ArticleInternational journal of biological sciences2018
Overexpression of human mitochondrial alanyl-tRNA synthetase suppresses biochemical defects of the mt-tRNA
Article in International journal of biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Gene Therapy Tools for Diseases Caused by Mutations of the Mitochondrial Genome.International journal of molecular sciences · 2026Review
- Mitochondrial alanyl-tRNA synthetase 2 mediates histone lactylation to promote ferroptosis in intestinal ischemia-reperfusion injury.World journal of gastrointestinal surgery · 2025Article
- AARS2 ameliorates myocardial ischemiaeLife · 2025Article
- Two novel likely pathogenic variants of HARS2 identified in a Chinese family with sensorineural hearing loss.Hereditas · 2020Article
- Overexpression of mitochondrial histidyl-tRNA synthetase restores mitochondrial dysfunction caused by a deafness-associated tRNAThe Journal of biological chemistry · 2020Article
- Mitochondrial Dysfunction in Primary Ovarian Insufficiency.Endocrinology · 2019Review
- Novel ACADVL variants resulting in mitochondrial defects in long-chain acyl-CoA dehydrogenase deficiency.Journal of Zhejiang University. Science. BArticle
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8 authors at 1 institution in 1 country.
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Abstract
Mutations of mitochondrial transfer RNAs (mt-tRNAs) play a major role in a wide range of mitochondrial diseases because of the vital role of these molecules in mitochondrial translation. It has previously been reported that the overexpression of mitochondrial aminoacyl tRNA synthetases is effective at partially suppressing the defects resulting from mutations in their cognate mt-tRNAs in cells. Here we report a detailed analysis of the suppressive activities of mitochondrial alanyl-tRNA synthetase (AARS2) on mt-tRNA
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