<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(5)</volume><submitter>Aaker JD</submitter><pubmed_abstract>The transcriptional program that controls oligodendrocyte maturation and central nervous system (CNS) myelination has not been fully characterized. In this study, we use high-throughput RNA sequencing to analyze how the loss of a key transcription factor, zinc finger protein 191 (ZFP191), results in oligodendrocyte development abnormalities and CNS hypomyelination. Using a previously described mutant mouse that is deficient in ZFP191 protein expression (Zfp191&lt;sup>null&lt;/sup>), we demonstrate that key transcripts are reduced in the whole brain as well as within oligodendrocyte lineage cells cultured in vitro To determine whether the loss of myelin seen in Zfp191&lt;sup>null&lt;/sup> mice contributes indirectly to these perturbations, we also examined the transcriptome of a well-characterized mous</pubmed_abstract><journal>ASN neuro</journal><pagination>1759091416670749</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5046175</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Transcriptional Fingerprint of Hypomyelination in Zfp191null and Shiverer (Mbpshi) Mice.</pubmed_title><pmcid>PMC5046175</pmcid><pubmed_authors>Aaker JD</pubmed_authors><pubmed_authors>Looney TJ</pubmed_authors><pubmed_authors>Elbaz B</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Lahn BT</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors><pubmed_authors>Popko B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcriptional Fingerprint of Hypomyelination in Zfp191null and Shiverer (Mbpshi) Mice.</name><description>The transcriptional program that controls oligodendrocyte maturation and central nervous system (CNS) myelination has not been fully characterized. In this study, we use high-throughput RNA sequencing to analyze how the loss of a key transcription factor, zinc finger protein 191 (ZFP191), results in oligodendrocyte development abnormalities and CNS hypomyelination. Using a previously described mutant mouse that is deficient in ZFP191 protein expression (Zfp191&lt;sup>null&lt;/sup>), we demonstrate that key transcripts are reduced in the whole brain as well as within oligodendrocyte lineage cells cultured in vitro To determine whether the loss of myelin seen in Zfp191&lt;sup>null&lt;/sup> mice contributes indirectly to these perturbations, we also examined the transcriptome of a well-characterized mous</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Oct</publication><modification>2026-04-07T17:54:40.434Z</modification><creation>2019-03-27T02:25:40Z</creation></dates><accession>S-EPMC5046175</accession><cross_references><pubmed>27683878</pubmed><doi>10.1177/1759091416670749</doi></cross_references></HashMap>