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Expression of connexin29 and 32 in the penumbra region after traumatic brain injury of mice

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dc.contributor.authorMoon, Younghye-
dc.contributor.authorChoi, So Yoen-
dc.contributor.authorKim, Kyungjin-
dc.contributor.authorKim, Hyun-
dc.contributor.authorSun, Woong-
dc.date.accessioned2021-09-07T22:06:39Z-
dc.date.available2021-09-07T22:06:39Z-
dc.date.created2021-06-14-
dc.date.issued2010-12-29-
dc.identifier.issn0959-4965-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/115092-
dc.description.abstractConnexins (Cx) are transmembrane proteins forming vertebrate gap junction channels for direct cell-cell communication. We found that the expressions of two Cx family members, Cx29 and Cx32, were progressively increased in the sharp border of injury penumbra regions after cryotraumatic brain injury. Although these two Cxs are expressed exclusively in the oligodendrocytes in the normal cerebral cortex, their expressions were increased in the astrocytes and microglia localized in the injury border. Highly selective induction of Cxs in the injury border suggests that altered Cxs may contribute to the propagations of injury-related and/or regeneration signals after acute brain injury. NeuroReport 21: 1135-1139 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherLIPPINCOTT WILLIAMS & WILKINS-
dc.subjectCENTRAL-NERVOUS-SYSTEM-
dc.subjectGAP-JUNCTION PROTEINS-
dc.subjectGLOBAL-ISCHEMIA-
dc.subjectGLIAL-CELLS-
dc.subjectCX32-
dc.subjectOLIGODENDROCYTES-
dc.subjectCOLOCALIZATION-
dc.subjectVULNERABILITY-
dc.subjectASTROCYTES-
dc.subjectCHANNELS-
dc.titleExpression of connexin29 and 32 in the penumbra region after traumatic brain injury of mice-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Hyun-
dc.contributor.affiliatedAuthorSun, Woong-
dc.identifier.doi10.1097/WNR.0b013e32834051c7-
dc.identifier.scopusid2-s2.0-78650516932-
dc.identifier.wosid000284607500001-
dc.identifier.bibliographicCitationNEUROREPORT, v.21, no.18, pp.1135 - 1139-
dc.relation.isPartOfNEUROREPORT-
dc.citation.titleNEUROREPORT-
dc.citation.volume21-
dc.citation.number18-
dc.citation.startPage1135-
dc.citation.endPage1139-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusCENTRAL-NERVOUS-SYSTEM-
dc.subject.keywordPlusGAP-JUNCTION PROTEINS-
dc.subject.keywordPlusGLOBAL-ISCHEMIA-
dc.subject.keywordPlusGLIAL-CELLS-
dc.subject.keywordPlusCX32-
dc.subject.keywordPlusOLIGODENDROCYTES-
dc.subject.keywordPlusCOLOCALIZATION-
dc.subject.keywordPlusVULNERABILITY-
dc.subject.keywordPlusASTROCYTES-
dc.subject.keywordPlusCHANNELS-
dc.subject.keywordAuthorconnexin-
dc.subject.keywordAuthorgap junction-
dc.subject.keywordAuthorhemichannel-
dc.subject.keywordAuthortraumatic brain injury-
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