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A conserved tryptophan at the membrane–water interface acts as a gatekeeper for Kir6.2/SUR1 channels and causes neonatal diabetes when mutated
ABSTRACT: We identified a novel heterozygous mutation, W68R, in the Kir6.2 subunit of the ATP-sensitive potassium (K(ATP)) channel, in a patient with transient neonatal diabetes. This tryptophan is absolutely conserved in mammalian Kir channels. The functional effects of mutations at residue 68 of K...
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| Main Authors: | , , , , , , |
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| Format: | Artigo |
| Jezik: | Inglês |
| Izdano: |
Blackwell Science Inc
2011
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| Teme: | |
| Online dostop: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3145925/ https://ncbi.nlm.nih.gov/pubmed/21540348 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1113/jphysiol.2011.209700 |
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