BAD antibody from Promab.
Know who made it. See the evidence. Buy through one marketplace.
BAD 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. BAD can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2.
For research use only.
Fully tested in-house by ABMIUM, or supported by an advanced validation report from a partner reviewed by ABMIUM. Highest confidence. Non-conformities fully supported under the ABMIUM Product Promise.
Quality verified. Independent collaborator or expected-performance data available. Product meets ABMIUM quality standards.
Expected to work based on structural and biochemical data. Not yet directly tested by ABMIUM or a collaborator. No non-conformity support for this combination.
Not recommended for this application or species/sample combination. This may indicate either evidence of unsuitability or that the combination has not been tested and therefore cannot currently be recommended.
Evidence status by application and model.
| Species | WB | IHC | IHC-P | IHC-F | IF/ICC | Flow Cytometry | ELISA | IP | ChIP |
|---|---|---|---|---|---|---|---|---|---|
| Human |
This product is manufactured by Promab and sold through ABMIUM without relabelling.
ABMIUM supports global orders. Availability, shipping requirements and applicable import arrangements are confirmed before fulfilment where required.
Yes. Send your target, sample, application and experimental conditions through ABMIUM MATCH or technical support.
Unless the listing expressly states otherwise, ABMIUM products are supplied for research use only and are not for diagnostic or therapeutic use.
BCL2 associated agonist of cell death (BAD) is a pro-apoptotic BH3-only BCL2-family regulator whose activity is strongly controlled by phosphorylation. When active, BAD can engage anti-apoptotic BCL2-family proteins and shift mitochondrial signalling toward intrinsic apoptosis. This page groups ABMIUM catalogue reagents for BAD signalling and cell-death research.
Biological function: BAD is regulated by phosphorylation at multiple serine residues. Survival signalling can promote phosphorylated BAD association with 14-3-3 proteins, limiting its pro-apoptotic activity. Dephosphorylated BAD can bind anti-apoptotic BCL2-family proteins such as BCL-XL and BCL2, favouring activation of the mitochondrial apoptosis programme.
