Threonyl-tRNA synthetase 2, mitochondrial (TARS2)

Threonyl-tRNA synthetase 2, mitochondrial (TARS2) is a class-II aminoacyl-tRNA synthetase that resides in mitochondria, where it catalyzes the attachment of threonine to its cognate tRNA (tRNA^Thr) as a critical step in mitochondrial protein synthesis[2][4]. It also possesses editing activity to ensure translation fidelity by removing mischarged serine-tRNA^Thr[5][3]. TARS2 is essential for proper mitochondrial function, cell energy metabolism, and viability. Mutations in TARS2 are causative for mitochondrial encephalomyopathies and broader mitochondrial diseases[3]. Dysregulation or overexpression of TARS2 contributes to tumorigenesis, particularly in lung adenocarcinoma, where it modulates cell proliferation (via the RB pathway) and apoptosis (through regulation of mitochondrial ROS)[1][5]. TARS2 is not currently targeted by approved drugs, but its unique roles in mitochondrial translation and cell signaling mark it as a candidate for future therapeutic research.

Other names

Threonine--tRNA ligase, mitochondrialThreonyl-tRNA synthetase-like 1TARSL1ThrRSFLJ12528COXPD21threonine tRNA ligase 2, mitochondrialthrRS

Not directly targeted by any drugs in clinical use or research as of now. Potential mechanisms for future targeting could involve inhibition of enzymatic activity or modulation of mitochondrial ROS production, affecting apoptotic pathways and cell proliferation[1].