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Mitochondrially encoded tRNA threonine (MT-TT, also known as tRNA-Thr or trnT) is a transfer RNA gene located in human mitochondrial DNA, spanning 66 nucleotides (mitochondrial position 15888-15953). Its primary molecular function is to transfer threonine to a growing polypeptide chain during mitochondrial translation, thus facilitating protein synthesis within mitochondria[1][2][4]. Like other mitochondrial tRNAs, MT-TT is essential for proper assembly of the oxidative phosphorylation complexes critical for energy production. Mutations in MT-TT can lead to a range of mitochondrial diseases, including MERRF, cytochrome c oxidase deficiency, cardiovascular disease, infantile myopathy, and Parkinson’s disease, mostly via effects on mitochondrial protein synthesis, energy metabolism, and cellular viability[1][2][3]. While not a direct drug target, pathogenic MT-TT variants are valuable disease biomarkers for screening and diagnosis[3][1][4].
Not applicable. Drugs do not directly target MT-TT; however, mitochondrial tRNA mutations can affect response to mitochondrial function–targeting drugs indirectly[1][3].
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