Target Name: ATXN7L3
NCBI ID: G56970
Review Report on ATXN7L3 Target / Biomarker Content of Review Report on ATXN7L3 Target / Biomarker
ATXN7L3
Other Name(s): AT7L3_HUMAN | Ataxin 7 like 3, transcript variant 1 | ataxin 7 like 3 | SGF11 | ATXN7L3 variant 1 | Ataxin-7-like protein 3 | Ataxin-7-like protein 3 (isoform a) | SAGA-associated factor 11 homolog

ATXN7L3 as A Potential Drug Target and Biomarker for Neurodegenerative Diseases

ATXN7L3 (AT7L3_HUMAN) is a protein that is expressed in the brain and is known for its role in the development and progression of neurodegenerative diseases, such as Alzheimer's disease. The protein is encoded by the HTATN7 gene and has been shown to be involved in the formation of beta-amyloid plaques, which are thought to contribute to the development of Alzheimer's disease.

Recent studies have suggested that ATXN7L3 may be a drug target or biomarker for the treatment of neurodegenerative diseases. One reason for this is that the protein has been shown to be involved in the formation of beta-amyloid plaques, which are thought to play a key role in the development of Alzheimer's disease. Researchers have also found that inhibiting the activity of ATXN7L3 has been shown to protect against the formation of beta-amyloid plaques in animal models of Alzheimer's disease.

Another reason for considering ATXN7L3 as a drug target is its role in the regulation of the immune system. Studies have shown that ATXN7L3 is involved in the regulation of T cell responses, which are important for the immune system's response to infection and disease. This suggests that ATXN7L3 may be a potential target for drugs that are used to treat autoimmune diseases, such as multiple sclerosis.

In addition to its potential as a drug target, ATXN7L3 has also been shown to be a potential biomarker for the diagnosis and progression of neurodegenerative diseases. Studies have shown that the level of ATXN7L3 is decreased in the brains of people with Alzheimer's disease, and that higher levels of the protein have been associated with a more severe form of the disease. This suggests that ATXN7L3 may be a useful biomarker for the diagnosis and progression of Alzheimer's disease.

Overall, the protein ATXN7L3 (AT7L3_HUMAN) is a promising candidate for drug targeting and biomarker research in the development of neurodegenerative diseases. Further studies are needed to fully understand its role in these conditions and to determine the best way to use it as a therapeutic agent.

Protein Name: Ataxin 7 Like 3

Functions: Component of the transcription regulatory histone acetylation (HAT) complex SAGA, a multiprotein complex that activates transcription by remodeling chromatin and mediating histone acetylation and deubiquitination. Within the SAGA complex, participates in a subcomplex that specifically deubiquitinates both histones H2A and H2B (PubMed:18206972, PubMed:21746879). The SAGA complex is recruited to specific gene promoters by activators such as MYC, where it is required for transcription. Required for nuclear receptor-mediated transactivation. Within the complex, it is required to recruit USP22 and ENY2 into the SAGA complex (PubMed:18206972). Regulates H2B monoubiquitination (H2Bub1) levels. Affects subcellular distribution of ENY2, USP22 and ATXN7L3B (PubMed:27601583)

The "ATXN7L3 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 ATXN7L3 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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