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Showing 1 - 8 results of 8 for search '(implications OR application) fork stalling', query time: 0.06s Refine Results
  1. 1

    Functional regulation of the structure-specific endonuclease FEN1 by the human cytomegalovirus protein IE1 suggests a role for the re-initiation of stalled viral replication forks. by Eva-Maria Schilling, Myriam Scherer, Franziska Rothemund, Thomas Stamminger

    Published 2021-03-01
    “…Furthermore, our results indicate that FEN1 is required for the formation of DSBs during HCMV infection suggesting that IE1 acts as viral activator of FEN1 in order to re-initiate stalled replication forks. In summary, we propose a novel mechanism of viral FEN1 activation to overcome replication fork barriers at difficult-to-replicate sites in viral genomes.…”
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  2. 2

    Genome-wide analysis of DNA replication and DNA double-strand breaks using TrAEL-seq. by Neesha Kara, Felix Krueger, Peter Rugg-Gunn, Jonathan Houseley

    Published 2021-03-01
    “…Faithful replication of the entire genome requires replication forks to copy large contiguous tracts of DNA, and sites of persistent replication fork stalling present a major threat to genome stability. …”
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  3. 3

    A high-resolution, nanopore-based artificial intelligence assay for DNA replication stress in human cancer cells by Mathew J. K. Jones, Subash Kumar Rai, Pauline L. Pfuderer, Alexis Bonfim-Melo, Julia K. Pagan, Paul R. Clarke, Francis Isidore Garcia Totañes, Catherine J. Merrick, Sarah E. McClelland, Michael A. Boemo

    Published 2025-08-01
    “…Our method can differentiate between fork slowing and fork stalling in cells treated with hydroxyurea, as well as inhibitors of ATR, WEE1, and PARP1. …”
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  4. 4

    Condensin II interacts with BLM helicase in S phase to maintain genome stability by Brian Rodemoyer, Ganesha Kariyawasam, Veena Subramanian, Kristina Schmidt

    Published 2025-03-01
    “…Disrupting the BLM-condensin II interaction reduced replication speed, increased fork stalling and sister-chromatid exchanges, delayed repair of DNA double-strand breaks, and led to micronuclei. …”
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  5. 5

    Molecular dependencies and genomic consequences of a global DNA damage tolerance defect by Daniel de Groot, Aldo Spanjaard, Ronak Shah, Maaike Kreft, Ben Morris, Cor Lieftink, Joyce J. I. Catsman, Shirley Ormel, Matilda Ayidah, Bas Pilzecker, Olimpia Alessandra Buoninfante, Paul C. M. van den Berk, Roderick L. Beijersbergen, Heinz Jacobs

    Published 2024-12-01
    “…Abstract Background DNA damage tolerance (DDT) enables replication to continue in the presence of fork stalling lesions. In mammalian cells, DDT is regulated by two independent pathways, controlled by the polymerase REV1 and ubiquitinated PCNA, respectively. …”
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  6. 6

    MMS exposure promotes increased MtDNA mutagenesis in the presence of replication-defective disease-associated DNA polymerase γ variants. by Jeffrey D Stumpf, William C Copeland

    Published 2014-10-01
    “…Increased mutagenesis could be explained by mutant variants stalling the replication fork, thereby predisposing the template DNA to irreparable damage that is bypassed with poor fidelity. …”
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  7. 7

    gammaH2AX foci form preferentially in euchromatin after ionising-radiation. by Ian G Cowell, Nicola J Sunter, Prim B Singh, Caroline A Austin, Barbara W Durkacz, Michael J Tilby

    Published 2007-10-01
    “…H2AX phosphorylation has also been demonstrated previously to occur at stalled replication forks induced by UV radiation or exposure to agents such as hydroxyurea. …”
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  8. 8

    Ataxia telangiectasia mutated and Rad3 related (ATR) protein kinase inhibition is synthetically lethal in XRCC1 deficient ovarian cancer cells. by Rebeka Sultana, Tarek Abdel-Fatah, Christina Perry, Paul Moseley, Nada Albarakti, Vivek Mohan, Claire Seedhouse, Stephen Chan, Srinivasan Madhusudan

    Published 2013-01-01
    “…<h4>Introduction</h4>Ataxia telangiectasia mutated and Rad3 Related (ATR) protein kinase is a key sensor of single-stranded DNA associated with stalled replication forks and repair intermediates generated during DNA repair. …”
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