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Cat. No.: DAB-0011800
| Product Information | |
|---|---|
| Clonality | Monoclonal |
| Isotype | IgG |
| Host Species | Rabbit |
| Reactivity | Human, Rat |
| Applications | WB, IP |
| Product Description | Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human Atg4A protein. |
| Format | Liquid |
| Purity | Affinity purity |
| Target Information | |
|---|---|
| Target Name | ATG4A |
| UniProt No. | Q8WYN0 |
| Gene ID | 115201 |
| Gene Description | Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents. Control of autophagy was largely discovered in yeast and involves proteins encoded by a set of autophagy-related genes. Formation of autophagic vesicles requires a pair of essential ubiquitin-like conjugation systems, Atg12-Atg5 and Atg8-phosphatidylethanolamine, which are widely conserved in eukaryotes. Numerous mammalian counterparts to yeast Atg proteins have been described, including three Atg8 proteins and four Atg4 homologs. The cysteine protease Atg4 is pivotal to autophagosome membrane generation and regulation. Atg4 primes the Atg8 homolog for lipidation by cleaving its carboxy terminus and exposing its glycine residue for E1-like enzyme Atg7. The Atg8 homolog is transferred to the E2-like enzyme Atg3 before forming the Atg8-PE conjugate. During later stages of autophagy, Atg4 can reverse this lipidation event by cleaving PE, thereby recycling the Atg8 homolog.Atg4A predominately cleaves GATE-16, athough it can cleave the other mammalian Atg8 homologues with lesser efficiencies. Mutation in the corresponding Atg4A gene is critical for redox regulation and inhibits autophagosome formation. Expression of this Atg4A mutation demonstrates a role for reactive oxygen species in nutrient-deprived autophagy. |
| Shipping & Storage | |
|---|---|
| Shipping | Shipped at 4 °C. |
| Storage Instructions | Store at –20 °C. Do not aliquot the antibody. |
| Storage Buffer | Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. |
Ace Therapeutics has a team of experts in the field of endocrine and metabolic research, aiming to provide innovative preclinical contract research solutions to cope with diabetes and its complications. We provide customized solutions and technical support, enabling the transformation of promising concepts into innovative treatments, thus accelerating the drug development process of diabetes.
