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Pediatric Diabetes|August 7, 2009
Successful sulfonylurea treatment of an insulin-naïve neonate with diabetes mellitus due to a KCNJ11 mutationJennifer A Wambach, Bess A Marshall, Joseph C Koster, et al.Diabetes|January 30, 2007
An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetesRicard Masia, Joseph C Koster, Stefano Tumini, et al.Developmental Biology|July 21, 2010
The ATP-sensitive K(+)-channel (K(ATP)) controls early left-right patterning in Xenopus and chick embryosSherry Aw, Joseph C Koster, Wade Pearson, et al.Plos Biology|January 13, 2006
Critical role of gap junction coupled KATP channel activity for regulated insulin secretionJonathan V Rocheleau, Maria S Remedi, Butch Granada, et al.Diabetes|November 25, 2004
Diet-induced glucose intolerance in mice with decreased beta-cell ATP-sensitive K+ channelsMaria S Remedi, Joseph C Koster, Kamelia Markova, et al.Diabetes|June 4, 2009
Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose toleranceDennis T Villareal, Joseph C Koster, Heather Robertson, et al.Cell Metabolism|February 4, 2009
Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitusMaria Sara Remedi, Harley T Kurata, Alexis Scott, et al.Diabetes|October 29, 2010
Congenital hyperinsulinism and glucose hypersensitivity in homozygous and heterozygous carriers of Kir6.2 (KCNJ11) mutation V290M mutation: K(ATP) channel inactivation mechanism and clinical managementKaren J Loechner, Alejandro Akrouh, Harley T Kurata, et al.Journal of the American Heart Association|August 27, 2013
Hypotension due to Kir6.1 gain-of-function in vascular smooth muscleAnlong Li, Russell H Knutsen, Haixia Zhang, et al.Pageof 2