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The Kir6.2-F333I mutation differentially modulates KATP channels composed of SUR1 or SUR2 subunits.

Abstract:

Mutations in Kir6.2, the pore-forming subunit of the KATP 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 KATP 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 S...

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Institution:
University of Oxford
Department:
Oxford, MSD, Pharmacology
Role:
Author
Journal:
The Journal of physiology
Volume:
581
Issue:
Pt 3
Pages:
1259-1269
Publication date:
2007-06-05
DOI:
EISSN:
1469-7793
ISSN:
0022-3751
URN:
uuid:9cea700c-e955-449d-8d6e-ceafc47f762e
Source identifiers:
376166
Local pid:
pubs:376166

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