A conserved tryptophan at the membrane-water interface acts as a gatekeeper for Kir6.2/SUR1 channels and causes neonatal diabetes when mutated.
about
A Conserved Residue Cluster That Governs Kinetics of ATP-dependent Gating of Kir6.2 Potassium ChannelsXenopus as a Model for GI/Pancreas Disease.The value of in vitro studies in a case of neonatal diabetes with a novel Kir6.2-W68G mutation.Phenotypic heterogeneity in monogenic diabetes: the clinical and diagnostic utility of a gene panel-based next-generation sequencing approach
P2860
A conserved tryptophan at the membrane-water interface acts as a gatekeeper for Kir6.2/SUR1 channels and causes neonatal diabetes when mutated.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
A conserved tryptophan at the ...... eonatal diabetes when mutated.
@en
A conserved tryptophan at the ...... eonatal diabetes when mutated.
@nl
type
label
A conserved tryptophan at the ...... eonatal diabetes when mutated.
@en
A conserved tryptophan at the ...... eonatal diabetes when mutated.
@nl
prefLabel
A conserved tryptophan at the ...... eonatal diabetes when mutated.
@en
A conserved tryptophan at the ...... eonatal diabetes when mutated.
@nl
P2093
P2860
P50
P1476
A conserved tryptophan at the ...... neonatal diabetes when mutated
@en
P2093
Alexandra S Ashcroft
Andrew T Hattersley
Frances M Ashcroft
P2860
P304
P356
10.1113/JPHYSIOL.2011.209700
P407
P577
2011-05-03T00:00:00Z