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The protein encoded by ATG16L1 is part of a large protein complex that is necessary for autophagy, the major process by which intracellular components are targeted to lysosomes for degradation. Additionally we are shipping ATG16L1 Proteins (8) and ATG16L1 Kits (5) and many more products for this protein.
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Cow (Bovine) Polyclonal ATG16L1 Primary Antibody for EM, IHC - ABIN258803
Plantinga, Crisan, Oosting, van de Veerdonk, de Jong, Philpott, van der Meer, Girardin, Joosten, Netea: Crohn's disease-associated ATG16L1 polymorphism modulates pro-inflammatory cytokine responses selectively upon activation of NOD2. in Gut 2011
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Human Polyclonal ATG16L1 Primary Antibody for IF, IHC (p) - ABIN388542
Baehrecke: Autophagy: dual roles in life and death? in Nature reviews. Molecular cell biology 2005
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Mouse (Murine) Polyclonal ATG16L1 Primary Antibody for ELISA, WB - ABIN451668
Rioux, Xavier, Taylor, Silverberg, Goyette, Huett, Green, Kuballa, Barmada, Datta, Shugart, Griffiths, Targan, Ippoliti, Bernard, Mei, Nicolae, Regueiro, Schumm, Steinhart, Rotter, Duerr, Cho, Daly et al.: Genome-wide association study identifies new susceptibility loci for Crohn disease and implicates autophagy in disease pathogenesis. ... in Nature genetics 2007
Human Polyclonal ATG16L1 Primary Antibody for IHC (p), WB - ABIN388543
Lum, DeBerardinis, Thompson: Autophagy in metazoans: cell survival in the land of plenty. in Nature reviews. Molecular cell biology 2005
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transient expression of ATG16L1 not only inhibited autophagosome biogenesis, but also aberrantly targeted RAB11-positive recycling endosomes, resulting in recycling endosome aggregates.
the ATG16L1 (T300A) variant is associated with necrotizing enterocolitis in premature infants
this study shows that the association between ATG16L1 and Crohn's disease is mediated at least in part through Rac1 hyperactivation and subsequent defective dendritic cell migration
the data suggested that genetic variants within the ATG16L1 gene promoter were not a risk factor for sporadic Parkinson's disease development
Polymorphism in ATG16L1 gene is associated withinflammatory bowel disease.
EVA1A (show FAM176A Antibodies) interacts with the WD repeats of ATG16L1 through its C-terminal and promotes ATG12 (show ATG12 Antibodies)-ATG5 (show ATG5 Antibodies)/ATG16L1 complex recruitment to the autophagic membrane and enhances the formation of the autophagosome.
Identified and present structure of the predicted WD40 domain (show DCAF12L2 Antibodies) boundaries of the autophagy-related protein 16-1 (ATG16L1).
this study revealed that ATG16L1 deficiency led to alterations in macrophage function that contribute to the severity of Crohn disease
The present results support the hypothesis that Trimethylamine N-oxide may be involved in the pathogenesis of inflammatory bowel disease by impacting ATG16L1-induced autophagy and activating NLRP3 (show NLRP3 Antibodies) inflammasome.
MicroRNA-410 regulates autophagy-related gene ATG16L1 expression and enhances chemosensitivity via autophagy inhibition in osteosarcoma.(
These findings indicate that, in contrast to tumor cells in which autophagy promotes caspase (show CASP3 Antibodies)-independent cell death, ATG16L1 maintains the intestinal barrier by inhibiting necroptosis in the epithelium.
Collectively, these data reveal that miR (show MLXIP Antibodies)-20a inhibits autophagic response and promotes BCG (show SLC11A1 Antibodies) survival in macrophages by targeting ATG7 (show ATG7 Antibodies) and ATG16L1.
this study shows that loss of Atg16l1 in myeloid cells exacerbated murine models of colitis
both TNF-R (show TNFRSF1A Antibodies) and nucleotide-binding oligomerization domain stimulation promote ATG16L1 stabilization via IKKalpha (show CHUK Antibodies)-dependent phosphorylation of ATG16L1 at Ser278.
defective autophagy in intestinal epithelial cells (IECs) may predispose to crohn disease ileitis via impaired clearance of IRE1alpha (show ERN1 Antibodies) aggregates during ER stress at this site.
Selective deletion of Atg16l1 in T cells in mice resulted in spontaneous intestinal inflammation that was characterized by aberrant type 2 responses to dietary and microbiota antigens, and by a loss of Foxp3 (show FOXP3 Antibodies)(+) Treg cells.
Arg-24 of Atg16L1 is crucial for its interaction with Atg5 (show ATG5 Antibodies) which has implications in the binding of the dimeric complex to Rab33B (show RAB33B Antibodies)
inhibition of IL-1beta (show IL1B Antibodies) signaling abrogates the ATG16L1-dependent protection from Urinary tract infections
A hypomorphic mutation in Atg16L1, a crucial autophagy gene, leads to developmental retention of early-stage cells in various tissues where the differentiation of stem cells is retarded.
The protein encoded by this gene is part of a large protein complex that is necessary for autophagy, the major process by which intracellular components are targeted to lysosomes for degradation. Defects in this gene are a cause of susceptibility to inflammatory bowel disease type 10 (IBD10). Several transcript variants encoding different isoforms have been found for this gene.
ATG16 autophagy related 16-like 1 (S. cerevisiae)
, APG16 autophagy 16-like
, autophagy-related protein 16
, APG16-like 1
, autophagy-related 16-like
, ATG16 autophagy related 16-like 1
, autophagy-related protein 16-1-like
, autophagy-related protein 16-1
, APG16L beta
, WD repeat domain 30
, Atg16L1 gamma
, autophagy-related 16-like 1 gamma
, autophagy-related 16-like 1