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Journal article

The Kir6.2-F333I mutation differentially modulates K ATP channels composed of SUR1 and SUR2 subunits

Abstract:

Mutations in Kir6.2, the pore-forming subunit of the K ATP channel, that reduce the ability of ATP to block the channel cause neonatal diabetes. The stimulatory effect of MgATP mediated by the regulatory sulphonylurea receptor (SUR) subunit of the channel may also be modified. We compared the effect of the Kir6.2-F333I mutation on K ATP channels containing SUR1, SUR2A or SUR2B. The open probability of Kir6.2/SUR1 channels, or a C-terminally truncated form of Kir6.2 expressed in the absence of...

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Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1113/jphysiol.2007.130211

Authors


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Institution:
University of Oxford
Division:
MSD
Department:
Physiology Anatomy & Genetics
Oxford college:
Wolfson College
Role:
Author
More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Physiology Anatomy & Genetics
Oxford college:
Trinity College
Role:
Author

Contributors

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Funding agency for:
Ashcroft, F
Wellcome Trust More from this funder
Royal Society More from this funder
Publisher:
Blackwell Publishing Publisher's website
Journal:
Journal of Physiology Journal website
Volume:
581
Issue:
3
Pages:
1259-1269
Publication date:
2007-06-01
DOI:
EISSN:
1469-7793
ISSN:
0022-3751
Language:
English
Keywords:
Subjects:
UUID:
uuid:9b1f8e79-d924-4ede-b0e3-e41d4a2b5a73
Local pid:
ora:1735
Deposit date:
2008-03-14

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