ArticleMolecular and cellular biology2005
Phosphorylation of BLM, dissociation from topoisomerase IIIalpha, and colocalization with gamma-H2AX after topoisomerase I-induced replication damage.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 88 citations in OpenAlex.
- Condensin II interacts with BLM helicase in S phase to maintain genome stability.Communications biology · 2025Article
- The kinase ATR controls meiotic crossover distribution at the genome scale in Arabidopsis.The Plant cell · 2024Article
- TOP3A coupling with replication forks and repair of TOP3A cleavage complexes.Cell cycle (Georgetown, Tex.) · 2024Review
- On the Prevalence and Roles of Proteins Undergoing Liquid-Liquid Phase Separation in the Biogenesis of PML-Bodies.Biomolecules · 2023Article
- A POLD3/BLM dependent pathway handles DSBs in transcribed chromatin upon excessive RNA:DNA hybrid accumulation.Nature communications · 2022Article
- The toposiomerase IIIalpha-RMI1-RMI2 complex orients human Bloom's syndrome helicase for efficient disruption of D-loops.Nature communications · 2022Article
- Checkpoint functions of RecQ helicases at perturbed DNA replication fork.Current genetics · 2021Review
- Heterozygous germlineProceedings of the National Academy of Sciences of the United States of America · 2020Article
- DNA- and DNA-Protein-Crosslink Repair in Plants.International journal of molecular sciences · 2019Review
- A tri-serine cluster within the topoisomerase IIα-interaction domain of the BLM helicase is required for regulating chromosome breakage in human cells.Human molecular genetics · 2018Article
- BLM helicase suppresses recombination at G-quadruplex motifs in transcribed genes.Nature communications · 2018Article
- A helical bundle in the N-terminal domain of the BLM helicase mediates dimer and potentially hexamer formation.The Journal of biological chemistry · 2017Article
- Bloom's Syndrome: Clinical Spectrum, Molecular Pathogenesis, and Cancer Predisposition.Molecular syndromology · 2017Review
- Regulation of BLM Nucleolar Localization.Genes · 2016Article
- Cellular defects caused by hypomorphic variants of the Bloom syndrome helicase gene BLM.Molecular genetics & genomic medicine · 2016Article
- Inhibition of Topoisomerase (DNA) I (TOP1): DNA Damage Repair and Anticancer Therapy.Biomolecules · 2015Review
- The role of post-translational modifications in fine-tuning BLM helicase function during DNA repair.DNA repair · 2014Review
- Molecular mechanism of double Holliday junction dissolution.Cell & bioscience · 2014Review
- Induction of homologous recombination following in utero exposure to DNA-damaging agents.DNA repair · 2013Article
- The BLM dissolvasome in DNA replication and repair.Cellular and molecular life sciences : CMLS · 2013Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Topoisomerase I-associated DNA single-strand breaks selectively trapped by camptothecins are lethal after being converted to double-strand breaks by replication fork collisions. BLM (Bloom's syndrome protein), a RecQ DNA helicase, and topoisomerase IIIalpha (Top3alpha) appear essential for the resolution of stalled replication forks (Holliday junctions). We investigated the involvement of BLM in the signaling response to Top1-mediated replication DNA damage. In BLM-complemented cells, BLM colocalized with promyelocytic leukemia protein (PML) nuclear bodies and Top3alpha. Fibroblasts without BLM showed an increased sensitivity to camptothecin, enhanced formation of Top1-DNA complexes, and delayed histone H2AX phosphorylation (gamma-H2AX). Camptothecin also induced nuclear relocalization of BLM, Top3alpha, and PML protein and replication-dependent phosphorylation of BLM on threonine 99 (T99p-BLM). T99p-BLM was also observed following replication stress induced by hydroxyurea. Ataxia telangiectasia mutated (ATM) protein and AT- and Rad9-related protein kinases, but not DNA-dependent protein kinase, appeared to play a redundant role in phosphorylating BLM. Following camptothecin treatment, T99p-BLM colocalized with gamma-H2AX but not with Top3alpha or PML. Thus, BLM appears to dissociate from Top3alpha and PML following its phosphorylation and facilitates H2AX phosphorylation in response to replication double-strand breaks induced by Top1. A defect in gamma-H2AX signaling in response to unrepaired replication-mediated double-strand breaks might, at least in part, explain the camptothecin-sensitivity of BLM-deficient cells.
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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.