<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Watanabe T</submitter><funding>Tokai University School of Medicine Research Aid</funding><funding>Japan Society for the Promotion of Science</funding><pagination>7112</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12920786</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>Ultraviolet (UV) radiation is a major environmental factor that induces DNA lesions. Cells have evolved repair pathways, in which the transcription-coupled nucleotide excision repair (TC-NER) has a central role in removing the lesions. Here we demonstrate that DGCR8, known as a crucial component in microRNA biogenesis, coordinates the UV-induced formation of the TC-NER complex by interacting with TC-NER factors. These interactions could depend on the phosphorylation of Serine 153 of DGCR8, potentially serving as a functional switch from miRNA biogenesis to the TC-NER process. Interestingly, DGCR8 is also involved in recruiting chromatin remodelers, SPT16 and SMARCA5, for the TC-NER initiation, regulating UV-induced DNA/RNA hybrids (R-loops), and modulating DNA replication through the ATR-C</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>DGCR8 regulates multiple processes of transcription coupled nucleotide excision repair.</pubmed_title><pmcid>PMC12920786</pmcid><funding_grant_id>2018, 2019, 2021 and 2023</funding_grant_id><funding_grant_id>KAKENHI 15K21771, 23K21303</funding_grant_id><funding_grant_id>KAKENHI 23K21303, 19K06493, 24K15292</funding_grant_id><funding_grant_id>2022 and 2023</funding_grant_id><pubmed_authors>Tanaka Y</pubmed_authors><pubmed_authors>Watanabe T</pubmed_authors><pubmed_authors>Yamasaki H</pubmed_authors><pubmed_authors>Ohtsuka M</pubmed_authors><pubmed_authors>Taniguchi T</pubmed_authors><pubmed_authors>Yoshinami D</pubmed_authors></additional><is_claimable>false</is_claimable><name>DGCR8 regulates multiple processes of transcription coupled nucleotide excision repair.</name><description>Ultraviolet (UV) radiation is a major environmental factor that induces DNA lesions. Cells have evolved repair pathways, in which the transcription-coupled nucleotide excision repair (TC-NER) has a central role in removing the lesions. Here we demonstrate that DGCR8, known as a crucial component in microRNA biogenesis, coordinates the UV-induced formation of the TC-NER complex by interacting with TC-NER factors. These interactions could depend on the phosphorylation of Serine 153 of DGCR8, potentially serving as a functional switch from miRNA biogenesis to the TC-NER process. Interestingly, DGCR8 is also involved in recruiting chromatin remodelers, SPT16 and SMARCA5, for the TC-NER initiation, regulating UV-induced DNA/RNA hybrids (R-loops), and modulating DNA replication through the ATR-C</description><dates><release>2026-01-01T00:00:00Z</release><publication>2026 Feb</publication><modification>2026-07-16T12:59:26.66Z</modification><creation>2026-07-09T10:57:00.35Z</creation></dates><accession>S-EPMC12920786</accession><cross_references><pubmed>41634336</pubmed><doi>10.1038/s41598-026-38338-5</doi></cross_references></HashMap>