SerRSmt Inhibitors

SerRSmt Inhibitors predominantly work by perturbing mitochondrial functionality or energy homeostasis, thereby exerting an influence on SerRSmt's role in aminoacylation. Agents like AICAR, an AMPK, target cellular energy regulation. AICAR modifies the AMP/ATP ratio, affecting SerRSmt which uses ATP in tRNA aminoacylation. mTOR inhibitors like Torin 1 and Rapamycin work by attenuating the global rate of protein synthesis. This reduction in translation rate can lessen the cellular requirement for tRNA ligases, including SerRSmt, altering their enzymatic activity indirectly. Compounds such as Oligomycin, a mitochondrial ATP synthase inhibitor, have an immediate effect on ATP pools, which are crucial for the ATP-dependent aminoacylation reactions that SerRSmt catalyzes.

Additional classes of indirect inhibitors include DNA intercalators and topoisomerase inhibitors such as Mitoxantrone and Etoposide, which affect mitochondrial gene expression. As SerRSmt is crucial for mitochondrial protein translation, disruption in the expression of mitochondrial genes could indirectly impair its function. Compounds like Actinonin, which inhibits peptide deformylase, can decrease the rate of protein turnover, thus affecting the demand for aminoacylated tRNAs and the activity of SerRSmt. Azathioprine, a purine synthesis inhibitor, can further affect ATP pools, causing downstream effects on any ATP-dependent activity of SerRSmt. Collectively, these compounds illuminate various indirect routes for inhibiting SerRSmt's enzymatic activity.