ATG16L1 Antibodies

Autophagy-related protein 16-1 (ATG16L1)

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Gene Information

Human
Gene Name:	ATG16L1
Uniprot:	Q676U5
Entrez:	55054

Family

Belongs to:
WD repeat ATG16 family

Alternative Names

APG16 autophagy 16-like (S. cerevisiae); APG16L beta; APG16LFLJ10828; APG16-like 1; ATG16 autophagy related 16-like (S. cerevisiae); ATG16 autophagy related 16-like 1 (S. cerevisiae); ATG16A; ATG16L; autophagy-related protein 16-1; FLJ00045; FLJ10035; FLJ22677; IBD10; WD repeat domain 30; WDR30

Molecular Weight

Mass (kDA):
68.265 kDA

Genomic Context

Human
Location:	2q37.1
Sequence:	2; NC_000002.12 (233251571..233295674)

Subcellular Localizations

Cytoplasm. Preautophagosomal structure membrane; Peripheral membrane protein. Recruited to omegasomes membranes by WIPI2. Omegasomes are endoplasmic reticulum connected strutures at the origin of preautophagosomal structures. Localized to preautophagosomal structure (PAS) where it is involved in the membrane targeting of ATG5. Localizes also to discrete punctae along the ciliary axoneme.

Diseases

• Crohn Disease
• Inflammatory Bowel Diseases
• Intestinal Diseases
• Ulcerative Colitis
• Colitis
• Ulcer
• Inflammation
• Inflammatory Disorder
• Malignant Neoplasms
• Bacterial Infections
• Chronic Inflammation
• Innate Immune Response
• Dysequilibrium Syndrome

• Neoplasms
• Inflammatory Response
• Paratuberculosis
• Salmonella Infections
• Psoriasis
• Cell Invasion
• Ileal Diseases

Interacting Proteins

• ATG5
• GABARAPL2
• MAP1LC3B
• MAP1LC3C
• RB1CC1

• TMEM59

Pathways

• Autophagy
• Pathogenesis
• Immune Response
• Secretion
• Macroautophagy
• Innate Immune Response
• Inflammatory Response
• Cytokine Production
• Localization
• Adaptive Immune Response
• Exocytosis
• Catabolic Process
• Conjugation

• Cell Adhesion
• Transport
• Cytokine Secretion
• Membrane Biogenesis
• Regulation Of Autophagy
• Translation
• Cell Differentiation

PTMs

• Phosphorylation

Research Areas

• Autophagy
• Cancer
• Cell Biology
• Macroautophagy
• Neurodegeneration

• Neuroscience
• Tumor Suppressors
• Ubiquitin Proteasome Pathway

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/ATG16L1

Best Uses Of The ATG16L1 Marker

Boster scientists make it easy when it comes to submitting results of special samples, species, or applications. Boster scientists can submit results for species-specific applications and get product credits. This program is open to scientists around the world. Continue reading to learn more about the ATG16L1 marker for scientists.

Inhibition autophagy in inflammatory intestinal disease

Numerous studies have linked lower levels of autophagy to IBD. Zeissig et.al. found XIAP variants within 4% of patients with CD. These results suggest that autophagy regulates immune related processes, including inflammation. Further research is needed in order to understand its role in IBD. IBD is a complicated disease, regardless of how autophagy plays a role.

Although existing medical therapies fail to relieve symptoms in most patients, a significant proportion still requires surgical intervention. Modern studies are beginning point to the importance of autophagy for the treatment of IBD. To understand how autophagy functions in IBD, further research is required and the development of new therapeutic drugs. Here are some examples of the most recent research. Hopefully, these will lead to new treatments for IBD.

Numerous genetic studies linked CD to autophagy reduction. Many of these genetic studies have focused on CD risk variants. Many studies have shown that autophagy plays an important role during the pathogenesis and progression of IBD. CD has also been shown to be linked with the deletion of genes associated autophagy. Inhibition of autophagy is an important step in treating IBD.

Autophagy regulates both the innate immune response to pathogens and metabolism. Multicellular organisms are protected from pathogens by the innate immune systems. When structural patterns of pathogen components can be identified, signaling pathways activate. Autophagy was initially thought to be a nonspecific method of degradation. Recent research has shown autophagosomes can selectively isolate substrates.

Autophagy has been implicated with many immune-related processes including the production of inflammasomes, and antigen presentation. Autophagy is also linked to cytokine regulation of inflammasome activities. Autophagy is an important homeostatic process in the intestinal mucosa. Its dysfunction can contribute to IBD's pathogenesis.

While CD can be caused by genetic predisposition, this does not mean that CD will develop if the NOD2 gene is present. In fact, most people with this mutation do not develop IBD. It is possible that IBD could be caused by genetic abnormalities, or environmental factors. Some genes involved with autophagy may also play a role in the pathogenesis IBD.

