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Mechanically, we found that thiotert dramatically inactivates the TRX1 and TERT, which facilitates redox system disequilibrate and telomeres dysfunction

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This aligns with the broader concept that genetic influences on pharmacodynamics and pharmacokinetics are interdependentwhere gene-driven differences in enzymatic metabolism directly alter drug exposure, influencing receptor interactions, signaling cascades, and ultimately clinical effectiveness (Li et al., 2024

Lysate preparation and binding for E.coli BL21 cells were transformed with E.coli SelO ppSumo and grown in LB media containing 50 g/ml of kanamycin at 37 C