ReviewCritical reviews in biochemistry and molecular biology2016
Structure, function and evolution of the animal mitochondrial replicative DNA helicase.
Review in Critical reviews in biochemistry and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Autoregulation of the real-time kinetics of the human mitochondrial replicative helicase.Nature communications · 2025Article
- The N-terminal domain of human mitochondrial helicase Twinkle has DNA-binding activity crucial for supporting processive DNA synthesis by polymerase γ.The Journal of biological chemistry · 2023Article
- Mitochondrial DNA maintenance in Drosophila melanogaster.Bioscience reports · 2022Review
- Method for the structural analysis of Twinkle mitochondrial DNA helicase by cryo-EM.Methods (San Diego, Calif.) · 2022Article
- Structural insight and characterization of human Twinkle helicase in mitochondrial disease.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Implications of Membrane Binding by the Fe-S Cluster-Containing N-Terminal Domain in theFrontiers in genetics · 2021Article
- Single-molecule level structural dynamics of DNA unwinding by human mitochondrial Twinkle helicase.The Journal of biological chemistry · 2020Article
- Roles of the mitochondrial replisome in mitochondrial DNA deletion formation.Genetics and molecular biology · 2020Article
- Arabidopsis thaliana organelles mimic the T7 phage DNA replisome with specific interactions between Twinkle protein and DNA polymerases Pol1A and Pol1B.BMC plant biology · 2019Article
- The Dictyostelium discoideum homologue of Twinkle, Twm1, is a mitochondrial DNA helicase, an active primase and promotes mitochondrial DNA replication.BMC molecular biology · 2018Article
- Developmental arrest in Drosophila melanogaster caused by mitochondrial DNA replication defects cannot be rescued by the alternative oxidase.Scientific reports · 2018Article
- Plant organellar DNA primase-helicase synthesizes RNA primers for organellar DNA polymerases using a unique recognition sequence.Nucleic acids research · 2017Article
- DNA2-An Important Player in DNA Damage Response or Just Another DNA Maintenance Protein?International journal of molecular sciences · 2017Review
- Pathogenicity in POLG syndromes: DNA polymerase gamma pathogenicity prediction server and database.BBA clinical · 2017Article
- Animal Mitochondrial DNA Replication.The EnzymesReview
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
The mitochondrial replicative DNA helicase is essential for animal mitochondrial DNA (mtDNA) maintenance. Deleterious mutations in the gene that encodes it cause mitochondrial dysfunction manifested in developmental delays, defects and arrest, limited life span, and a number of human pathogenic phenotypes that are recapitulated in animals across taxa. In fact, the replicative mtDNA helicase was discovered with the identification of human disease mutations in its nuclear gene, and based upon its deduced amino acid sequence homology with bacteriophage T7 gene 4 protein (T7 gp4), a bi-functional primase-helicase. Since that time, numerous investigations of its structure, mechanism, and physiological relevance have been reported, and human disease alleles have been modeled in the human, mouse, and Drosophila systems. Here, we review this literature and draw evolutionary comparisons that serve to shed light on its divergent features.
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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.