Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/5051
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dc.contributor.authorLevit, Noah A.-
dc.contributor.authorMeşe, Gülistan-
dc.contributor.authorBasaly, Mena George R.-
dc.contributor.authorWhite, Thomas W.-
dc.date.accessioned2017-03-14T12:38:35Z-
dc.date.available2017-03-14T12:38:35Z-
dc.date.issued2012-08-
dc.identifier.citationLevit, N. A., Meşe, G., Basaly, M. G. R., and White, T. W. (2012). Pathological hemichannels associated with human Cx26 mutations causing Keratitis-Ichthyosis-Deafness syndrome. Biochimica et Biophysica Acta - Biomembranes, 1818(8), 2014-2019. doi:10.1016/j.bbamem.2011.09.003en_US
dc.identifier.issn0005-2736-
dc.identifier.urihttp://doi.org/10.1016/j.bbamem.2011.09.003-
dc.identifier.urihttp://hdl.handle.net/11147/5051-
dc.description.abstractAbstract Connexin (Cx) proteins form intercellular gap junction channels by first assembling into single membrane hemichannels that then dock to connect the cytoplasm of two adjacent cells. Gap junctions are highly specialized structures that allow the direct passage of small molecules between cells to maintain tissue homeostasis. Functional activity of nonjunctional hemichannels has now been shown in several experimental systems. Hemichannels may constitute an important diffusional exchange pathway with the extracellular space, but the extent of their normal physiological role is currently unknown. Aberrant hemichannel activity has been linked to mutations of connexin proteins involved in genetic diseases. Here, we review a proposed role for hemichannels in the pathogenesis of Keratitis-Ichthyosis-Deafness (KID) syndrome associated with connexin26 (Cx26) mutations. Continued functional evaluation of mutated hemichannels linked to human hereditary disorders may provide additional insights into the mechanisms governing their regulation in normal physiology and dysregulation in disease. This article is part of a Special Issue entitled: The Communicating junctions, composition, structure and characteristics. © 2011 Elsevier B.V.en_US
dc.description.sponsorshipNIH Grant R01 AR059505en_US
dc.language.isoenen_US
dc.publisherElsevier Ltd.en_US
dc.relation.ispartofBiochimica et Biophysica Acta - Biomembranesen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectGenetic diseaseen_US
dc.subjectMutationen_US
dc.subjectEpidermisen_US
dc.subjectConnexin 26en_US
dc.subjectHemichannelsen_US
dc.titlePathological hemichannels associated with human Cx26 mutations causing Keratitis-Ichthyosis-Deafness syndromeen_US
dc.typeArticleen_US
dc.authorid0000-0003-0458-8684en_US
dc.institutionauthorMeşe, Gülistan-
dc.departmentİzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.identifier.volume1818en_US
dc.identifier.issue8en_US
dc.identifier.startpage2014en_US
dc.identifier.endpage2019en_US
dc.identifier.wosWOS:000305359000022en_US
dc.identifier.scopus2-s2.0-84055168825en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1016/j.bbamem.2011.09.003-
dc.identifier.pmid21933663en_US
dc.relation.doi10.1016/j.bbamem.2011.09.003en_US
dc.coverage.doi10.1016/j.bbamem.2011.09.003en_US
dc.identifier.scopusqualityQ1-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.grantfulltextopen-
crisitem.author.dept04.03. Department of Molecular Biology and Genetics-
Appears in Collections:Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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