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The first clinical case of a mutation at residue K185 of Kir6.2 (KCNJ11): a major ATP-binding residue.

Abstract:

BACKGROUND: Closure of the adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel plays a key role in insulin secretion from the pancreatic beta-cells. Many mutations in KCNJ11 and ABCC8, which respectively encode the pore-forming (Kir6.2) and regulatory (SUR1) subunits of the K(ATP) channel, cause neonatal diabetes. All such mutations impair the ability of metabolically generated ATP to close the channel. Although lysine 185 is predicted to be a major contributor to the ATP-bindi...

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Publication status:
Published

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Journal:
Diabetic medicine : a journal of the British Diabetic Association
Volume:
27
Issue:
2
Pages:
225-229
Publication date:
2010-02-05
DOI:
EISSN:
1464-5491
ISSN:
0742-3071
URN:
uuid:396dbbac-6ef6-481b-b66a-2fc87b5792ef
Source identifiers:
113385
Local pid:
pubs:113385

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