EC Number   |
Application |
Reference |
|---|
    6.1.1.4 | drug development |
leucyl-tRNA synthetase (LeuRS) is an attractive therapeutic target and a target for development of drugs |
-, 745458 |
| 6.1.1.4 | drug development |
LeuRS is a potential target for antiparasitic drug development |
715854 |
| 6.1.1.4 | medicine |
LARS1 plays roles in migration and growth of lung cancer cells, which suggest its potential implication in lung tumorigenesis |
692229 |
| 6.1.1.4 | medicine |
pretreatment of mice with zinc sulfate solution favors to protection of protein synthesis and acceptor activity of tRNALeu against cadmium-induced inhibition. Under co-exposure of mouse liver to cadmium and zinc, activity of the leucyl-tRNA synthetase is at the level of control. Zinc does not influence TUNEL-positive cell number in cadmium-exposed mouse liver |
693987 |
| 6.1.1.4 | medicine |
suppression of a tRNA gene mutation by increasing the steady-state levels of its cognate aminoacyl-tRNA synthetase is a model for potential therapies for human pathogenic tRNA mutations |
695107 |
| 6.1.1.4 | medicine |
the A3243G mutation of the tRNALeu gene causes mitochondrial encephalomyopathy, lactic acidosis, and stroke-like symptoms and 2% of cases of type 2 diabetes. The alteration of aminoacylation of tRNALeu(UUR) caused by the A3243G mutation leads to mitochondrial translational defects and thereby reduces the aminoacylating efficiencies of tRNALeu(UUR) as well as of tRNAAla and tRNAMet. The transfer of human mitochondrial leucyl-tRNA synthetase into the cybrid cells carrying the A3243G mutation improve the efficiency of aminoacylation and stability of mitochondrial tRNAs and then increase the rates of mitochondrial translation and respiration, consequently correcting the mitochondrial dysfunction |
705705 |
