ArticlePflugers Archiv : European journal of physiology2016
Gap-junctional channel and hemichannel activity of two recently identified connexin 26 mutants associated with deafness.
Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
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- Inhibition of Connexin Hemichannels by New Amphiphilic Aminoglycosides without Antibiotic Activity.ACS medicinal chemistry letters · 2018Article
- Mast Cells Interact with Endothelial Cells to Accelerate In Vitro Angiogenesis.International journal of molecular sciences · 2017Article
- Inhibition by Commercial Aminoglycosides of Human Connexin Hemichannels Expressed in Bacteria.Molecules (Basel, Switzerland) · 2017Article
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Authors and funding
10 authors at 8 institutions in 3 countries.
Funding
Abstract
Gap-junction channels (GJCs) are formed by head-to-head association of two hemichannels (HCs, connexin hexamers). HCs and GJCs are permeable to ions and hydrophilic molecules of up to Mr ~1 kDa. Hearing impairment of genetic origin is common, and mutations of connexin 26 (Cx26) are its major cause. We recently identified two novel Cx26 mutations in hearing-impaired subjects, L10P and G109V. L10P forms functional GJCs with slightly altered voltage dependence and HCs with decrease ATP/cationic dye selectivity. G109V does not form functional GJCs, but forms functional HCs with enhanced extracellular Ca(2+) sensitivity and subtle alterations in voltage dependence and ATP/cationic dye selectivity. Deafness associated with G109V could result from decreased GJCs activity, whereas deafness associated to L10P may have a more complex mechanism that involves changes in HC permeability.
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