<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sartor MA</submitter><funding>NIEHS NIH HHS</funding><funding>NHGRI NIH HHS</funding><funding>NLM NIH HHS</funding><pagination>1139-46</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2717142</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>117(7)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The vertebrate aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that regulates cellular responses to environmental polycyclic and halogenated compounds. The naive receptor is believed to reside in an inactive cytosolic complex that translocates to the nucleus and induces transcription of xenobiotic detoxification genes after activation by ligand.&lt;h4>Objectives&lt;/h4>We conducted an integrative genomewide analysis of AHR gene targets in mouse hepatoma cells and determined whether AHR regulatory functions may take place in the absence of an exogenous ligand.&lt;h4>Methods&lt;/h4>The network of AHR-binding targets in the mouse genome was mapped through a multipronged approach involving chromatin immunoprecipitation/chip and global gene expression signature</pubmed_abstract><journal>Environmental health perspectives</journal><pubmed_title>Genomewide analysis of aryl hydrocarbon receptor binding targets reveals an extensive array of gene clusters that control morphogenetic and developmental programs.</pubmed_title><pmcid>PMC2717142</pmcid><funding_grant_id>R01 ES006273</funding_grant_id><funding_grant_id>R01 ES010807</funding_grant_id><funding_grant_id>R21 LM009662</funding_grant_id><funding_grant_id>T32 ES07250</funding_grant_id><funding_grant_id>P30 ES06096</funding_grant_id><funding_grant_id>P30 ES006096</funding_grant_id><funding_grant_id>R01 ES10807</funding_grant_id><funding_grant_id>R01 HG003749</funding_grant_id><funding_grant_id>T32 ES007250</funding_grant_id><funding_grant_id>R01 ES06273</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Marlowe JL</pubmed_authors><pubmed_authors>Ma C</pubmed_authors><pubmed_authors>Medvedovic M</pubmed_authors><pubmed_authors>Fan Y</pubmed_authors><pubmed_authors>Karyala S</pubmed_authors><pubmed_authors>Puga A</pubmed_authors><pubmed_authors>Halbleib D</pubmed_authors><pubmed_authors>Reichard JF</pubmed_authors><pubmed_authors>Sartor MA</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Schnekenburger M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genomewide analysis of aryl hydrocarbon receptor binding targets reveals an extensive array of gene clusters that control morphogenetic and developmental programs.</name><description>&lt;h4>Background&lt;/h4>The vertebrate aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that regulates cellular responses to environmental polycyclic and halogenated compounds. The naive receptor is believed to reside in an inactive cytosolic complex that translocates to the nucleus and induces transcription of xenobiotic detoxification genes after activation by ligand.&lt;h4>Objectives&lt;/h4>We conducted an integrative genomewide analysis of AHR gene targets in mouse hepatoma cells and determined whether AHR regulatory functions may take place in the absence of an exogenous ligand.&lt;h4>Methods&lt;/h4>The network of AHR-binding targets in the mouse genome was mapped through a multipronged approach involving chromatin immunoprecipitation/chip and global gene expression signature</description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 Jul</publication><modification>2025-04-19T13:25:59.082Z</modification><creation>2019-06-06T21:32:40Z</creation></dates><accession>S-EPMC2717142</accession><cross_references><pubmed>19654925</pubmed><doi>10.1289/ehp.0800485</doi></cross_references></HashMap>