Anti-Human ATG4B Antikörper mit von Kollaborateuren getestetem IHC-Nachweis.
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Anti-Human ATG4B Antibody is a research-use antibody from Elabscience for studying ATG4B in 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, 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-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.
ATG4B (autophagy related 4B cysteine peptidase), also called cysteine protease ATG4B or autophagin-1, is an ATG4-family cysteine protease central to ATG8-family protein processing during macroautophagy.
Biological function: ATG4B is a peptidase family C54 cysteine protease that processes ATG8-family proteins, including LC3 and GABARAP family members, to expose the C-terminal glycine required for lipidation. It also removes lipid modifications from ATG8-family proteins, regulating autophagosome membrane dynamics and autophagic flux.
