ArticleJournal of human genetics2023
Compound heterozygous variants of THG1L result in autosomal recessive cerebellar ataxia.
Article in Journal of human genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Syntaxin-3 Regulates Tight Junction Assembly in Human Retinal Pigment Epithelium.Cell biochemistry and function · 2026Article
- THG1L- associated early childhood-onset cerebellar ataxia with atrophy and developmental delay.Neurogenetics · 2026Article
- Deciphering Autoantigen Signatures in Chikungunya Virus Infection Using Machine Learning: A Data-Driven Approach to Understand Host Immunity.Current microbiology · 2025Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
tRNA-histidine guanyltransferase 1-like protein (THG1L), located in the mitochondria, plays a crucial role in the tRNA maturation process. Dysfunction of THG1L results in abnormal mitochondrial tRNA modification and neurodevelopmental disorders. To date, few studies have focused on THG1L-related cerebellar ataxia. Whole-exome sequencing revealed compound heterozygous variants NM_017872.5: [c.224A > G]; [c.369-8T > G] in THG1L in a 6-year-old boy with moderate cerebellar ataxia. The variant c.224A > G was demonstrated to downregulate its RNA and protein expression, and c.369-8 T > G resulted in a 7 bp insertion before exon 3. Our case expanded the gene variation and clinical spectrum of THG1L-related cerebellar ataxia.
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Registered trials
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