HIGHLIGHTS
- who: TYPE and collaborators from the Glasgow Caledonian University, United Kingdom have published the research work: Expression of KID syndromic mutation Cx26S17F produces hyperactive hemichannels in supporting cells of the organ of Corti, in the Journal: (JOURNAL)
- what: The authors show that mutant Cx26S17F can associate with Cx30, producing hyperactive HCs with reduced sensitivity to extracellular Ca2+ and standard HC blockers. The authors explore this possibility in HeLa Frontiers in Cell and Developmental Biology frontiersin.org 10.3389/fcell.2022.1071202 this mutation impaired the traffic of Cxs to the plasma_membrane .
- how: Through . . .
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