These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Journal Abstract Search

192 related items for PubMed ID: 15962003

  • 1. Kir6.2 mutations causing neonatal diabetes provide new insights into Kir6.2-SUR1 interactions.
    Tammaro P, Girard C, Molnes J, Njølstad PR, Ashcroft FM.
    EMBO J; 2005 Jul 06; 24(13):2318-30. PubMed ID: 15962003
    [Abstract] [Full Text] [Related]

  • 2. The Kir6.2-F333I mutation differentially modulates KATP channels composed of SUR1 or SUR2 subunits.
    Tammaro P, Ashcroft F.
    J Physiol; 2007 Jun 15; 581(Pt 3):1259-69. PubMed ID: 17395632
    [Abstract] [Full Text] [Related]

  • 3. 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; 2006 Dec 15; 453(3):323-32. PubMed ID: 17021801
    [Abstract] [Full Text] [Related]

  • 4. Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels.
    Tammaro P, Proks P, Ashcroft FM.
    J Physiol; 2006 Feb 15; 571(Pt 1):3-14. PubMed ID: 16339180
    [Abstract] [Full Text] [Related]

  • 5. Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features.
    Proks P, Antcliff JF, Lippiat J, Gloyn AL, Hattersley AT, Ashcroft FM.
    Proc Natl Acad Sci U S A; 2004 Dec 14; 101(50):17539-44. PubMed ID: 15583126
    [Abstract] [Full Text] [Related]

  • 6. 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; 2011 Jun 14; 60(6):1813-22. PubMed ID: 21617188
    [Abstract] [Full Text] [Related]

  • 7. Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1.
    Proks P, de Wet H, Ashcroft FM.
    J Gen Physiol; 2010 Oct 14; 136(4):389-405. PubMed ID: 20876358
    [Abstract] [Full Text] [Related]

  • 8. 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; 2009 Jul 14; 94(7):2551-7. PubMed ID: 19351728
    [Abstract] [Full Text] [Related]

  • 9. 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; 2006 Jun 14; 55(6):1731-7. PubMed ID: 16731836
    [Abstract] [Full Text] [Related]

  • 10. 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; 2007 Nov 01; 584(Pt 3):743-53. PubMed ID: 17855752
    [Abstract] [Full Text] [Related]

  • 11. Involvement of the n-terminus of Kir6.2 in coupling to the sulphonylurea receptor.
    Reimann F, Tucker SJ, Proks P, Ashcroft FM.
    J Physiol; 1999 Jul 15; 518 ( Pt 2)(Pt 2):325-36. PubMed ID: 10381582
    [Abstract] [Full Text] [Related]

  • 12. 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; 2007 Aug 15; 16(16):2011-9. PubMed ID: 17584766
    [Abstract] [Full Text] [Related]

  • 13. Functional effects of KCNJ11 mutations causing neonatal diabetes: enhanced activation by MgATP.
    Proks P, Girard C, Ashcroft FM.
    Hum Mol Genet; 2005 Sep 15; 14(18):2717-26. PubMed ID: 16087682
    [Abstract] [Full Text] [Related]

  • 14. 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; 2007 Nov 15; 9 Suppl 2():46-55. PubMed ID: 17919178
    [Abstract] [Full Text] [Related]

  • 15. A cytosolic factor that inhibits KATP channels expressed in Xenopus oocytes by impairing Mg-nucleotide activation by SUR1.
    Tammaro P, Ashcroft FM.
    J Physiol; 2009 Apr 15; 587(Pt 8):1649-56. PubMed ID: 19237428
    [Abstract] [Full Text] [Related]

  • 16. Increased ATPase activity produced by mutations at arginine-1380 in nucleotide-binding domain 2 of ABCC8 causes neonatal diabetes.
    de Wet H, Rees MG, Shimomura K, Aittoniemi J, Patch AM, Flanagan SE, Ellard S, Hattersley AT, Sansom MS, Ashcroft FM.
    Proc Natl Acad Sci U S A; 2007 Nov 27; 104(48):18988-92. PubMed ID: 18025464
    [Abstract] [Full Text] [Related]

  • 17. Analysis of the differential modulation of sulphonylurea block of beta-cell and cardiac ATP-sensitive K+ (K(ATP)) channels by Mg-nucleotides.
    Reimann F, Dabrowski M, Jones P, Gribble FM, Ashcroft FM.
    J Physiol; 2003 Feb 15; 547(Pt 1):159-68. PubMed ID: 12562963
    [Abstract] [Full Text] [Related]

  • 18. 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; 2008 Jan 15; 131(1):43-58. PubMed ID: 18079561
    [Abstract] [Full Text] [Related]

  • 19. N-terminal transmembrane domain of SUR1 controls gating of Kir6.2 by modulating channel sensitivity to PIP2.
    Pratt EB, Tewson P, Bruederle CE, Skach WR, Shyng SL.
    J Gen Physiol; 2011 Mar 15; 137(3):299-314. PubMed ID: 21321069
    [Abstract] [Full Text] [Related]

  • 20. Compound heterozygous mutations in the SUR1 (ABCC 8) subunit of pancreatic K(ATP) channels cause neonatal diabetes by perturbing the coupling between Kir6.2 and SUR1 subunits.
    Lin YW, Akrouh A, Hsu Y, Hughes N, Nichols CG, De León DD.
    Channels (Austin); 2012 Mar 15; 6(2):133-8. PubMed ID: 22562119
    [Abstract] [Full Text] [Related]

    Page: [Next] [New Search]
    of 10.