Mechanism of the defect in gap-junctional communication by expression of a connexin 26 mutant associated with dominant deafness Y. Chen 1 , Y. Deng 1 , X. Bao, L. Reuss and G. A. Altenberg 2 Department of Neuroscience and Cell Biology, and Membrane Protein Laboratory of the Sealy Center for Structural Biology, The University of Texas Medical Branch Galveston, Texas, USA 2 Correspondence: E-mail: galtenbe@utmb.edu <h3>SPECIFIC AIMS</h3> Gap-junctional channels (connexin oligomers) are large-diameter aqueous pores formed by head-to-head association of two gap-junctional hemichannels (connexons), one from each of the adjacent cells. Mutations of connexin 26 (Cx26) are the most frequent cause of genetic deafness. The aim of this work was to elucidate the mechanism of the dominant defect on gap-junctional communication produced by expression of Cx26 R75W. To accomplish this task, we measured gap-junctional channel and hemichannel activities in Xenopus laevis oocytes. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Cx26 R75W is expressed at the plasma membrane where it forms gap-junctional hemichannels (GJH) that are functional and blocked by extracellular divalent cations</h3> We found that the R75W mutant is expressed at the plasma membrane, but does not form gap junctions permeable to small inorganic ions, which is in agreement with previous reports.
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Mechanism of the defect in gap-junctional communication by expression of a connexin 26 mutant associated with dominant deafness
Chen, Y.; Deng, Y.; Bao, X.; Reuss, L.; Altenberg, G. A.
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, Volume 19 (11): 1516
Fed of American Socs for Experimental Biology – Sep 1, 2005
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