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(Redirected from TARS3)
TARS1
Identifiers
AliasesTARS1, ThrRS, threonyl-tRNA synthetase, TARS, threonyl-tRNA synthetase 1, TTD7
External IDsOMIM: 187790; MGI: 106314; GeneCards: TARS1
Available structures
PDBOrtholog search: PDBe RCSB
Enzyme activity
EC #BRENDAExPASyKEGGMetaCyc
6.1.1.3↗↗↗↗
Orthologs
DatabasesNCBI: entry; OMA: entry
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_001258437
NM_001258438
NM_152295

NM_033074

RefSeq (protein)

NP_001245366
NP_001245367
NP_689508

NP_149065

Location (UCSC)Chr 5: 33.44 – 33.47 MbChr 15: 11.38 – 11.4 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Threonine–tRNA ligase 1, cytoplasmic, also called threonyl-tRNA synthetase 1, is an enzyme that in humans is encoded by the TARS1 gene.[5] Like its relatives, TARS2 and TARS3, this enzyme functions as a threonine–tRNA ligase,[5][6] which means it attaches the animo acid threonine to its corresponding transfer RNA as part of RNA-to-protein translation.[7]

Function

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Aminoacyl tRNA synthetases catalyze the aminoacylation of tRNA by their cognate amino acid. Because of their central role in linking amino acids with nucleotide triplets contained in tRNAs, aminoacyl-tRNA synthetases are thought to be among the first proteins that appeared in evolution. Threonyl-tRNA synthetase belongs to the class-II aminoacyl-tRNA synthetase family.[5]

Comparison with TARS3

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Cytoplasmic threonine–tRNA ligase is unique in vertebrate aminoacyl-tRNA synthetases in having a second form, TARS3 (previously called TARSL2), evolved from a gene duplication.[8] In mice, the TARS1 enzyme is significantly more prevalent (55x in lungs, and 3x in muscles).[9] Structurally, TARS1 functions as a homodimer,[10] while TARS3 may instead be a component of the protein complex: multisynthetase complex (MSC).[9] TARS1 is also smaller, 83 kD vs. 93 kD, and this has been used to infer that it is the primary target of the antibodies involved in antisynthetase syndrome.[9]

Medical significance

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Pathogenic (homozygous and compound heterozygous) mutations in TARS1 are associated with trichothiodystrophy (a type of hair fragility disorder), with the type caused by TARS1 mutation designated as: nonphotosensitive trichothiodystrophy-7 (TTD7).[11]

References

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This article incorporates text from the United States National Library of Medicine, which is in the public domain.

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000113407 – Ensembl, May 2017
  2. 1 2 3 GRCm38: Ensembl release 89: ENSMUSG00000022241 – Ensembl, May 2017
  3. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. 1 2 3 "Entrez Gene: TARS threonyl-tRNA synthetase".
  6. ↑ EC 3.1.1.3
  7. ↑ Gomez MA, Ibba M (2020-04-17). "Aminoacyl-tRNA synthetases". Rna. doi:10.1261/rna.071720.119. PMC 7373986.
  8. ↑ Zeng QY, Zhang F, Zhang JH, Hei Z, Li ZH, Huang MH, Fang P, Wang ED, Sun XJ, Zhou XL (2023-05-01). "Loss of threonyl-tRNA synthetase-like protein Tarsl2 has little impact on protein synthesis but affects mouse development". Journal of Biological Chemistry. 299 (5). doi:10.1016/j.jbc.2023.104704.
  9. 1 2 3 Kanaji S, Chen W, Morodomi Y, Shapiro R, Kanaji T, Yang XL (2023-03-01). "Mechanistic perspectives on anti-aminoacyl-tRNA synthetase syndrome". Trends in biochemical sciences. 48 (3): 288–302. doi:10.1016/j.tibs.2022.09.011.
  10. ↑ "Threonine--tRNA ligase 1, cytoplasmic". UniProt consortium. Retrieved 2026-10-01.
  11. ↑ "TRICHOTHIODYSTROPHY 7, NONPHOTOSENSITIVE; TTD7". Online Mendelian Inheritance in Man. Johns Hopkins University. Retrieved 2026-09-27.

Further reading

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