ADH1C: A Potential Drug Target and Biomarker for Alcohol-Related Disorders

Target Name: ADH1C

NCBI ID: G126

ADH1C

ADH1C: A Potential Drug Target and Biomarker for Alcohol-Related Disorders

Abstract:
Alcohol-related disorders are a significant public health issue worldwide, affecting millions of individuals and causing significant morbidity and mortality. The aim of this article is to provide an overview of ADH1C, a gene that has been identified as a potential drug target and biomarker for alcohol-related disorders. The article will cover the molecular and cellular mechanisms of ADH1C function, its potential as a drug target, and its potential as a biomarker for assessing the severity and progression of alcohol-related disorders.

Introduction:
Alcohol use disorder (AUD) is a chronic condition that can lead to significant physical, emotional, and social consequences. The World Health Organization (WHO) estimates that in 2019, approximately 214 million adults worldwide consumed alcohol. Unfortunately, many individuals with AUD do not seek or receive proper treatment, leading to significant morbidity and mortality associated with alcohol-related disorders.

One of the known genetic risk factors for AUD is the ADH gene family. The ADH gene family encodes the subunit gamma (ADH1C) gene, which is responsible for the production of the enzyme alcohol dehydrogenase (ADH). The primary function of ADH is to Convert alcohol to ethyl acetate, thereby reducing alcohol damage to the liver. However, mutations in the ADH1C gene can lead to reduced ADH activity, thereby increasing the risk of liver damage from drinking alcohol.

Molecular and cellular mechanisms:
The protein encoded by the ADH1C gene is an 8kDa polypeptide consisting of 114 amino acids. The protein encoded by the ADH1C gene is synthesized by ribosomes in cells, then modified by the endoplasmic reticulum and Golgi, and finally secreted out of the cell.

Variations in the ADH1C gene can lead to changes in the structure and function of the ADH1C protein. Studies have found that mutations in the ADH1C gene will lead to changes in the amino acid composition of the ADH1C protein, especially the increased content of lysine (Lysine) and threonine (Threonine), while the content of tryptophan (Serine) and histidine (Histidine) content decreased. These changes may affect the activity of ADH1C, preventing it from functioning normally.

Variations in the ADH1C gene may also lead to changes in the localization of ADH1C within cells. Research has found that mutations in the ADH1C gene may cause changes in the localization of ADH1C protein within cells, moving from the cytoplasm to the nucleus. This change may affect the transcription and expression of the ADH1C gene, thereby affecting the activity of ADH1C.

Drug target:
Variations in the ADH1C gene are closely related to the occurrence and development of AUD. Therefore, using the ADH1C gene as a drug target to treat AUD has important clinical value. Currently, there are a variety of drug targets related to the ADH1C gene, including AUD, cirrhosis and other diseases.

potential drug targets:
1.

Protein Name: Alcohol Dehydrogenase 1C (class I), Gamma Polypeptide

Functions: Alcohol dehydrogenase. Exhibits high activity for ethanol oxidation and plays a major role in ethanol catabolism

The "ADH1C 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 ADH1C 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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