Papers associated with epithelium∨derBy=4 (and kcnj11)

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	Neonatal diabetes caused by a homozygous KCNJ11 mutation demonstrates that tiny changes in ATP sensitivity markedly affect diabetes risk., Vedovato N., Diabetologia. July 1, 2016; 59 (7): 1430-1436.
	Bioelectric signalling via potassium channels: a mechanism for craniofacial dysmorphogenesis in KCNJ2-associated Andersen-Tawil Syndrome., Adams DS., J Physiol. June 15, 2016; 594 (12): 3245-70.
	Sulfonylureas suppress the stimulatory action of Mg-nucleotides on Kir6.2/SUR1 but not Kir6.2/SUR2A KATP channels: a mechanistic study., Proks P., J Gen Physiol. November 1, 2014; 144 (5): 469-86.
	Recessive mutations in PCBD1 cause a new type of early-onset diabetes., Simaite D., Diabetes. October 1, 2014; 63 (10): 3557-64.
	Molecular mechanism of sulphonylurea block of K(ATP) channels carrying mutations that impair ATP inhibition and cause neonatal diabetes., Proks P., Diabetes. November 1, 2013; 62 (11): 3909-19.
	Mutations of the same conserved glutamate residue in NBD2 of the sulfonylurea receptor 1 subunit of the KATP channel can result in either hyperinsulinism or neonatal diabetes., Männikkö R., Diabetes. June 1, 2011; 60 (6): 1813-22.
	Relapsing diabetes can result from moderately activating mutations in KCNJ11., Gloyn AL., Hum Mol Genet. April 1, 2005; 14 (7): 925-34.
	The novel diazoxide analog 3-isopropylamino-7-methoxy-4H-1,2,4-benzothiadiazine 1,1-dioxide is a selective Kir6.2/SUR1 channel opener., Dabrowski M., Diabetes. June 1, 2002; 51 (6): 1896-906.
	Glimepiride block of cloned beta-cell, cardiac and smooth muscle K(ATP) channels., Song DK., Br J Pharmacol. May 1, 2001; 133 (1): 193-9.
	Effects of mitiglinide (S 21403) on Kir6.2/SUR1, Kir6.2/SUR2A and Kir6.2/SUR2B types of ATP-sensitive potassium channel., Reimann F., Br J Pharmacol. April 1, 2001; 132 (7): 1542-8.
	Sensitivity of Kir6.2-SUR1 currents, in the absence and presence of sodium azide, to the K(ATP) channel inhibitors, ciclazindol and englitazone., McKay NG., Br J Pharmacol. June 1, 2000; 130 (4): 857-66.
	Sensitivity of a renal K+ channel (ROMK2) to the inhibitory sulfonylurea compound glibenclamide is enhanced by coexpression with the ATP-binding cassette transporter cystic fibrosis transmembrane regulator., McNicholas CM., Proc Natl Acad Sci U S A. July 23, 1996; 93 (15): 8083-8.

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