ArticleInternational journal of molecular sciences2020
Molecular Basis of the Pathogenic Mechanism Induced by the m.9191T>C Mutation in Mitochondrial
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Analysis of MT-ATP8 gene variants reported in patients by modeling in silico and in yeast model organism.Scientific reports · 2023Article
- Molecular basis of diseases induced by the mitochondrial DNA mutation m.9032T>C.Human molecular genetics · 2023Article
- Probing the pathogenicity of patient-derived variants of MT-ATP6 in yeast.Disease models & mechanisms · 2023Article
- Creation of Mitochondrial Disease Models Using Mitochondrial DNA Editing.Biomedicines · 2023Review
- Yeast as a Model to Find New Drugs and Drug Targets forInternational journal of molecular sciences · 2022Review
- Assembly-dependent translation of subunits 6 (Atp6) and 9 (Atp9) of ATP synthase in yeast mitochondria.Genetics · 2022Article
- Yeast Models and Molecular Mechanisms of Neurodegenerative Diseases.International journal of molecular sciences · 2021Article
- The pathogenic m.8993 T > G mutation in mitochondrial ATP6 gene prevents proton release from the subunit c-ring rotor of ATP synthase.Human molecular genetics · 2021Article
- Human Mitochondrial Pathologies of the Respiratory Chain and ATP Synthase: Contributions from Studies ofLife (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Probing the pathogenicity and functional consequences of mitochondrial DNA (mtDNA) mutations from patient's cells and tissues is difficult due to genetic heteroplasmy (co-existence of wild type and mutated mtDNA in cells), occurrence of numerous mtDNA polymorphisms, and absence of methods for genetically transforming human mitochondria. Owing to its good fermenting capacity that enables survival to loss-of-function mtDNA mutations, its amenability to mitochondrial genome manipulation, and lack of heteroplasmy,
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.