AGXT2

AGXT2 activity may be affected by oxidative stress due to the potential modification of critical cysteine residues in the enzyme's active site. Such modifications might impact its ability to detoxify glyoxylate effectively.

Yes, mutations in the AGXT2 gene have been linked to primary hyperoxaluria type 3 (PH3), a rare genetic disorder characterized by excessive oxalate production, leading to kidney stone formation and renal failure.

AGXT2 may interact with specific signaling pathways related to oxidative stress, inflammation, and calcium homeostasis, which could contribute to kidney stone formation and renal health.

AGXT2 and AGXT share similarities in their enzymatic functions, but AGXT is primarily expressed in the liver and catalyzes the conversion of glyoxylate and alanine to glycine, while AGXT2 is expressed in various tissues and has a broader substrate specificity.

AGXT2 has potential as a therapeutic target for managing oxalate-related diseases, such as PH3. Modulating AGXT2 activity might help reduce oxalate levels and prevent kidney stone formation.

Identification of AGXT2-related biomarkers could aid in early detection and diagnosis of metabolic disorders, especially those involving oxalate metabolism and kidney stone disease.

AGXT2 expression is regulated by various factors, including nuclear receptors and transcription factors. Post-translational modifications, such as phosphorylation and acetylation, can also modulate its enzymatic activity.

AGXT2 is primarily expressed in the liver, kidneys, and the central nervous system, where it localizes to mitochondria.

AGXT2 is involved in the detoxification of glyoxylate, preventing its accumulation, which is crucial in avoiding calcium oxalate kidney stone formation and various metabolic disorders.

AGXT2 requires pyridoxal 5'-phosphate (PLP), the active form of vitamin B6, as a cofactor for its enzymatic activity. PLP assists in the transfer of amino groups during the transamination reactions.