ArticleMolecular and cellular biology2008
Characterization of human GTPBP3, a GTP-binding protein involved in mitochondrial tRNA modification.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Pathogenicity Analysis of a Novel Variant inGenes · 2023Pooled it
- Biallelic variants in GTPBP3: New patients, phenotypic spectrum, and outcome.Annals of clinical and translational neurology · 2024Article
- Insights into the Mechanism of Installation of 5-Carboxymethylaminomethyl Uridine Hypermodification by tRNA-Modifying Enzymes MnmE and MnmG.Journal of the American Chemical Society · 2023Article
- Modopathies Caused by Mutations in Genes Encoding for Mitochondrial RNA Modifying Enzymes: Molecular Mechanisms and Yeast Disease Models.International journal of molecular sciences · 2023Review
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- Role of Oxidative Stress and Antioxidants in Acquired Inner Ear Disorders.Antioxidants (Basel, Switzerland) · 2022Review
- DNA methylation signatures associated with cardiometabolic risk factors in children from India and The Gambia: results from the EMPHASIS study.Clinical epigenetics · 2022Article
- Mitochondrial noncoding RNAs: new wine in an old bottle.RNA biology · 2021Review
- The human tRNA taurine modification enzyme GTPBP3 is an active GTPase linked to mitochondrial diseases.Nucleic acids research · 2021Article
- Human-induced pluripotent stem cells for modelling metabolic perturbations and impaired bioenergetics underlying cardiomyopathies.Cardiovascular research · 2021Review
- Novel Mutations in theFrontiers in genetics · 2021Article
- A Natural Variation inThe Plant cell · 2020Article
- tRNA cleavage: a new insight.Neural regeneration research · 2020Review
- Deletion of Gtpbp3 in zebrafish revealed the hypertrophic cardiomyopathy manifested by aberrant mitochondrial tRNA metabolism.Nucleic acids research · 2019Article
- The mammalian mitochondrial epitranscriptome.Biochimica et biophysica acta. Gene regulatory mechanisms · 2019Review
- Article
- Mitochondrial transcription and translation: overview.Essays in biochemistry · 2018Review
- microRNA-mediated differential expression of TRMU, GTPBP3 and MTO1 in cell models of mitochondrial-DNA diseases.Scientific reports · 2017Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human GTPBP3 is an evolutionarily conserved, multidomain protein involved in mitochondrial tRNA modification. Characterization of its biochemical properties and the phenotype conferred by GTPBP3 inactivation is crucial to understanding the role of this protein in tRNA maturation and its effects on mitochondrial respiration. We show that the two most abundant GTPBP3 isoforms exhibit moderate affinity for guanine nucleotides like their bacterial homologue, MnmE, although they hydrolyze GTP at a 100-fold lower rate. This suggests that regulation of the GTPase activity, essential for the tRNA modification function of MnmE, is different in GTPBP3. In fact, potassium-induced dimerization of the G domain leads to stimulation of the GTPase activity in MnmE but not in GTPBP3. The GTPBP3 N-terminal domain mediates a potassium-independent dimerization, which appears as an evolutionarily conserved property of the protein family, probably related to the construction of the binding site for the one-carbon-unit donor in the modification reaction. Partial inactivation of GTPBP3 by small interfering RNA reduces oxygen consumption, ATP production, and mitochondrial protein synthesis, while the degradation of these proteins slightly increases. It also results in mitochondria with defective membrane potential and increased superoxide levels. These phenotypic traits suggest that GTPBP3 defects contribute to the pathogenesis of some oxidative phosphorylation diseases.
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