BIM(Phospho-Ser69) antibody from Promab.
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BCL2L11 induces apoptosis and anoikis. Isoform BimL is more potent than isoform BimEL. Isoform Bim-alpha1, isoform Bim-alpha2 and isoform Bim-alpha3 induce apoptosis, although less potent than isoform BimEL, isoform BimL and isoform BimS.
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 | |||||||||
| Mouse | |||||||||
| Rat |
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.
BCL2L11 (BCL2 like 11), commonly called BIM or Bcl-2-like protein 11, is a BH3-only BCL-2-family regulator that helps initiate mitochondrial apoptosis in response to developmental and cellular stress signals.
Biological function: BCL2L11 encodes a BH3-only pro-apoptotic BCL-2-family protein. BIM engages anti-apoptotic BCL-2-family members and helps shift mitochondrial signalling toward activation of the intrinsic apoptosis machinery. Alternative splicing generates multiple BCL2L11 isoforms whose abundance and activity are regulated by cell state and signalling inputs.
