Papers associated with embryonic structure (and kcnj11)

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	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.
	Xenopus as a model system for studying pancreatic development and diabetes., Kofent J., Semin Cell Dev Biol. March 1, 2016; 51 106-16.
	Recessive mutations in PCBD1 cause a new type of early-onset diabetes., Simaite D., Diabetes. October 1, 2014; 63 (10): 3557-64.
	A universally conserved residue in the SUR1 subunit of the KATP channel is essential for translating nucleotide binding at SUR1 into channel opening., de Wet H., J Physiol. October 15, 2012; 590 (20): 5025-36.
	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.
	Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1., Proks P., J Gen Physiol. October 1, 2010; 136 (4): 389-405.
	A Kir6.2 mutation causing severe functional effects in vitro produces neonatal diabetes without the expected neurological complications., Tammaro P., Diabetologia. May 1, 2008; 51 (5): 802-10.
	A novel mutation causing DEND syndrome: a treatable channelopathy of pancreas and brain., Shimomura K., Neurology. September 25, 2007; 69 (13): 1342-9.
	Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels., Tammaro P., J Physiol. February 15, 2006; 571 (Pt 1): 3-14.
	Arylcyanoguanidines as activators of Kir6.2/SUR1K ATP channels and inhibitors of insulin release., Tagmose TM., J Med Chem. June 3, 2004; 47 (12): 3202-11.
	K(ATP) channel activity is required for hatching in Xenopus embryos., Cheng SM., Dev Dyn. December 1, 2002; 225 (4): 588-91.
	Open state destabilization by ATP occupancy is mechanism speeding burst exit underlying KATP channel inhibition by ATP., Li L., J Gen Physiol. January 1, 2002; 119 (1): 105-16.
	Amiloride derivatives are potent blockers of KATP channels., Bollensdorff C., Naunyn Schmiedebergs Arch Pharmacol. October 1, 2001; 364 (4): 351-8.
	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.
	Nucleotide modulation of pinacidil stimulation of the cloned K(ATP) channel Kir6.2/SUR2A., Gribble FM., Mol Pharmacol. June 1, 2000; 57 (6): 1256-61.
	Altered functional properties of KATP channel conferred by a novel splice variant of SUR1., Sakura H., J Physiol. December 1, 1999; 521 Pt 2 337-50.
	Differential sensitivity of beta-cell and extrapancreatic K(ATP) channels to gliclazide., Gribble FM., Diabetologia. July 1, 1999; 42 (7): 845-8.
	Phentolamine block of KATP channels is mediated by Kir6.2., Proks P., Proc Natl Acad Sci U S A. October 14, 1997; 94 (21): 11716-20.

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