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Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions.

Abstract:

ATP-sensitive K(+) (K(ATP)) channels, comprised of pore-forming Kir6.2 and regulatory SUR1 subunits, play a critical role in regulating insulin secretion. Binding of ATP to Kir6.2 inhibits, whereas interaction of MgATP with SUR1 activates, K(ATP) channels. We tested the functional effects of two Kir6.2 mutations (Y330C, F333I) that cause permanent neonatal diabetes mellitus, by heterologous expression in Xenopus oocytes. Both mutations reduced ATP inhibition and increased whole-cell currents,...

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Publication status:
Published

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Publisher copy:
10.1038/sj.emboj.7600715

Authors


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Institution:
University of Oxford
Department:
Oxford, MSD, Pharmacology
Njølstad, PR More by this author
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Institution:
University of Oxford
Department:
Oxford, MSD, Physiology Anatomy and Genetics
Journal:
The EMBO journal
Volume:
24
Issue:
13
Pages:
2318-2330
Publication date:
2005-07-05
DOI:
EISSN:
1460-2075
ISSN:
0261-4189
URN:
uuid:bc4b5503-a9c5-4781-a082-9a36442607a0
Source identifiers:
113900
Local pid:
pubs:113900

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