The class of AASS inhibitors encompasses a diverse array of compounds that directly or indirectly modulate the activity of the enzyme involved in the biosynthesis of essential amino acids. Aminooxyacetic acid and Methoxyacetic acid serve as indirect inhibitors by disrupting the serine biosynthesis pathway, specifically inhibiting serine hydroxymethyltransferase (SHMT). These compounds alter the availability of serine, a precursor for AASS, indirectly influencing its expression and function within the context of branched-chain amino acid synthesis. Hydroxycitrate and Fluorooxalate act as indirect inhibitors by disrupting the tricarboxylic acid (TCA) cycle and oxalate metabolism, respectively. These compounds indirectly influence AASS by perturbing the availability of substrates required for amino acid synthesis, underscoring the interconnectedness of metabolic pathways and their impact on AASS-mediated processes.
Gabaculine, Homocysteine, Propargylglycine, and Acivicin represent indirect inhibitors affecting AASS through various mechanisms. Gabaculine disrupts pyridoxal phosphate-dependent enzymes, Homocysteine influences the folate-dependent one-carbon metabolism, Propargylglycine interferes with cysteine biosynthesis, and Acivicin hinders glutamine-dependent amidotransferase activity. These compounds collectively showcase the diverse regulatory mechanisms governing AASS activity within the broader landscape of amino acid metabolism. D-Cysteine, serving as a direct activator of AASS, exemplifies how specific amino acids can positively regulate the enzyme's function by providing essential substrates. Oxythiamine and alpha-Methyltryptophan act as indirect inhibitors by disrupting thiamine-dependent enzymes and tryptophan metabolism, respectively, showcasing additional layers of complexity in the modulation of AASS activity. In summary, the class of AASS inhibitors comprises a nuanced collection of chemicals that intricately regulate the enzyme's expression and function, shedding light on the multifaceted interconnections between amino acid metabolism and cellular homeostasis.
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Gabaculine | 59556-17-1 | sc-200473 sc-200473A sc-200473B | 10 mg 50 mg 250 mg | $354.00 $884.00 $3069.00 | 5 | |
Gabaculine inhibits AASS indirectly by disrupting the pyridoxal phosphate-dependent enzymes involved in amino acid metabolism. As a potent inhibitor of aminotransferases, it affects the interconversion of amino acids, indirectly influencing the substrate availability for AASS. This sheds light on the complex regulatory network governing AASS activity within the broader context of amino acid metabolism. | ||||||
Homocysteine | 6027-13-0 | sc-507315 | 250 mg | $195.00 | ||
Homocysteine acts as an indirect inhibitor of AASS by influencing the folate-dependent one-carbon metabolism. Through its impact on the methionine cycle, homocysteine alters the availability of precursors for AASS activity, indirectly modulating its expression and function. Understanding the regulatory role of homocysteine provides insights into the intricate connections between amino acid metabolism and cellular homeostasis. | ||||||
Acivicin | 42228-92-2 | sc-200498B sc-200498C sc-200498 sc-200498D | 1 mg 5 mg 10 mg 25 mg | $104.00 $416.00 $655.00 $1301.00 | 10 | |
Acivicin inhibits AASS indirectly by interfering with the glutamine-dependent amidotransferase activity. As a competitive inhibitor of glutamine amidotransferases, it disrupts the synthesis of amino acids, indirectly influencing the substrate availability for AASS activity. This modulation highlights the intricate connections between glutamine metabolism and the regulation of AASS-mediated processes. | ||||||
Oxythiamine chloride hydrochloride | 614-05-1 | sc-236265 sc-236265A sc-236265B | 1 g 5 g 25 g | $40.00 $121.00 $446.00 | 2 | |
Oxythiamine inhibits AASS indirectly by interfering with thiamine-dependent enzymes involved in amino acid metabolism. As a thiamine antagonist, it disrupts key enzymatic reactions, influencing the availability of precursors for AASS activity. This modulation sheds light on the complex regulatory network governing AASS activity within the broader context of thiamine-dependent pathways. | ||||||