WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7150
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Conference Object Nanometer Scale Surface Protein Patterns for Spatially Controlled Cell Adhesion(American Society for Cell Biology, 2012) Vurmaz, D.; Pesen Okvur, Devrim; Oyman, G.; Heinz, W. F.; Werbin, J. L.; Hoh, J. H.; Haviland, D. B.; Okvur, D. Pesen; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology[No abstract available]Conference Object Cell Adhesion on Nanometer Scale Protein Patterns With Micrometer Scale Spacings(American Society for Cell Biology, 2012) Vurmaz, Deniz; Pesen Okvur, Devrim; Oyman, Gizem; Okvur, Devrim Pesen; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology[No abstract available]Conference Object Differential Changes in Cell Shape on Nanopatterned Surfaces for Normal and Cancer Cells(American Society for Cell Biology, 2013) Özdil, B.; Pesen Okvur, Devrim; Horzum, U.; Okvur, Devrim Pesen; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology[No abstract available]Conference Object O-Coumaric Acid, Caffeic Acid, Vanilic Acid Inhibits Stat Pathway on Malignant Mesothelioma Cell Lines(American Society for Cell Biology, 2015) Ulupınar, Z.; Soyer, Ferda; Cavus, O.; Gul, H.; Soyer, Ferda; Zergeroğlu, A. Demiroğlu; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of Technology[No abstract available]Conference Object Role of Connexin 32 on Gap Junctions in Breast Cancer Cells With Varying Metastatic Potential.(American Society for Cell Biology, 2017) Özçivici, Engin; Meşe Özçivici, Gülistan; Uğur, Deniz; 03.01. Department of Bioengineering; 04.03. Department of Molecular Biology and Genetics; 01. Izmir Institute of Technology; 03. Faculty of Engineering; 04. Faculty of Science[No abstract available]Conference Object Investigating the Role of Connexin 32 in Cell Cycle, Cell Viability and Epithelial To Mesenchymal Transition of Normal Breast and Breast Cancer Cells(American Society for Cell Biology, 2017) Özçivici, Engin; Meşe Özçivici, Gülistan; Meşe, Gülistan; 03.01. Department of Bioengineering; 04.03. Department of Molecular Biology and Genetics; 03. Faculty of Engineering; 04. Faculty of Science; 01. Izmir Institute of Technology[No abstract available]Article Citation - WoS: 79Citation - Scopus: 80The Cx26-G45e Mutation Displays Increased Hemichannel Activity in a Mouse Model of the Lethal Form of Keratitis-Ichthyosis Syndrome(American Society for Cell Biology, 2011) Meşe Özçivici, Gülistan; Sellitto, Caterina; Li, Leping; Wang, Hongzhan; Valiunas, Virginijus; Richard, Gabriele; Brink, Peter R.; White, Thomas W.; 04.03. Department of Molecular Biology and Genetics; 04. Faculty of Science; 01. Izmir Institute of TechnologyMutations in the GJB2 gene (Cx26) cause deafness in humans. Most are loss-of-function mutations and cause nonsyndromic deafness. Some mutations produce a gain of function and cause syndromic deafness associated with skin disorders, such as keratitis-ichthyosis-deafness syndrome (KIDS). Cx26-G45E is a lethal mutation linked to KIDS that forms constitutively active connexin hemichannels. The pathomechanism(s) by which mutant Cx26 hemichannels perturb normal epidermal cornification are poorly understood. We created an animal model for KIDS by generating an inducible transgenic mouse expressing Cx26-G45E in keratinocytes. Cx26-G45E mice displayed reduced viability, hyperkeratosis, scaling, skin folds, and hair loss. Histopathology included hyperplasia, acanthosis, papillomatosis, increased cell size, and osteal plugging. These abnormalities correlated with human KIDS pathology and were associated with increased hemichannel currents in transgenic keratinocytes. These results confirm the pathogenic nature of the G45E mutation and provide a new model for studying the role of aberrant connexin hemichannels in epidermal differentiation and inherited connexin disorders.