Mice expressing a human K(ATP) channel mutation have altered channel ATP sensitivity but no cardiac abnormalities.
AIMS/HYPOTHESIS: Patients with severe gain-of-function mutations in the Kir6.2 subunit of the ATP-sensitive potassium (K(ATP)) channel, have neonatal diabetes, muscle hypotonia and mental and motor developmental delay-a condition known as iDEND syndrome. However, despite the fact that Kir6.2 forms t...
| Main Authors: | , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
2012
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