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RAD52 prevents accumulation of Polα-dependent replication gaps at perturbed replication forks in human cells

Replication gaps can arise as a consequence of perturbed DNA replication and their accumulation might undermine the stability of the genome. Loss of RAD52, a protein involved in the regulation of fork reversal, promotes accumulation of parental ssDNA gaps during replication perturbation. Here, we de...

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Detalles Bibliográficos
Autores principales: Di Biagi, Ludovica, Malacaria, Eva, Aiello, Francesca Antonella, Valenzisi, Pasquale, Marozzi, Giorgia, Franchitto, Annapaola, Pichierri, Pietro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10120653/
https://www.ncbi.nlm.nih.gov/pubmed/37090680
http://dx.doi.org/10.1101/2023.04.12.536536

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