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Journal article

A Kir6.2 mutation causing neonatal diabetes impairs electrical activity and insulin secretion from INS-1 beta-cells.

Abstract:

ATP-sensitive K(+) channels (K(ATP) channels) couple beta-cell metabolism to electrical activity and thereby play an essential role in the control of insulin secretion. Gain-of-function mutations in Kir6.2 (KCNJ11), the pore-forming subunit of this channel, cause neonatal diabetes. We investigated the effect of the most common neonatal diabetes mutation (R201H) on beta-cell electrical activity and insulin secretion by stable transfection in the INS-1 cell line. Expression was regulated by pla...

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Publication status:
Published

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Publisher copy:
10.2337/db06-0637

Authors


Tarasov, AI More by this author
Welters, HJ More by this author
Ryffel, GU More by this author
Hattersley, AT More by this author
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Journal:
Diabetes
Volume:
55
Issue:
11
Pages:
3075-3082
Publication date:
2006-11-05
DOI:
EISSN:
1939-327X
ISSN:
0012-1797
URN:
uuid:a17dc798-26a2-46d4-aefd-e73597f5de93
Source identifiers:
114072
Local pid:
pubs:114072

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