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Engineered Kir6.2 mutations that correct the trafficking defect of K(ATP) channels caused by specific SUR1 mutations

K(ATP) channels consisting of Kir6.2 and SUR1 couple cell metabolism to membrane excitability and regulate insulin secretion. The molecular interactions between SUR1 and Kir6.2 that govern channel gating and biogenesis are incompletely understood. In a recent study, we showed that a SUR1 and Kir6.2...

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Bibliografski detalji
Glavni autori: Zhou, Qing, Pratt, Emily B, Shyng, Show-Ling
Format: Artigo
Jezik:Inglês
Izdano: Landes Bioscience 2013
Teme:
Online pristup:https://ncbi.nlm.nih.gov/pmc/articles/PMC3989359/
https://ncbi.nlm.nih.gov/pubmed/23695995
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.4161/chan.25003
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