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A mutation in the ATP-binding site of the Kir6.2 subunit of the K(ATP) channel alters coupling with the SUR2A subunit
Mutations in the pore-forming subunit of the ATP-sensitive K(+) (K(ATP)) channel Kir6.2 cause neonatal diabetes. Understanding the molecular mechanism of action of these mutations has provided valuable insight into the relationship between the structure and function of the K(ATP) channel. When Kir6....
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| Autors principals: | , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
Blackwell Science Inc
2007
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2277002/ https://ncbi.nlm.nih.gov/pubmed/17855752 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1113/jphysiol.2007.143149 |
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