<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yoshikawa F</submitter><funding>Tokyo University of Science</funding><funding>Hamaguchi Foundation for the Advancement of Biochemistry</funding><funding>Japan Society for the Promotion of Science</funding><funding>Exchange Program between Tokyo University of Science and the University of Strasbourg</funding><pagination>e0166732</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5113975</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(11)</volume><pubmed_abstract>Opalin, a central nervous system-specific myelin protein phylogenetically unique to mammals, has been suggested to play a role in mammalian-specific myelin. To elucidate the role of Opalin in mammalian myelin, we disrupted the Opalin gene in mice and analyzed the impacts on myelination and behavior. Opalin-knockout (Opalin-/-) mice were born at a Mendelian ratio and had a normal body shape and weight. Interestingly, Opalin-/- mice had no obvious abnormalities in major myelin protein compositions, expression of oligodendrocyte lineage markers, or domain organization of myelinated axons compared with WT mice (Opalin+/+) mice. Electron microscopic observation of the optic nerves did not reveal obvious differences between Opalin+/+ and Opalin-/- mice in terms of fine structures of paranodal lo</pubmed_abstract><journal>PloS one</journal><pubmed_title>Mammalian-Specific Central Myelin Protein Opalin Is Redundant for Normal Myelination: Structural and Behavioral Assessments.</pubmed_title><pmcid>PMC5113975</pmcid><funding_grant_id>Research Grant</funding_grant_id><funding_grant_id>KAKENHI 20300134, 23300137, 26290026, 15K14356</funding_grant_id><pubmed_authors>Yoshikawa F</pubmed_authors><pubmed_authors>Ghandour MS</pubmed_authors><pubmed_authors>Furuse T</pubmed_authors><pubmed_authors>Sano Y</pubmed_authors><pubmed_authors>Wakana S</pubmed_authors><pubmed_authors>Furuichi T</pubmed_authors><pubmed_authors>Sato Y</pubmed_authors><pubmed_authors>Sadakata T</pubmed_authors><pubmed_authors>Shinoda Y</pubmed_authors><pubmed_authors>Tohyama K</pubmed_authors><pubmed_authors>Itohara S</pubmed_authors><pubmed_authors>Tanaka M</pubmed_authors><pubmed_authors>Hashikawa T</pubmed_authors><pubmed_authors>Akagi T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mammalian-Specific Central Myelin Protein Opalin Is Redundant for Normal Myelination: Structural and Behavioral Assessments.</name><description>Opalin, a central nervous system-specific myelin protein phylogenetically unique to mammals, has been suggested to play a role in mammalian-specific myelin. To elucidate the role of Opalin in mammalian myelin, we disrupted the Opalin gene in mice and analyzed the impacts on myelination and behavior. Opalin-knockout (Opalin-/-) mice were born at a Mendelian ratio and had a normal body shape and weight. Interestingly, Opalin-/- mice had no obvious abnormalities in major myelin protein compositions, expression of oligodendrocyte lineage markers, or domain organization of myelinated axons compared with WT mice (Opalin+/+) mice. Electron microscopic observation of the optic nerves did not reveal obvious differences between Opalin+/+ and Opalin-/- mice in terms of fine structures of paranodal lo</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016</publication><modification>2025-04-26T20:48:04.496Z</modification><creation>2019-03-26T22:48:50Z</creation></dates><accession>S-EPMC5113975</accession><cross_references><pubmed>27855200</pubmed><doi>10.1371/journal.pone.0166732</doi></cross_references></HashMap>