<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ding N</submitter><funding>NIEHS NIH HHS</funding><funding>National Natural Science Foundation of China</funding><funding>National Institutes of Health</funding><pagination>862592</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9046994</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12</volume><pubmed_abstract>H3K56 acetylation (H3K56Ac) was reported to play a critical role in chromatin assembly; thus, H3K56ac participates in the regulation of DNA replication, cell cycle progression, DNA repair, and transcriptional activation. To investigate the influence of DNA damage regulators on the acetylation of histone H3 and gene transcription, U2OS cells expressing SNAP-labeled H3.1 or SNAP-labeled H3.3 were treated with ATM, ATR, or a Chk1 inhibitor after ultraviolet (UV) radiation. The levels of H3.1K56ac, H3.3K56ac, and other H3 site-specific acetylation were checked at different time points until 24 h after UV radiation. The difference in gene transcription levels was also examined by mRNA sequencing. The results identified Chk1 as an important regulator of histone H3K56 acetylation in the restorati</pubmed_abstract><journal>Frontiers in oncology</journal><pubmed_title>Chk1 Inhibition Hinders the Restoration of H3.1K56 and H3.3K56 Acetylation and Reprograms Gene Transcription After DNA Damage Repair.</pubmed_title><pmcid>PMC9046994</pmcid><funding_grant_id>U1932208</funding_grant_id><funding_grant_id>R01 ES012991</funding_grant_id><funding_grant_id>ES012991</funding_grant_id><pubmed_authors>Yuan F</pubmed_authors><pubmed_authors>Qu P</pubmed_authors><pubmed_authors>Shao Z</pubmed_authors><pubmed_authors>Ding N</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Lu D</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Zhu Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>Chk1 Inhibition Hinders the Restoration of H3.1K56 and H3.3K56 Acetylation and Reprograms Gene Transcription After DNA Damage Repair.</name><description>H3K56 acetylation (H3K56Ac) was reported to play a critical role in chromatin assembly; thus, H3K56ac participates in the regulation of DNA replication, cell cycle progression, DNA repair, and transcriptional activation. To investigate the influence of DNA damage regulators on the acetylation of histone H3 and gene transcription, U2OS cells expressing SNAP-labeled H3.1 or SNAP-labeled H3.3 were treated with ATM, ATR, or a Chk1 inhibitor after ultraviolet (UV) radiation. The levels of H3.1K56ac, H3.3K56ac, and other H3 site-specific acetylation were checked at different time points until 24 h after UV radiation. The difference in gene transcription levels was also examined by mRNA sequencing. The results identified Chk1 as an important regulator of histone H3K56 acetylation in the restorati</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-06-01T01:30:41.547Z</modification><creation>2024-11-14T00:50:37.072Z</creation></dates><accession>S-EPMC9046994</accession><cross_references><pubmed>35494003</pubmed><doi>10.3389/fonc.2022.862592</doi></cross_references></HashMap>