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Showing 1 - 7 results of 7 for search 'implications (fork OR form) stalling', query time: 0.09s 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

    Brain endothelial cells as phagocytes: mechanisms and implications by Rudy T. Chang, Mark J. Fisher, Rachita K. Sumbria

    Published 2025-04-01
    “…Phagocytic activity by BECs has significant clinical implications ranging from regulation of cerebral microvascular patency (particularly by contributing to and resolving capillary stalling), clearance of brain parenchymal debris, and brain parenchymal invasion by pathogens. …”
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  3. 3

    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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  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

    Addressing Shortcomings in Contingency Standards of Care by Alexander Quan

    Published 2022-09-01
    “…Crisis standards of care require formal activation at the state level, and in the absence of clear triggers or governmental willingness to use them, hospitals may adopt informal strategies to manage allocation in the form of contingency measures. The contingency phase is defined by two simultaneous goals: prevent or stall crisis-level scarcity by managing limited resources and providing patient care that is functionally equivalent to usual care.[3] In other words, allocate scarce resources with no significant health consequences to patients. …”
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