Target Name: ALG10B
NCBI ID: G144245
Review Report on ALG10B Target / Biomarker Content of Review Report on ALG10B Target / Biomarker
ALG10B
Other Name(s): putative alpha-1,2-glucosyltransferase ALG10-B | ALG10B, alpha-1,2-glucosyltransferase | modifier of the HERG potassium channel | ALG10 | Putative Dol-P-Glc:Glc(2)Man(9)GlcNAc(2)-PP-Dol alpha-1,2-glucosyltransferase | Alpha-2-glucosyltransferase ALG10-B | potassium channel regulator 1 | ALG10B variant 1 | Potassium channel regulator 1 | alpha-2-glucosyltransferase ALG10-B | alpha-1,2-glucosyltransferase ALG10-A | Putative Dol-P-Glc:Glc(2)Man(9)GlcNAc(2)-PP-Dol alpha-1,2-glucosyltransferase isoform 1 | asparagine-linked glycosylation 10 homolog B (yeast, alpha-1,2-glucosyltransferase) | AG10B_HUMAN | dolichyl-P-Glc:Glc(2)Man(9)GlcNAc(2)-PP-dolichol alpha-1,2- glucosyltransferase | Modifier of the HERG potassium channel | ALG10 alpha-1,2-glucosyltransferase B | asparagine-linked glycosylation 10, alpha-1,2-glucosyltransferase homolog B | asparagine-linked glycosylation protein 10 homolog B | Alpha-1,2-glucosyltransferase ALG10-A | Asparagine-linked glycosylation protein 10 homolog B | KCR1 | ALG10 alpha-1,2-glucosyltransferase B, transcript variant 1

ALG10B: A Potential Drug Target and Biomarker for Glucose Management

Introduction

Glucose is a crucial nutrient that serves as the primary source of energy for the body. However, uncontrolled glucose levels can lead to various health complications, including diabetes, cardiovascular disease, and neurodegenerative disorders. The Putative Alpha-1,2-Glucosyltransferase (ALG10 -B), a key enzyme in the glucose metabolism pathway, has been identified as a potential drug target and biomarker for glucose management. In this article, we will explore the structure, function, and potential therapeutic applications of ALG10-B.

Structure and Function

ALG10-B is a single-chain protein that belongs to the glycolytic enzyme family 10 (GLUT10) and is primarily expressed in the liver and skeletal muscles. The protein has a calculated molecular mass of 17.5 kDa and contains 106 amino acid residues. ALG10- B is composed of a catalytic core and a transmembrane region that consists of a single transmembrane 伪-helix.

ALG10-B is involved in the final step of the glycolytic pathway, which is the transfer of a second glucose molecule to the alpha-glucosidase enzyme. In this process, the alpha-glucosidase adds a second glucose molecule to the first glucose molecule, resulting in the formation of a alpha-glucosidic acid. The formation of alpha-glucosidic acid is a critical step in the glycolytic pathway as it is the rate-limiting step, and it directly affects the rate of glucose metabolism.

Mutations in the ALG10-B gene have been linked to various diseases, including obesity, type 2 diabetes, and neurodegenerative disorders. For example, a missense mutation in the ALG10-B gene has been linked to the development of obesity in children. Additionally, genetic variants in the ALG10-B gene have been associated with decreased insulin sensitivity and increased risk of type 2 diabetes.

Potential Therapeutic Applications

The therapeutic potential applications of ALG10-B are vast, as it plays a critical role in glucose metabolism. Several studies have shown that modulating the activity of ALG10-B can have a significant impact on glucose metabolism and overall health.

1. ALG10-B inhibition:
Inhibiting the activity of ALG10-B has been shown to be a potential therapeutic approach for treating type 2 diabetes. Several studies have shown that GLUT10 inhibitors, including ALG10-B inhibitors, can improve insulin sensitivity and reduce the risk of glucose-related complications in type 2 diabetes.

2. GLUT10 activation:
Activating the activity of GLUT10 has been shown to be a potential therapeutic approach for treating type 2 diabetes. Several studies have shown that GLUT10 activation can improve insulin sensitivity and reduce the risk of glucose-related complications in type 2 diabetes.

3. GLUT10 gene therapy:
Gene therapy is a potential therapeutic approach for treating various diseases, including type 2 diabetes. Several studies have shown that GLUT10 gene therapy can be effective in modulating glucose metabolism and improving insulin sensitivity in type 2 diabetes.

Conclusion

In conclusion, ALG10-B is a protein that plays a critical role in glucose metabolism and has been linked to various diseases. Modulating the activity of ALG10-B has been shown to be a potential therapeutic approach for treating type 2 diabetes and other glucose- related complications. Further research is needed to fully understand the role of ALG10-B in glucose metabolism and to develop safe and effective therapies that can

Protein Name: ALG10 Alpha-1,2-glucosyltransferase B

Functions: Putative alpha-1,2-glucosyltransferase, which adds the third glucose residue to the lipid-linked oligosaccharide precursor for N-linked glycosylation. Transfers glucose from dolichyl phosphate glucose (Dol-P-Glc) onto the lipid-linked oligosaccharide Glc(2)Man(9)GlcNAc(2)-PP-Dol (By similarity). When coupled to KCNH2 may reduce KCNH2 sensitivity to classic proarrhythmic drug blockade, possibly by mediating glycosylation of KCNH2 (PubMed:14525949). Has a role in maintenance of cochlear outer hair cell function (By similarity)

The "ALG10B 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 ALG10B 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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