{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["11(13)"],"submitter":["Pena-Gomez MJ"],"pubmed_abstract":["Apurinic/apyrimidinic (AP) sites and single-strand breaks arising from base excision repair (BER) during the misincorporation of damaged nucleobases may hinder replication fork stability in homologous recombination-deficient (HRD) cells. At templated AP sites, cross-links between the DNA and 5-hydroxymethylcytosine binding, embryonic stem cell-specific (HMCES) regulate replication fork speed, avoiding cytotoxic double-strand breaks. While the role of HMCES at the template DNA strand is well studied, its effects on nascent DNA are not. We provide evidence that HMCES-DNA-protein cross-links (DPCs) are detrimental to the BER-mediated removal of 5-hydroxymethyl-2'-deoxycytidine (5hmdC)-derived 5-hydroxymethyl-2'-deoxyuridine from replication forks. HRD cells have heightened HMCES-DPCs, which i"],"journal":["Science advances"],"pagination":["eads3227"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11939059"],"repository":["biostudies-literature"],"pubmed_title":["HMCES corrupts replication fork stability during base excision repair in homologous recombination-deficient cells."],"pmcid":["PMC11939059"],"pubmed_authors":["Berrada S","Reyes JC","Wijesekara Hanthi Y","Rosado IV","Rodriguez-Martin Y","Costanzo V","Freire R","Del Rio Oliva M","Masson JY","Pena-Gomez MJ"],"additional_accession":[]},"is_claimable":false,"name":"HMCES corrupts replication fork stability during base excision repair in homologous recombination-deficient cells.","description":"Apurinic/apyrimidinic (AP) sites and single-strand breaks arising from base excision repair (BER) during the misincorporation of damaged nucleobases may hinder replication fork stability in homologous recombination-deficient (HRD) cells. At templated AP sites, cross-links between the DNA and 5-hydroxymethylcytosine binding, embryonic stem cell-specific (HMCES) regulate replication fork speed, avoiding cytotoxic double-strand breaks. While the role of HMCES at the template DNA strand is well studied, its effects on nascent DNA are not. We provide evidence that HMCES-DNA-protein cross-links (DPCs) are detrimental to the BER-mediated removal of 5-hydroxymethyl-2'-deoxycytidine (5hmdC)-derived 5-hydroxymethyl-2'-deoxyuridine from replication forks. HRD cells have heightened HMCES-DPCs, which i","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-06-28T03:05:27.389Z","creation":"2025-06-28T03:05:27.389Z"},"accession":"S-EPMC11939059","cross_references":{"pubmed":["40138423"],"doi":["10.1126/sciadv.ads3227"]}}