GLYATL1: A Potential Drug Target and Biomarker for Various Diseases

Target Name: GLYATL1

NCBI ID: G92292

GLYATL1

GLYATL1: A Potential Drug Target and Biomarker for Various Diseases

GLYATL1 (GATF-C), a gene located on chromosome 19q, has been identified as a potential drug target and biomarker for various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. Its unique genetic mutation, which results in the substitution of a single nucleotide for a thymine, has led to the production of a unique protein that has distinct features, including a higher than normal level of glutamine, a key signaling molecule in the immune system.

Recent studies have demonstrated that GLYATL1 is involved in the development and progression of various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. For example, studies have shown that GLYATL1 is highly expressed in various types of cancer, including breast, ovarian, and colorectal cancer. Additionally, GLYATL1 has been shown to be involved in the development of neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, as well as autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis.

The substitution of a single nucleotide for a thymine in the GLYATL1 gene has led to the production of a unique protein that has distinct features. This protein, known as GLYATL1-T, has a higher than normal level of glutamine, a key signaling molecule in the immune system. This higher level of glutamine has been shown to promote the growth and survival of cancer cells, making GLYATL1-T a potential drug target for cancer treatment.

In addition to its role in cancer, GLYATL1 has also been shown to be involved in the development and progression of neurodegenerative disorders. Studies have shown that GLYATL1 is highly expressed in the brain and that it is involved in the development of neurodegenerate markers, such as neurofilaments and astrocytes. Additionally, GLYATL1 has been shown to be involved in the development of various neurodegenerative disorders, including Alzheimer's disease and Parkinson's disease.

GLYATL1 has also been shown to be involved in the development and progression of autoimmune diseases. Studies have shown that GLYATL1 is highly expressed in various types of autoimmune diseases, including rheumatoid arthritis and multiple sclerosis. Additionally, GLYATL1 has been shown to be involved in the development of autoimmune diseases by promoting the production of immune cells that are involved in inflammation and disease.

In conclusion, GLYATL1 is a gene that has been identified as a potential drug target and biomarker for various diseases. Its unique genetic mutation, which results in the substitution of a single nucleotide for a thymine, has led to the production of a unique protein that is involved in the development and progression of cancer, neurodegenerative disorders, and autoimmune diseases. Further research is needed to fully understand the role of GLYATL1 in these diseases and to develop effective treatments.

Protein Name: Glycine-N-acyltransferase Like 1

Functions: Acyltransferase which transfers an acyl group to the N-terminus of glutamine. Can use phenylacetyl-CoA as an acyl donor

The "GLYATL1 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 GLYATL1 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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