Papers associated with cranial nerve (and kcnj11)

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	Distinct action of the α-glucosidase inhibitor miglitol on SGLT3, enteroendocrine cells, and GLP1 secretion., Lee EY., J Endocrinol. March 1, 2015; 224 (3): 205-14.
	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.
	Three C-terminal residues from the sulphonylurea receptor contribute to the functional coupling between the K(ATP) channel subunits SUR2A and Kir6.2., Dupuis JP., J Physiol. July 1, 2008; 586 (13): 3075-85.
	Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy., Proks P., Diabetes. June 1, 2006; 55 (6): 1731-7.
	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.
	Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP., Proks P., Hum Mol Genet. September 15, 2005; 14 (18): 2717-26.
	Ligand-dependent linkage of the ATP site to inhibition gate closure in the KATP channel., Li L., J Gen Physiol. September 1, 2005; 126 (3): 285-99.
	A gating mutation at the internal mouth of the Kir6.2 pore is associated with DEND syndrome., Proks P., EMBO Rep. May 1, 2005; 6 (5): 470-5.
	Relapsing diabetes can result from moderately activating mutations in KCNJ11., Gloyn AL., Hum Mol Genet. April 1, 2005; 14 (7): 925-34.
	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.
	Mapping the architecture of the ATP-binding site of the KATP channel subunit Kir6.2., Dabrowski M., J Physiol. June 1, 2004; 557 (Pt 2): 347-54.
	Na(+) current through KATP channels: consequences for Na(+) and K(+) fluxes during early myocardial ischemia., Bollensdorff C., Am J Physiol Heart Circ Physiol. January 1, 2004; 286 (1): H283-95.
	Pyridine nucleotide regulation of the KATP channel Kir6.2/SUR1 expressed in Xenopus oocytes., Dabrowski M., J Physiol. July 15, 2003; 550 (Pt 2): 357-63.
	Identification of residues contributing to the ATP binding site of Kir6.2., Trapp S., EMBO J. June 16, 2003; 22 (12): 2903-12.
	A threonine residue (Thr71) at the intracellular end of the M1 helix plays a critical role in the gating of Kir6.2 channels by intracellular ATP and protons., Cui N., J Membr Biol. March 15, 2003; 192 (2): 111-22.
	K(ATP) channel activity is required for hatching in Xenopus embryos., Cheng SM., Dev Dyn. December 1, 2002; 225 (4): 588-91.
	Protons activate homomeric Kir6.2 channels by selective suppression of the long and intermediate closures., Wu J., J Membr Biol. November 15, 2002; 190 (2): 105-16.

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