<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hinman JD</submitter><funding>National Institute for Nanotechnology</funding><funding>COST</funding><funding>Landes-Offensive zur Entwicklung Wissenschaftlichökonomischer Exzellenz</funding><funding>Deutsche Forschungsgemeinschaft</funding><funding>Universtätsklinikum Giessen Marburg</funding><funding>National Multiple Sclerosis Society</funding><funding>Ural Federal University</funding><funding>NINDS NIH HHS</funding><funding>University of California, Los Angeles</funding><funding>German Center for Lung Research</funding><pagination>103-118</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8496370</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>30(1)</volume><pubmed_abstract>Oligodendrocytes exist in a heterogenous state and are implicated in multiple neuropsychiatric diseases including dementia. Cortical oligodendrocytes are a glial population uniquely positioned to play a key role in neurodegeneration by synchronizing circuit connectivity but molecular pathways specific to this role are lacking. We utilized oligodendrocyte-specific translating ribosome affinity purification and RNA-seq (TRAP-seq) to transcriptionally profile adult mature oligodendrocytes from different regions of the central nervous system. Weighted gene co-expression network analysis reveals distinct region-specific gene networks. Two of these mature myelinating oligodendrocyte gene networks uniquely define cortical oligodendrocytes and differentially regulate cortical myelination (M8) and </pubmed_abstract><journal>Human molecular genetics</journal><pubmed_title>miR-142-3p regulates cortical oligodendrocyte gene co-expression networks associated with tauopathy.</pubmed_title><pmcid>PMC8496370</pmcid><funding_grant_id>CRC1213</funding_grant_id><funding_grant_id>PP1892</funding_grant_id><funding_grant_id>DZL</funding_grant_id><funding_grant_id>R01 NS082094</funding_grant_id><funding_grant_id>K08 NS083740</funding_grant_id><funding_grant_id>BE4443/4-1</funding_grant_id><funding_grant_id>BE4443/6-1</funding_grant_id><funding_grant_id>BM1201</funding_grant_id><pubmed_authors>Kushner SA</pubmed_authors><pubmed_authors>Kim D</pubmed_authors><pubmed_authors>Ghanbari M</pubmed_authors><pubmed_authors>Bellusci S</pubmed_authors><pubmed_authors>Kawaguchi R</pubmed_authors><pubmed_authors>Chen C</pubmed_authors><pubmed_authors>Fogel BL</pubmed_authors><pubmed_authors>Coppola G</pubmed_authors><pubmed_authors>Abraham CR</pubmed_authors><pubmed_authors>Ngo KJ</pubmed_authors><pubmed_authors>Hernandez I</pubmed_authors><pubmed_authors>Kosik KS</pubmed_authors><pubmed_authors>Ikram MA</pubmed_authors><pubmed_authors>Hinman JD</pubmed_authors><pubmed_authors>Goth K</pubmed_authors></additional><is_claimable>false</is_claimable><name>miR-142-3p regulates cortical oligodendrocyte gene co-expression networks associated with tauopathy.</name><description>Oligodendrocytes exist in a heterogenous state and are implicated in multiple neuropsychiatric diseases including dementia. Cortical oligodendrocytes are a glial population uniquely positioned to play a key role in neurodegeneration by synchronizing circuit connectivity but molecular pathways specific to this role are lacking. We utilized oligodendrocyte-specific translating ribosome affinity purification and RNA-seq (TRAP-seq) to transcriptionally profile adult mature oligodendrocytes from different regions of the central nervous system. Weighted gene co-expression network analysis reveals distinct region-specific gene networks. Two of these mature myelinating oligodendrocyte gene networks uniquely define cortical oligodendrocytes and differentially regulate cortical myelination (M8) and </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Mar</publication><modification>2025-04-05T14:05:39.557Z</modification><creation>2025-04-05T14:05:39.557Z</creation></dates><accession>S-EPMC8496370</accession><cross_references><pubmed>33555315</pubmed><doi>10.1093/hmg/ddaa252</doi></cross_references></HashMap>