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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...
| Autores principales: | , , , , , |
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| Formato: | Online Artículo Texto |
| Lenguaje: | English |
| Publicado: |
Springer-Verlag
2012
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| Materias: | |
| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3296019/ https://www.ncbi.nlm.nih.gov/pubmed/22252471 http://dx.doi.org/10.1007/s00125-011-2428-6 |