There are many targets for miRNAs involved in the autophagy process. The miRNA miR-196 suppresses autophagy and inhibits LC3II. MiR-665 regulates a cellular response to unfolded proteins and may be involved in intestinal fibrosis. The miRNA miR-146b, meanwhile, regulates the NF-kB and mTOR signaling pathways.

The accumulation of macrophages in the submucosa layer contributes to the overinduction of inflammatory responses in IBD. Inhibiting autophagy in IBD patients may prove to be a useful therapeutic approach. Increased inflammatory infiltration and increased body weight have been linked to autophagy inhibition. Recent research showed that autophagy blockade could inhibit intestinal damage, which in turn led to a higher DAI score.

Incubation with secondary antibody of ATG16L1 marker

In a cell-free experiment, we used the antibody specific to ATG16L1 for immunohistochemistry and found that the protein was present on dense-core vesicles. The primary antibody was specific to Atg16L1 lipidation, while the secondary antibody was specific to LC3 lipidation. These results show that Atg16L1 plays a role in the removal active STING signaling compounds. Our studies show that Atg16l1 can cause ER-mitochondria axis to be aggravated and may impair DNA integrity. We also found that the protein is involved with the generation of the endogenous activate principle, which may impair DNA integrity and dsDNA releases.

You could also use ATG16L1's full-length or truncated version in a double stranded peptide to serve as a source of reference. In either of these cases, the secondary antigen should be added in a single tube. The PCR product can be viewed using a JEOL JEM1200 electron microscope. Itoh et al. (2008) performed experiments on human ULK1 cDNAs.

Autophagy-related protein Atg16L1 directs the secretion of LC3 to autophagosomes. It is a member of the ATG16 family with WD repeats and interacts with ATG5 and RAB33B to form minor and major complexes. It is found in preautophagosomal structures. This has been implicated for membrane targeting of ATG5.

ATG16L1 plays an important role in dense-core vehicle secretion. NPY fused with GST targets dense-core vesicles. This assay measures the amount of protein that is secreted into extracellular space. This test is used to identify the function Ofg16L1 in autophagosomes. This study also revealed that ATG16L1 was involved in the Gigaxonin E3 ligase. This regulates the maturation process of autophagosomes.

ATG16L1 represents a large protein compound that is essential for autophagy. This refers to the process of transferring an intracellular constituent to lysosomes where it can be degraded. There are several forms of the protein. For western blots, we use an ATG16L1 antibody at 1:500 in blocking solution.

Secondary antibodies were obtained by Abcam and Thermofisher. Next, we used mouse anti-LC3B, CT813, Flag(M2) and rat anti-TMEM59 antibodies. After incubating the primary and secondary antibodies with each other, we added Hoechst 3342 to the coverslips. Afterwards, images were obtained using a 63x Apochromat Lens.

We can also use modified siRNA duplexes, which target the ATG16L1 genetic gene, in addition to anti–ATG16L1 antibodies. These siRNA duplexes can be used to target the ATG16L1 or control stealth genes. Invitrogen has modified siRNAs available for purchase. The modified siRNAs have been created to inhibit HeLa cell inclusion.

Rab33A is required in order to localize Atg16L1's dense-core, vesicle in PC12 cell cells. ATG16L1 is colocalized on dense-core vessels. Rab33A knockdown partially rescues hyper-sprouting vascular phenotypes in PKA-deficient mice.

Atg16l1 deficiencies, in addition to IL-22, can lead to epithelial cells dying. In addition, IL-22-induced activation of cGAS-STING signaling is responsible for concomitant induction of ISG and TNF. The IL-22-induced cGAS–STING response can be physiologically detected in primary intestinal epithelial cell lines. In the absence of functional Atg16l1, this response increases.

Atg16L1 is also known to interact with two Rab33 isoforms (A and B), which are a part of the Rab33 protein family. These proteins are involved with membrane trafficking and regulate different secretion events. Atg16L1's functional significance has not been determined. Its interaction with Rab33A has not been fully studied.

ATG16L1 marker can be incubated with secondary antibodies. This is a simple but highly effective method to detect ATG16L1 proteins. GE Healthcare Life Sciences offers enhanced chemiluminescence-conjugated antibody. Detection of protein-bound ATG16L1 by using the corresponding enzymes and secondary antibodies improves the sensitivity of the technique.

The NPYT7-GST secretion assays in Atg16L1 knockdown cells PC12 were performed. These cells did no respond to wortmannin, or the drug at the exact same concentration, as shown by Table 3. In addition, wortmannin treatment did not affect the total level of NPY-T7-GST expression and secretion.