Bad monoclonal Antibody
Purified Mouse Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB |
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Primary Accession | Q92934 |
Reactivity | Human, Mouse, Rat |
Host | Mouse |
Clonality | Monoclonal |
Isotype | IgG1 |
Calculated MW | 18392 Da |
Gene ID | 572 |
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Other Names | Bcl2-associated agonist of cell death, BAD, Bcl-2-binding component 6, Bcl-2-like protein 8, Bcl2-L-8, Bcl-xL/Bcl-2-associated death promoter, Bcl2 antagonist of cell death, BAD, BBC6, BCL2L8 |
Target/Specificity | Bad |
Formulation | 100 µg (200 µg/ml) in PBS containing 1 mg/ml BSA and 1.5 mM sodium azide and 50% glycerol. |
Handling | The antibody solution should be gently mixed before use. |
Background Descriptions | |
Precautions | Bad monoclonal Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | BAD |
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Synonyms | BBC6, BCL2L8 |
Function | Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2 (By similarity). Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. |
Cellular Location | Mitochondrion outer membrane. Cytoplasm {ECO:0000250|UniProtKB:Q61337}. Note=Colocalizes with HIF3A in the cytoplasm (By similarity). Upon phosphorylation, locates to the cytoplasm. {ECO:0000250|UniProtKB:Q61337} |
Tissue Location | Expressed in a wide variety of tissues. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Bad is a member of the Bcl-2 family proteins. Within the Bcl-2 homology domains 1 and 2 (BH1 and BH2), Bad shows significant homology to Bcl-2 and Bcl-x. Bcl-2 is known to block several apoptosis signals and is considered to be a central downstream cell death repressor. Bcl-XL represses apoptosis, but its short form, Bcl-XS, 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-xL and Bcl-2, but not with Bax, Bcl-xS, Mcl-1, A1, or itself. In mammalian cells, Bad binds more strongly to Bcl-xL than Bcl-2, which may explain why Bad reverse the death repressor activity of Bcl-xL, but not that of Bcl-2. The formation of the Bad-Bcl-xL heterodimer displaces Bax and restores favorable conditions for apoptosis.
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