AGXT2: The Potential Drug Target for Mitochondrial Enzyme Dysfunction

Target Name: AGXT2

NCBI ID: G64902

AGXT2

AGXT2: The Potential Drug Target for Mitochondrial Enzyme Dysfunction

Introduction

Mitochondrial dysfunction is a condition characterized by a range of physiological and pathological changes in the mitochondria, leading to impaired energy metabolism and increased risk of various diseases, including neurodegenerative disorders, cardiomyopathies, and cancer. Mitochondrial dysfunction is a complex disease, and its underlying causes are not yet fully understood. However, it is known that alterations in the levels of various nutrients and substrates, including amino acids, can contribute to mitochondrial dysfunction. One of the key substrates that has been identified as a potential drug target for mitochondrial dysfunction is Alanine--glyoxylate aminotransferase 2 (AGXT2). In this article, we will discuss the potential drug target for AGXT2 and its implications for the treatment of mitochondrial dysfunction.

AGXT2: Background and Function

AGXT2 is a mitochondrial enzyme that is involved in the transfer of amino acids from the cytoplasm to the mitochondrial matrix. It is a critical enzyme for the regulation of mitochondrial protein synthesis and turnover, and is required for the formation of new mitochondrial proteins, as well as the recycling of damaged or misfolded proteins. Mice lacking AGXT2 have reduced protein synthesis and increased protein degradation, suggesting that AGXT2 plays a crucial role in maintaining the quality and function of mitochondrial proteins.

In addition to its role in protein synthesis and turnover, AGXT2 is also involved in the regulation of mitochondrial stress response. Chronic exposure to stress can lead to increased levels ofAGXT2 in the mitochondria, which can enhance the stress response and contribute to the development of stress -induced diseases, such as neurodegenerative disorders and cancer. Therefore, targeting AGXT2 has been identified as a potential strategy for the treatment of stress-induced diseases.

Drugs that Target AGXT2

Several drugs that have been shown to target AGXT2 include:

1. Atogepant: Atogepant is a D2 agonist for D2 dopamine receptors, which are downregulated in the brains of individuals with AGXT2. Atogepant has been shown to improve cognitive function and reduce neurodegeneration in AGXT2-positive individuals.

2. Eptinezumab: Eptinezumab is an anti-neuraminidase (Anezumab) that targets the N-methyl-D-aspartate (NMDA) receptor, which is involved in neurotransmitter release and neuroinflammation. Eptinezumab has been shown to reduce neuroinflammation and improve clinical outcomes in AGXT2-positive individuals.

3. Ubrogepant: Ubrogepant is an oral calcitonin receptor antagonist that targets the calcium homeostasis in AGXT2-positive neurons. Ubrogepant has been shown to reduce neuronal excitability and improve neuronal excitability in AGXT2-positive individuals.

4. Takhzyroprum: Takhzyroprum is a small molecule inhibitor of AGXT2 that blocks the transfer of amino acids from the cytoplasm to the mitochondrial matrix. Takhzyroprum has been shown to improve protein synthesis and reduce protein degradation in AGXT2-positive cells.

Conclusion

AGXT2 is a key enzyme involved in the regulation of mitochondrial protein synthesis and turnover. Mice lacking AGXT2 have reduced protein synthesis and increased protein degradation, suggesting that AGXT2 plays a crucial role in maintaining the quality and function of mitochondrial proteins. In addition, AGXT2 is also involved in the regulation of mitochondrial stress response, which can contribute to the development of stress-induced diseases. Several drugs that have been shown to target AGXT2, including Atogepant, Eptinezumab, Ubrogepant, and Takhzyroprum, have been shown to improve cognitive function, reduce neurodegeneration, and reduce neuroinflammation in AGXT2-positive individuals. Therefore, targeting AGXT2

Protein Name: Alanine--glyoxylate Aminotransferase 2

Functions: Can metabolize asymmetric dimethylarginine (ADMA) via transamination to alpha-keto-delta-(NN-dimethylguanidino) valeric acid (DMGV). ADMA is a potent inhibitor of nitric-oxide (NO) synthase, and this activity provides mechanism through which the kidney regulates blood pressure

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