<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Duong HA</submitter><funding>NEI NIH HHS</funding><funding>U.S. Department of Health &amp;amp; Human Services | NIH | National Institute of General Medical Sciences</funding><funding>U.S. Department of Health &amp; Human Services | NIH | National Institute of General Medical Sciences (NIGMS)</funding><funding>NCRR NIH HHS</funding><funding>NIMHD NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>5537</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11220080</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>Circadian gene expression is fundamental to the establishment and functions of the circadian clock, a cell-autonomous and evolutionary-conserved timing system. Yet, how it is affected by environmental-circadian disruption (ECD) such as shiftwork and jetlag are ill-defined. Here, we provided a comprehensive and comparative description of male liver circadian gene expression, encompassing transcriptomes, whole-cell proteomes and nuclear proteomes, under normal and after ECD conditions. Under both conditions, post-translation, rather than transcription, is the dominant contributor to circadian functional outputs. After ECD, post-transcriptional and post-translational processes are the major contributors to whole-cell or nuclear circadian proteome, respectively. Furthermore, ECD re-writes the </pubmed_abstract><journal>Nature communications</journal><pubmed_title>Environmental circadian disruption re-writes liver circadian proteomes.</pubmed_title><pmcid>PMC11220080</pmcid><funding_grant_id>SC1 GM127260</funding_grant_id><funding_grant_id>1R16GM146703-01</funding_grant_id><funding_grant_id>U54 MD007602</funding_grant_id><funding_grant_id>G12 RR003034</funding_grant_id><funding_grant_id>R21 EY031821</funding_grant_id><funding_grant_id>R01 EY026291</funding_grant_id><funding_grant_id>R16 GM146703</funding_grant_id><funding_grant_id>SC1 GM135112</funding_grant_id><funding_grant_id>R35 GM136661</funding_grant_id><funding_grant_id>R35 GM127044</funding_grant_id><pubmed_authors>Duong HA</pubmed_authors><pubmed_authors>Ehlen C</pubmed_authors><pubmed_authors>DeBruyne JP</pubmed_authors><pubmed_authors>Baba K</pubmed_authors><pubmed_authors>Tosini G</pubmed_authors><pubmed_authors>Davidson AJ</pubmed_authors><pubmed_authors>Powell M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Environmental circadian disruption re-writes liver circadian proteomes.</name><description>Circadian gene expression is fundamental to the establishment and functions of the circadian clock, a cell-autonomous and evolutionary-conserved timing system. Yet, how it is affected by environmental-circadian disruption (ECD) such as shiftwork and jetlag are ill-defined. Here, we provided a comprehensive and comparative description of male liver circadian gene expression, encompassing transcriptomes, whole-cell proteomes and nuclear proteomes, under normal and after ECD conditions. Under both conditions, post-translation, rather than transcription, is the dominant contributor to circadian functional outputs. After ECD, post-transcriptional and post-translational processes are the major contributors to whole-cell or nuclear circadian proteome, respectively. Furthermore, ECD re-writes the </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-05-29T11:20:27.888Z</modification><creation>2025-04-04T12:54:18.317Z</creation></dates><accession>S-EPMC11220080</accession><cross_references><pubmed>38956413</pubmed><doi>10.1038/s41467-024-49852-3</doi></cross_references></HashMap>