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Summary Expression Gene Literature (137) GO Terms (0) Nucleotides (19) Proteins (10) Interactants (210) Wiki
XB-GENEPAGE-996922

Papers associated with abcc8

Search for abcc8 morpholinos using Textpresso

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4 paper(s) referencing morpholinos

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Binding of sulphonylureas to plasma proteins - A KATP channel perspective., Proks P, Kramer H, Haythorne E, Ashcroft FM., PLoS One. January 1, 2018; 13 (5): e0197634.        


Role of the C-terminus of SUR in the differential regulation of β-cell and cardiac KATP channels by MgADP and metabolism., Vedovato N, Rorsman O, Hennis K, Ashcroft FM, Proks P., J Physiol. January 1, 2018; 596 (24): 6205-6217.            


A novel high-affinity inhibitor against the human ATP-sensitive Kir6.2 channel., Ramu Y, Xu Y, Lu Z., J Gen Physiol. January 1, 2018; 150 (7): 969-976.              


Xenopus as a model system for studying pancreatic development and diabetes., Kofent J, Spagnoli FM., Semin Cell Dev Biol. March 1, 2016; 51 106-16.  


Sensitivity of KATP channels to cellular metabolic disorders and the underlying structural basis., Li CG, Cui WY, Wang H., Acta Pharmacol Sin. January 1, 2016; 37 (1): 134-42.        


Kir6.2 activation by sulfonylurea receptors: a different mechanism of action for SUR1 and SUR2A subunits via the same residues., Principalli MA, Dupuis JP, Moreau CJ, Vivaudou M, Revilloud J., Physiol Rep. September 1, 2015; 3 (9):         


Sulfonylureas suppress the stimulatory action of Mg-nucleotides on Kir6.2/SUR1 but not Kir6.2/SUR2A KATP channels: a mechanistic study., Proks P, de Wet H, Ashcroft FM., J Gen Physiol. November 1, 2014; 144 (5): 469-86.                  


Recessive mutations in PCBD1 cause a new type of early-onset diabetes., Simaite D, Kofent J, Gong M, Rüschendorf F, Jia S, Arn P, Bentler K, Ellaway C, Kühnen P, Hoffmann GF, Blau N, Spagnoli FM, Hübner N, Raile K., Diabetes. October 1, 2014; 63 (10): 3557-64.


Purinergic receptor-induced Ca2+ signaling in the neuroepithelium of the vomeronasal organ of larval Xenopus laevis., Dittrich K, Sansone A, Hassenklöver T, Manzini I., Purinergic Signal. January 1, 2014; 10 (2): 327-36.          


The unusual stoichiometry of ADP activation of the KATP channel., Hosy E, Vivaudou M., Front Physiol. January 1, 2014; 5 11.        


Molecular mechanism of sulphonylurea block of K(ATP) channels carrying mutations that impair ATP inhibition and cause neonatal diabetes., Proks P, de Wet H, Ashcroft FM., Diabetes. November 1, 2013; 62 (11): 3909-19.              


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, Shimomura K, Aittoniemi J, Ahmad N, Lafond M, Sansom MS, Ashcroft FM., J Physiol. October 15, 2012; 590 (20): 5025-36.            


Homeoprotein hhex-induced conversion of intestinal to ventral pancreatic precursors results in the formation of giant pancreata in Xenopus embryos., Zhao H, Han D, Dawid IB, Pieler T, Chen Y, Chen Y., Proc Natl Acad Sci U S A. May 29, 2012; 109 (22): 8594-9.                              


Transient expression of Ngn3 in Xenopus endoderm promotes early and ectopic development of pancreatic beta and delta cells., Oropeza D, Horb M., Genesis. March 1, 2012; 50 (3): 271-85.                        


Engineering of an artificial light-modulated potassium channel., Caro LN, Moreau CJ, Estrada-Mondragón A, Ernst OP, Vivaudou M., PLoS One. January 1, 2012; 7 (8): e43766.        


Neurally Derived Tissues in Xenopus laevis Embryos Exhibit a Consistent Bioelectrical Left-Right Asymmetry., Pai VP, Vandenberg LN, Blackiston D, Levin M., Stem Cells Int. January 1, 2012; 2012 353491.          


A conserved tryptophan at the membrane-water interface acts as a gatekeeper for Kir6.2/SUR1 channels and causes neonatal diabetes when mutated., Männikkö R, Stansfeld PJ, Ashcroft AS, Hattersley AT, Sansom MS, Ellard S, Ashcroft FM., J Physiol. July 1, 2011; 589 (Pt 13): 3071-83.


