Product Description
Polyclonal Antibody for studying ATG16L1 (Ser278) phosphate. Validated for Western Blotting. Highly specific and rigorously validated in-house, Phospho-Atg16L1 (Ser278) Antibody (CST #84300) is ready to ship.
Product Usage Information
Western Blotting: 1:1000
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at -20°C. Do not aliquot the antibody.
Protocol
Available protocols: Western Blotting
Specificity / Sensitivity
Phospho-Atg16L1 (Ser278) Antibody recognizes endogenous levels of Atg16L1 protein only when phosphorylated at Ser278. This site is present on Atg16L1β, but not Atg16L1α.
Species Reactivity: Human, Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser278 of human Atg16L1 protein. Antibodies are purified by peptide affinity chromatography.
Background
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 (Atg) (1). Formation of autophagic vesicles requires a pair of essential ubiquitin-like conjugation systems, Atg12-Atg5 and Atg8 (LC3)-phosphatidylethanolamine (LC3-PE), which are widely conserved in eukaryotes (2).Mammalian Atg16L1, containing an amino-terminal coiled-coil domain and carboxyl-terminal WD-repeats, has multiple isoforms produced by alternative splicing (3,4). Atg16L1 provides a functional link between the two crucial ubiquitin-like conjugation systems of autophagy. Atg16L1 binds Atg5 of the Atg12-Atg5 conjugate forming an 800 kDa multimeric complex (3). The Atg12-Atg-5-Atg16L1 complex localizes to pre-autophagosomal membranes, where it determines the site of LC3 lipidation and catalyzes the reaction required for the formation of mature autophagosomes (3,5). Genome-wide association scanning revealed variations in the gene associated with Crohn's disease (6,7). Mice lacking the coiled-coil domain of Atg16L1 have impaired autophagosome formation and elevated inflammatory cytokines, consistent with its role in inflammatory disease pathogenesis (8). Hypomorphic Atg16L1 mice also show defects in autophagy and abnormalities in intestinal Paneth cell function similar to that found in Crohn's disease (9). ULK1-mediated phosphorylation of Atg16L1 at Ser278 promotes xenophagy, a selective autophagic process directed against pathogens (10).
Alternate Names
A16L1; APG16 autophagy 16-like; APG16-like 1; APG16L; APG16L beta; ATG16; ATG16 autophagy related 16-like 1; ATG16 autophagy related 16-like 1 (S. cerevisiae); ATG16 autophagy related 16-like protein 1; ATG16A; ATG16L; ATG16L1; autophagy related 16 like 1; Autophagy-related protein 16-1; FLJ00045; FLJ10035; FLJ10828; FLJ22677; IBD10; WD repeat domain 30; WDR30
Specification
REACTIVITY: H M R
SENSITIVITY: Endogenous
MW (kDa): 68
SOURCE: Rabbit
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Collaboration
Tony Tang
Email: Tony.Tang@iright.com
Mobile/WhatsApp/Wechat: +86-17717886924