{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThreonyl-tRNA synthetase‐like protein, also known as TARSL2 (sometimes referred to as TARS3), was recently identified as a novel component of the multi–tRNA synthetase complex (MSC). Although canonical aminoacyl-tRNA synthetases are chiefly responsible for linking amino acids to their cognate tRNAs during protein synthesis, TARSL2 appears to be evolutionarily derived from the canonical threonyl-tRNA synthetase gene and has acquired unique features that facilitate its integration into the MSC. Its enrichment within the ARS core complex suggests a role not only in translation but possibly also in supporting non‐canonical functions of the MSC."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMolecular investigations into TARSL2 have revealed that its distinct N-terminal extension, which is different from that of the canonical ThrRS, is both necessary and sufficient for its incorporation into the MSC. This N-extension contains two leucine zipper motifs that mediate protein–protein interactions, thereby targeting TARSL2—and even heterologous proteins fused to this region—into the complex. Notably, while TARSL2 is a bona fide MSC component, its deletion does not disturb the overall structural integrity of the MSC, indicating a regulatory rather than an essential structural role within the complex."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a pathological context, TARSL2 plays an intriguing role in the behavior of glioma cells. Studies have shown that microRNA-720 is significantly upregulated in glioma, where it directly targets TARSL2, leading to its downregulation. The loss of TARSL2 correlates with enhanced glioma cell migration and invasion, while reintroduction of TARSL2 mitigates these effects. This inverse relationship suggests that TARSL2 may function as a negative regulator of glioma invasiveness, highlighting its potential importance not only in normal translational regulation within the MSC but also in influencing aberrant cell motility in cancer."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Kyutae Kim, Seong-Jun Park, Seungjin Na, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Reinvestigation of aminoacyl-tRNA synthetase core complex by affinity purification-mass spectrometry reveals TARSL2 as a potential member of the complex."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0081734"}], "href": "https://doi.org/10.1371/journal.pone.0081734"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "24312579"}], "href": "https://pubmed.ncbi.nlm.nih.gov/24312579"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Xiao-Long Zhou, Yun Chen, Qi-Yu Zeng, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Newly acquired N-terminal extension targets threonyl-tRNA synthetase-like protein into the multiple tRNA synthetase complex."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nucleic Acids Res (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/nar/gkz588"}], "href": "https://doi.org/10.1093/nar/gkz588"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31287872"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31287872"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Yinlong Liu, Kuan Jiang, Tongle Zhi, et al. "}, {"type": "b", "children": [{"type": "t", "text": "miR-720 is a key regulator of glioma migration and invasion by controlling TARSL2 expression."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Cell (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s13577-021-00551-x"}], "href": "https://doi.org/10.1007/s13577-021-00551-x"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "34024034"}], "href": "https://pubmed.ncbi.nlm.nih.gov/34024034"}]}]}]}