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, Flanagan SE, Sim X, Segal D, Hussain K, Ellard S, Hattersley AT, Ashcroft FM., Diabetes. June 1, 2011; 60 (6): 1813-22.              


β2-Adrenergic ion-channel coupled receptors as conformational motion detectors., Caro LN, Moreau CJ, Revilloud J, Vivaudou M., PLoS One. March 2, 2011; 6 (3): e18226.            


Constitutive recycling of the store-operated Ca2+ channel Orai1 and its internalization during meiosis., Yu F, Sun L, Machaca K., J Cell Biol. November 1, 2010; 191 (3): 523-35.                  


The ATP-sensitive K(+)-channel (K(ATP)) controls early left-right patterning in Xenopus and chick embryos., Aw S, Koster JC, Pearson W, Nichols CG, Shi NQ, Carneiro K, Levin M., Dev Biol. October 1, 2010; 346 (1): 39-53.        


Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1., Proks P, de Wet H, Ashcroft FM., J Gen Physiol. October 1, 2010; 136 (4): 389-405.                    


Disease progression and search for monogenic diabetes among children with new onset type 1 diabetes negative for ICA, GAD- and IA-2 Antibodies., Pörksen S, Laborie LB, Nielsen L, Louise Max Andersen M, Sandal T, de Wet H, Schwarcz E, Aman J, Swift P, Kocova M, Schönle EJ, de Beaufort C, Hougaard P, Ashcroft F, Molven A, Knip M, Mortensen HB, Hansen L, Njølstad PR, null null., BMC Endocr Disord. September 23, 2010; 10 16.      


Targeting hypertension with a new adenosine triphosphate-sensitive potassium channel opener iptakalim., Pan Z, Huang J, Cui W, Long C, Zhang Y, Wang H., J Cardiovasc Pharmacol. September 1, 2010; 56 (3): 215-28.


The first clinical case of a mutation at residue K185 of Kir6.2 (KCNJ11): a major ATP-binding residue., Shimomura K, de Nanclares GP, Foutinou C, Caimari M, Castaño L, Ashcroft FM., Diabet Med. February 1, 2010; 27 (2): 225-9.


Impact of disease-causing SUR1 mutations on the KATP channel subunit interface probed with a rhodamine protection assay., Hosy E, Dupuis JP, Vivaudou M., J Biol Chem. January 29, 2010; 285 (5): 3084-91.


An in-frame deletion in Kir6.2 (KCNJ11) causing neonatal diabetes reveals a site of interaction between Kir6.2 and SUR1., Craig TJ, Shimomura K, Holl RW, Flanagan SE, Ellard S, Ashcroft FM., J Clin Endocrinol Metab. July 1, 2009; 94 (7): 2551-7.


Xenopus pancreas development., Pearl EJ, Bilogan CK, Mukhi S, Brown DD, Horb ME., Dev Dyn. June 1, 2009; 238 (6): 1271-86.          


A cytosolic factor that inhibits KATP channels expressed in Xenopus oocytes by impairing Mg-nucleotide activation by SUR1., Tammaro P, Ashcroft FM., J Physiol. April 15, 2009; 587 (Pt 8): 1649-56.


Coassembly of different sulfonylurea receptor subtypes extends the phenotypic diversity of ATP-sensitive potassium (KATP) channels., Wheeler A, Wang C, Yang K, Fang K, Davis K, Styer AM, Mirshahi U, Moreau C, Revilloud J, Vivaudou M, Liu S, Mirshahi T, Chan KW., Mol Pharmacol. November 1, 2008; 74 (5): 1333-44.


How ATP inhibits the open K(ATP) channel., Craig TJ, Ashcroft FM, Proks P., J Gen Physiol. July 1, 2008; 132 (1): 131-44.            


A Kir6.2 mutation causing severe functional effects in vitro produces neonatal diabetes without the expected neurological complications., Tammaro P, Flanagan SE, Zadek B, Srinivasan S, Woodhead H, Hameed S, Klimes I, Hattersley AT, Ellard S, Ashcroft FM., Diabetologia. May 1, 2008; 51 (5): 802-10.            


Sulfonylurea receptors type 1 and 2A randomly assemble to form heteromeric KATP channels of mixed subunit composition., Chan KW, Wheeler A, Csanády L., J Gen Physiol. January 1, 2008; 131 (1): 43-58.                    


Expression of complement components coincides with early patterning and organogenesis in Xenopus laevis., McLin VA, Hu CH, Shah R, Jamrich M., Int J Dev Biol. January 1, 2008; 52 (8): 1123-33.                                              


Functional analysis of two Kir6.2 (KCNJ11) mutations, K170T and E322K, causing neonatal diabetes., Tarasov AI, Girard CA, Larkin B, Tammaro P, Flanagan SE, Ellard S, Ashcroft FM., Diabetes Obes Metab. November 1, 2007; 9 Suppl 2 46-55.


