{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yang Z"],"funding":["HHS | NIH | National Institute of Environmental Health Sciences"],"pagination":["e2025948118"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8536359"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["118(35)"],"pubmed_abstract":["Global genome repair (GGR), a subpathway of nucleotide excision repair, corrects bulky helix-distorting DNA lesions across the whole genome and is essential for preventing mutagenesis and skin cancer. Here, we show that METTL14 (methyltransferase-like 14), a critical component of the N6-methyladenosine (m6A) RNA methyltransferase complex, promotes GGR through regulating m6A mRNA methylation-mediated DDB2 translation and suppresses ultraviolet B (UVB) radiation-induced skin tumorigenesis. UVB irradiation down-regulates METTL14 protein through NBR1-dependent selective autophagy. METTL14 knockdown decreases GGR and DDB2 abundance. Conversely, overexpression of wild-type METTL14 but not its enzymatically inactive mutant increases GGR and DDB2 abundance. METTL14 knockdown decreases m6A methylat"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["METTL14 facilitates global genome repair and suppresses skin tumorigenesis."],"pmcid":["PMC8536359"],"funding_grant_id":["ES030576","ES024373","ES030546"],"pubmed_authors":["Park G","Yang Z","He C","Shah P","He YY","Cui X","Wei J","Yang S","Cui YH"],"additional_accession":[]},"is_claimable":false,"name":"METTL14 facilitates global genome repair and suppresses skin tumorigenesis.","description":"Global genome repair (GGR), a subpathway of nucleotide excision repair, corrects bulky helix-distorting DNA lesions across the whole genome and is essential for preventing mutagenesis and skin cancer. Here, we show that METTL14 (methyltransferase-like 14), a critical component of the N6-methyladenosine (m6A) RNA methyltransferase complex, promotes GGR through regulating m6A mRNA methylation-mediated DDB2 translation and suppresses ultraviolet B (UVB) radiation-induced skin tumorigenesis. UVB irradiation down-regulates METTL14 protein through NBR1-dependent selective autophagy. METTL14 knockdown decreases GGR and DDB2 abundance. Conversely, overexpression of wild-type METTL14 but not its enzymatically inactive mutant increases GGR and DDB2 abundance. METTL14 knockdown decreases m6A methylat","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Aug","modification":"2025-04-05T14:05:23.39Z","creation":"2025-04-05T14:05:23.39Z"},"accession":"S-EPMC8536359","cross_references":{"pubmed":["34452996"],"doi":["10.1073/pnas.2025948118"]}}