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Comparative proteomic approach in rat model of absence epilepsy.

dc.contributor.authorGürol, Gönül
dc.contributor.authorDemiralp, Duygu Özel
dc.contributor.authorYılmaz, Ayça Kasapoğlu
dc.contributor.authorAkman, Özlem
dc.contributor.authorAteş, Nurbay
dc.contributor.authorKarson, Ayşe
dc.date.accessioned2015-09-16T13:17:42Z
dc.date.available2015-09-16T13:17:42Z
dc.date.issued2015
dc.identifier.citationGürol G, Demiralp DÖ, Yılmaz AK, Akman Ö, Ateş N, Karson A. Comparative proteomic approach in rat model of absence epilepsy. J Mol Neurosci. 2015; 55(3): 632-643. doi: 10.1007/s12031-014-0402-8.en_US
dc.identifier.issn0895-8696
dc.identifier.urihttp://link.springer.com/article/10.1007%2Fs12031-014-0402-8en_US
dc.identifier.urihttps://hdl.handle.net/11446/794en_US
dc.descriptionİstanbul Bilim Üniversitesi, Tıp Fakültesi.en_US
dc.description.abstractThe aim of this study was to investigate cellular proteins in the pathogenesis of the genetic rat model of absence epilepsy. Protein spots were identified with peptide mass fingerprinting analysis using matrix-assisted laser desorption ionization time of flight mass spectrometry. Data were gathered from the frontoparietal cortex and thalamus of Wistar Albino Glaxo/Rij (WAG/Rij) and Wistar by using two-dimensional gel electrophoresis (2D-PAGE). Six proteins (Clathrin light chain-A protein, Transmembrane EMP24 Domain-Containing Protein, Stathmin-4, Myosin Light Chain4, Rheb, phosphoserine phosphatase) were found to be differentially expressed in the frontoparietal cortex of WAG/Rij and Wistar rats in both age groups. Another set of six proteins (Protein FAM89A and Oasl1, Gemin2, NuDEL1, Pur-beta, 3-alpha HSD) were found to be differentially expressed in the thalamus of WAG/Rij and Wistar rats.en_US
dc.language.isoengen_US
dc.publisherHumana Pressen_US
dc.identifier.doi10.1007/s12031-014-0402-8en_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectWAG/Rijen_US
dc.subjectRheben_US
dc.subjectmTORen_US
dc.subject3α-HSDen_US
dc.subjectRB3en_US
dc.titleComparative proteomic approach in rat model of absence epilepsy.en_US
dc.typearticleen_US
dc.relation.journalJournal of Molecular Neuroscienceen_US
dc.departmentDBÜ, Tıp Fakültesien_US
dc.identifier.issue3
dc.identifier.volume55
dc.identifier.startpage632
dc.identifier.endpage643
dc.contributor.authorIDTR153088en_US
dc.contributor.authorIDTR121373en_US
dc.contributor.authorIDTR45271en_US
dc.contributor.authorIDTR25866en_US
dc.contributor.authorIDTR155950en_US
dc.relation.publicationcategoryBelirsizen_US


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