A mutation in the ATP-binding site of the Kir6.2 subunit of the KATP channel alters coupling with the SUR2A subunit., Tammaro P, Ashcroft FM., J Physiol. November 1, 2007; 584 (Pt 3): 743-53.


Uncoupling by (--)-epigallocatechin-3-gallate of ATP-sensitive potassium channels from phosphatidylinositol polyphosphates and ATP., Jin JY, Park SH, Bae JH, Cho HC, Lim JG, Park WS, Han J, Lee JH, Song DK., Pharmacol Res. September 1, 2007; 56 (3): 237-47.


Mechanism of action of a sulphonylurea receptor SUR1 mutation (F132L) that causes DEND syndrome., Proks P, Shimomura K, Craig TJ, Girard CA, Ashcroft FM., Hum Mol Genet. August 15, 2007; 16 (16): 2011-9.


Iptakalim, a vascular ATP-sensitive potassium (KATP) channel opener, closes rat pancreatic beta-cell KATP channels and increases insulin release., Misaki N, Mao X, Lin YF, Suga S, Li GH, Liu Q, Chang Y, Wang H, Wakui M, Wu J., J Pharmacol Exp Ther. August 1, 2007; 322 (2): 871-8.


Single residue (K332A) substitution in Kir6.2 abolishes the stimulatory effect of long-chain acyl-CoA esters: indications for a long-chain acyl-CoA ester binding motif., Bränström R, Leibiger IB, Leibiger B, Klement G, Nilsson J, Arhem P, Aspinwall CA, Corkey BE, Larsson O, Berggren PO., Diabetologia. August 1, 2007; 50 (8): 1670-7.


Remodelling of the SUR-Kir6.2 interface of the KATP channel upon ATP binding revealed by the conformational blocker rhodamine 123., Hosy E, Dérand R, Revilloud J, Vivaudou M., J Physiol. July 1, 2007; 582 (Pt 1): 27-39.


The Kir6.2-F333I mutation differentially modulates KATP channels composed of SUR1 or SUR2 subunits., Tammaro P, Ashcroft F., J Physiol. June 15, 2007; 581 (Pt 3): 1259-69.


Electrophysiological and pharmacological characterization of the K(ATP) channel involved in the K+-current responses to FSH and adenosine in the follicular cells of Xenopus oocyte., Fujita R, Kimura S, Kawasaki S, Watanabe S, Watanabe N, Hirano H, Matsumoto M, Sasaki K., J Physiol Sci. February 1, 2007; 57 (1): 51-61.


Functional analysis of six Kir6.2 (KCNJ11) mutations causing neonatal diabetes., Girard CA, Shimomura K, Proks P, Absalom N, Castano L, Perez de Nanclares G, Ashcroft FM., Pflugers Arch. December 1, 2006; 453 (3): 323-32.


Scavenging of 14-3-3 proteins reveals their involvement in the cell-surface transport of ATP-sensitive K+ channels., Heusser K, Yuan H, Neagoe I, Tarasov AI, Ashcroft FM, Schwappach B., J Cell Sci. October 15, 2006; 119 (Pt 20): 4353-63.


The N-terminal transmembrane domain (TMD0) and a cytosolic linker (L0) of sulphonylurea receptor define the unique intrinsic gating of KATP channels., Fang K, Csanády L, Chan KW., J Physiol. October 15, 2006; 576 (Pt 2): 379-89.


Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy., Proks P, Girard C, Baevre H, Njølstad PR, Ashcroft FM., Diabetes. June 1, 2006; 55 (6): 1731-7.


Mutations at the same residue (R50) of Kir6.2 (KCNJ11) that cause neonatal diabetes produce different functional effects., Shimomura K, Girard CA, Proks P, Nazim J, Lippiat JD, Cerutti F, Lorini R, Ellard S, Hattersley AT, Barbetti F, Ashcroft FM., Diabetes. June 1, 2006; 55 (6): 1705-12.


A heterozygous activating mutation in the sulphonylurea receptor SUR1 (ABCC8) causes neonatal diabetes., Proks P, Arnold AL, Bruining J, Girard C, Flanagan SE, Larkin B, Colclough K, Hattersley AT, Ashcroft FM, Ellard S., Hum Mol Genet. June 1, 2006; 15 (11): 1793-800.


Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels., Tammaro P, Proks P, Ashcroft FM., J Physiol. February 15, 2006; 571 (Pt 1): 3-14.

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