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Article

Human mitochondrial leucyl tRNA synthetase can suppress non cognate pathogenic mt-tRNA mutations.

EMBO molecular medicine - 1 Feb 2014

Hornig-Do Hue Tran, Montanari Arianna, Rozanska Agata, Tuppen Helen A, Almalki Abdulraheem A, Abg-Kamaludin Dyg P, Frontali Laura, Francisci Silvia, Lightowlers Robert N, Chrzanowska-Lightowlers Zofia M

Abstract excerpt

Disorders of the mitochondrial genome cause a wide spectrum of disease, these present mainly as neurological and/or muscle related pathologies. Due to the intractability of the human mitochondrial genome there are currently no effective treatments for these disorders. The majority of the pathogenic mutations lie in the genes encoding mitochondrial tRNAs. Consequently, the biochemical deficiency is due to...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Mitochondria

Share to Oxidative Phosphorylation

Share to Protein Binding

Share to Protein Structure, Tertiary

Share to RNA, Transfer, Leu

Share to Suppression, Genetic

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Identifiers

PMID: 24413189
DOI: 10.1002/emmm.201303202
PMCID: PMC3927954

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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