Target Name: ATG16L1
NCBI ID: G55054
Review Report on ATG16L1 Target / Biomarker Content of Review Report on ATG16L1 Target / Biomarker
ATG16L1
Other Name(s): ATG16A | autophagy related 16 like 1 | ATG16L | FLJ10035 | Autophagy-related protein 16-1 | FLJ00045 | A16L1_HUMAN | APG16-like 1 | IBD10 | Autophagy related 16 like 1, transcript variant 1 | ATG16L1 variant 2 | FLJ22677 | Autophagy-related protein 16-1 (isoform 2) | WD repeat domain 30 | ATG16 autophagy related 16-like 1 | OTTHUMP00000165877 | ATG16L1 variant 1 | Autophagy related 16 like 1, transcript variant 2 | APG16L beta | Autophagy-related protein 16-1 (isoform 1) | FLJ10828 | WDR30 | APG16L

ATG16L1: A Potential Drug Target Or Biomarker

ATG16L1, also known as ATG16A, is a protein that is expressed in various tissues of the body, including the brain, pancreas, and gastrointestinal tract. It is a member of the TATA-protein family, which is known for their role in gene regulation and DNA binding.

ATG16L1 has been identified as a potential drug target or biomarker for various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. Its function in these diseases is still being explored, but its potential as a drug target is based on its known biology and the results of preclinical studies.

One of the reasons for its potential as a drug target is its involvement in several signaling pathways that are involved in various diseases. For example, ATG16L1 has been shown to be involved in the regulation of cell proliferation, apoptosis (programmed cell death), and autophagy (the breakdown of cells by macrophages).

In addition, ATG16L1 has also been shown to be involved in the regulation of inflammation and immune cell function. Its expression has been shown to be elevated in various inflammatory diseases, including cancer, and its levels have been shown to be reduced in autoimmune disorders.

Another potential reason for its potential as a drug target is its role in the development and progression of neurodegenerative diseases. ATG16L1 has been shown to be involved in the regulation of neurotransmitter synthesis and release, as well as the maintenance of cellular homeostasis. Its expression has been shown to be elevated in neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease.

In addition, ATG16L1 has also been shown to be involved in the regulation of pain perception and neuroinflammation. Its expression has been shown to be elevated in conditions that cause pain, including neuroinflammation.

The potential benefits of ATG16L1 as a drug target are vast and varied. Its involvement in multiple signaling pathways and its potential involvement in a wide range of diseases make it an attractive target for drug development. Additionally, its relatively simple structure and the fact that it is expressed in multiple tissues make it easier to study and develop drugs.

However, it is important to note that while ATG16L1 is a promising drug target, further research is needed to fully understand its function and potential as a drug. Additionally, the development of drugs that target ATG16L1 will likely require the collaboration of experts in various fields, including pharmacology, biochemistry, and neuroscience.

In conclusion, ATG16L1 is a protein that has the potential to be a drug target or biomarker for a wide range of diseases. Its involvement in multiple signaling pathways and its potential involvement in a wide range of diseases make it an attractive target for drug development. While further research is needed to fully understand its function and potential, the potential benefits of ATG16L1 as a drug target are vast and varied.

Protein Name: Autophagy Related 16 Like 1

Functions: Plays an essential role in both canonical and non-canonical autophagy: interacts with ATG12-ATG5 to mediate the lipidation to ATG8 family proteins (MAP1LC3A, MAP1LC3B, MAP1LC3C, GABARAPL1, GABARAPL2 and GABARAP) (PubMed:23376921, PubMed:23392225, PubMed:29317426, PubMed:30778222, PubMed:33909989, PubMed:24553140, PubMed:24954904, PubMed:27273576). Acts as a molecular hub, coordinating autophagy pathways via distinct domains that support either canonical or non-canonical signaling (PubMed:29317426, PubMed:30778222). During canonical autophagy, interacts with ATG12-ATG5 to mediate the conjugation of phosphatidylethanolamine (PE) to ATG8 proteins, to produce a membrane-bound activated form of ATG8 (PubMed:23376921, PubMed:23392225, PubMed:24553140, PubMed:24954904, PubMed:27273576). Thereby, controls the elongation of the nascent autophagosomal membrane (PubMed:23376921, PubMed:23392225, PubMed:24553140, PubMed:24954904, PubMed:27273576). Also involved in non-canonical autophagy, a parallel pathway involving conjugation of ATG8 proteins to single membranes at endolysosomal compartments, probably by catalyzing conjugation of phosphatidylserine (PS) to ATG8 (PubMed:33909989). Non-canonical autophagy plays a key role in epithelial cells to limit lethal infection by influenza A (IAV) virus (By similarity). Regulates mitochondrial antiviral signaling (MAVS)-dependent type I interferon (IFN-I) production (PubMed:22749352, PubMed:25645662). Negatively regulates NOD1- and NOD2-driven inflammatory cytokine response (PubMed:24238340). Instead, promotes with NOD2 an autophagy-dependent antibacterial pathway (PubMed:20637199). Plays a role in regulating morphology and function of Paneth cell (PubMed:18849966)

The "ATG16L1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about ATG16L1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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