of biological chemistry, Vol. 275, Issue 34, pp. 25939-48, 2000

Wang, Yin, Chao, Milliman, Korsmeyer: "BID: a novel BH3 domain-only death agonist." in: Genes & development, Vol. 10, Issue 22, pp. 2859-69, 1996