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...

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Detalles Bibliográficos
Autores principales: Clark, R., Männikkö, R., Stuckey, D. J., Iberl, M., Clarke, K., Ashcroft, F. M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2012
Materias:
Article
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

Internet

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

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