{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["13(1)"],"submitter":["Paniagua I"],"pubmed_abstract":["Protection of stalled replication forks is essential to prevent genome instability, a major driving force of tumorigenesis. Several key regulators of DNA double-stranded break (DSB) repair, including 53BP1 and RIF1, have been implicated in fork protection. MAD2L2, also known as REV7, plays an important role downstream of 53BP1/RIF1 by counteracting resection at DSBs in the recently discovered shieldin complex. The ability to bind and counteract resection at exposed DNA ends at DSBs makes MAD2L2/shieldin a prime candidate for also suppressing nucleolytic processing at stalled replication forks. However, the function of MAD2L2/shieldin outside of DNA repair is unknown. Here we address this by using genetic and single-molecule analyses and find that MAD2L2 is required for protecting and resta"],"journal":["Nature communications"],"pagination":["5167"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9458726"],"repository":["biostudies-literature"],"pubmed_title":["MAD2L2 promotes replication fork protection and recovery in a shieldin-independent and REV3L-dependent manner."],"pmcid":["PMC9458726"],"pubmed_authors":["Tayeh Z","Cerutti A","Falcone M","Hernandez Perez S","Paniagua I","Jacobs JJL"],"additional_accession":[]},"is_claimable":false,"name":"MAD2L2 promotes replication fork protection and recovery in a shieldin-independent and REV3L-dependent manner.","description":"Protection of stalled replication forks is essential to prevent genome instability, a major driving force of tumorigenesis. Several key regulators of DNA double-stranded break (DSB) repair, including 53BP1 and RIF1, have been implicated in fork protection. MAD2L2, also known as REV7, plays an important role downstream of 53BP1/RIF1 by counteracting resection at DSBs in the recently discovered shieldin complex. The ability to bind and counteract resection at exposed DNA ends at DSBs makes MAD2L2/shieldin a prime candidate for also suppressing nucleolytic processing at stalled replication forks. However, the function of MAD2L2/shieldin outside of DNA repair is unknown. Here we address this by using genetic and single-molecule analyses and find that MAD2L2 is required for protecting and resta","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2025-04-05T10:25:45.089Z","creation":"2025-04-05T10:25:45.089Z"},"accession":"S-EPMC9458726","cross_references":{"pubmed":["36075897"],"doi":["10.1038/s41467-022-32861-5"]}}