ArticleScientific reports2021
Leucyl-tRNA synthetase deficiency systemically induces excessive autophagy in zebrafish.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- LARS promotes osteosarcoma proliferation through leucine-dependent PRIM2 translation and DNA replication activation.Journal of experimental & clinical cancer research : CR · 2026Article
- Autophagy: Are Amino Acid Signals Dependent on the mTORC1 Pathway or Independent?Current issues in molecular biology · 2024Review
- Biallelic variants in LARS1 induce steatosis in developing zebrafish liver via enhanced autophagy.Orphanet journal of rare diseases · 2024Article
- Hepatic extracellular ATP/adenosine dynamics in zebrafish models of alcoholic and metabolic steatotic liver disease.Scientific reports · 2024Article
- Recessive aminoacyl-tRNA synthetase disorders: lessons learned fromFrontiers in neuroscience · 2023Review
- Transcriptome-Based Identification of Genes Responding to the Organophosphate Pesticide Phosmet inGenes · 2021Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
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Abstract
Leucyl-tRNA synthetase (LARS) is an enzyme that catalyses the ligation of leucine with leucine tRNA. LARS is also essential to sensitize the intracellular leucine concentration to the mammalian target of rapamycin complex 1 (mTORC1) activation. Biallelic mutation in the LARS gene causes infantile liver failure syndrome type 1 (ILFS1), which is characterized by acute liver failure, anaemia, and neurological disorders, including microcephaly and seizures. However, the molecular mechanism underlying ILFS1 under LARS deficiency has been elusive. Here, we generated Lars deficient (larsb
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