ReviewCell cycle (Georgetown, Tex.)2024
TOP3A coupling with replication forks and repair of TOP3A cleavage complexes.
Review in Cell cycle (Georgetown, Tex.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Brain age gap as biomarker linking cardiovascular diseases genetic susceptibility and causality.iScience · 2026Article
- Topoisomerase IIIα controls alternative lengthening of telomeres.Cell reports · 2025Article
- Mitochondrial DNA depletion syndrome and its cardiac complication.Frontiers in cardiovascular medicine · 2025Review
- Temporospatial control of topoisomerases by essential cellular processes.Current opinion in microbiology · 2024Review
- Mechanisms and pathologies of human mitochondrial DNA replication and deletion formation.The Biochemical journal · 2024Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Humans have two Type IA topoisomerases, topoisomerase IIIα (TOP3A) and topoisomerase IIIβ (TOP3B). In this review, we focus on the role of human TOP3A in DNA replication and highlight the recent progress made in understanding TOP3A in the context of replication. Like other topoisomerases, TOP3A acts by a reversible mechanism of cleavage and rejoining of DNA strands allowing changes in DNA topology. By cleaving and resealing single-stranded DNA, it generates TOP3A-linked single-strand breaks as TOP3A cleavage complexes (TOP3Accs) with a TOP3A molecule covalently bound to the 5´-end of the break. TOP3A is critical for both mitochondrial and for nuclear DNA replication. Here, we discuss the formation and repair of irreversible TOP3Accs, as their presence compromises genome integrity as they form TOP3A DNA-protein crosslinks (TOP3A-DPCs) associated with DNA breaks. We discuss the redundant pathways that repair TOP3A-DPCs, and how their defects are a source of DNA damage leading to neurological diseases and mitochondrial disorders.
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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.