Premature Termination Codons (PTC) introduced by nonsense mutations (NSM) in genetic diseases lead to the synthesis of truncated proteins and are consequently linked to loss-of-function phenotype. The goal of my project is to refactor natural tRNAs into suppressor tRNAs (sup-tRNAs) to alleviate protein synthesis and combat PTC-associated diseases. Additionally, I am working on modulating promoter and terminator sequences to control the sup-tRNA expression, stability, and functional efficiency in a tissue-specific manner. This optimization is crucial for maximizing the therapeutic potential of sup-tRNA therapeutics.
