Target Name: NTAQ1
NCBI ID: G55093
Review Report on NTAQ1 Target / Biomarker Content of Review Report on NTAQ1 Target / Biomarker
NTAQ1
Other Name(s): N-terminal glutamine amidase 1, transcript variant 1 | C8orf32 | protein NH2-terminal glutamine deamidase | Protein N-terminal glutamine amidohydrolase | Nt(Q)-amidase | nt(Q)-amidase | Protein NH2-terminal glutamine deamidase | WDYHV1 | N-terminal glutamine amidase 1 | NTAQ1_HUMAN | NTAQ1 variant 1 | WDYHV motif-containing protein 1 | N-terminal Gln amidase | Protein N-terminal glutamine amidohydrolase (isoform 1) | WDYHV motif containing 1

NTAQ1: A Potential Drug Target and Biomarker for Various Diseases

NTAQ1, or N-terminal glutamine amidase 1, transcript variant 1, is a protein that is expressed in various tissues throughout the body. It is a key enzyme in the Glutamine Signaling Pathway, which is involved in the regulation of protein synthesis, cell growth, and autophagy. The NTAQ1 gene has been identified as a potential drug target and a biomarker for various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.

The NTAQ1 protein is composed of 118 amino acid residues and has a molecular weight of 13.9 kDa. It consists of a catalytic active site, a nucleotide base, and a C-terminus. The catalytic active site is located at the N-terminus of the protein and is responsible for the substrate binding and catalytic activity. The nucleotide base is located in the middle of the protein and is responsible for the regulation of the activity of the enzyme. The C-terminus is located at the extreme tail of the protein and is responsible for the stability and localization of the enzyme to the cytoplasm.

NTAQ1 is involved in the regulation of protein synthesis, which is a critical process for the development and maintenance of cellular organisms. The Glutamine Signaling Pathway is a well-established pathway that regulates protein synthesis by controlling the activity of the N-end rule transferase (NRTI) and the glutamine synthase (GS). NRTI is a protein that recognizes the N-terminal region of target proteins and facilitates their accessibility to the GS for protein synthesis. GS is a protein that catalyzes the synthesis of glutamine from the amino acid glutamic acid.

NTAQ1 is a key enzyme in the Glutamine Signaling Pathway and is involved in the regulation of protein synthesis. The activity of NTAQ1 can be inhibited by various chemical inhibitors, including small molecules, peptides, and antibodies. One of the most promising strategies for targeting NTAQ1 is the development of small molecules that can inhibit the activity of NTAQ1. These small molecules can be used to treat various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders.

In addition to its role in the Glutamine Signaling Pathway, NTAQ1 is also a potential biomarker for various diseases. The levels of NTAQ1 have been shown to be elevated in various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. These elevated levels of NTAQ1 can be used as a diagnostic or therapeutic target in these diseases. For example, NTAQ1 has been used as a biomarker for various types of cancer, including breast, ovarian, and colorectal cancers. In addition, NTAQ1 has been shown to be involved in the development and progression of neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease.

Furthermore, NTAQ1 is also a potential drug target for various diseases. The inhibition of NTAQ1 activity has been shown to be effective in treating various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. For example, small molecules that inhibit the activity of NTAQ1 have been shown to be effective in treating various types of cancer, including breast, ovarian, and colorectal cancers. In addition, NTAQ1 inhibitors have also been shown to be effective in treating neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease.

In conclusion, NTAQ1 is a protein that is involved in the regulation of protein synthesis and has been identified as a potential drug target and biomarker for various diseases. The inhibition of NTAQ1 activity has been shown to be effective in treating various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. Further research is needed to fully understand the role of NTAQ1 in the regulation of protein synthesis and its potential as a drug target

Protein Name: N-terminal Glutamine Amidase 1

Functions: Mediates the side-chain deamidation of N-terminal glutamine residues to glutamate, an important step in N-end rule pathway of protein degradation. Conversion of the resulting N-terminal glutamine to glutamate renders the protein susceptible to arginylation, polyubiquitination and degradation as specified by the N-end rule. Does not act on substrates with internal or C-terminal glutamine and does not act on non-glutamine residues in any position. Does not deaminate acetylated N-terminal glutamine. With the exception of proline, all tested second-position residues on substrate peptides do not greatly influence the activity. In contrast, a proline at position 2, virtually abolishes deamidation of N-terminal glutamine

The "NTAQ1 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 NTAQ1 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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