Anti-Human BAK1 Antibody with collaborator-tested evidence for WB, IHC.
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Anti-Human BAK1 Antibody is a research-use antibody from Elabscience for studying BAK1 in WB, IHC workflows with listed reactivity for Human. Specifications and supporting documents below should be reviewed when planning the experiment.
Fully tested in-house 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-P | IHC-Fr | IF/ICC | Flow Cyt | IP | ChIP | IHC |
|---|---|---|---|---|---|---|---|---|
| Human |
This product is manufactured by Elabscience 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 antagonist/killer 1 (BAK1/BAK) is a pro-apoptotic BCL2-family effector located at the mitochondrial outer membrane. Following apoptotic activation, BAK changes conformation and oligomerizes to drive mitochondrial outer-membrane permeabilization. This page groups ABMIUM catalogue reagents for intrinsic-apoptosis research.
Biological function: BAK1 is a mitochondrial apoptosis effector. Pro-apoptotic activation promotes BAK conformational change and homo-oligomerization in the outer mitochondrial membrane, increasing membrane permeability and enabling release of cytochrome c and other apoptogenic factors that support downstream caspase activation.
