Colin Nichols

Summary

Affiliation: Washington University School of Medicine
Country: USA

Publications

  1. pmc KATP channels and cardiovascular disease: suddenly a syndrome
    Colin G Nichols
    Center for the Investigation of Membrane Excitability Diseases and Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Circ Res 112:1059-72. 2013
  2. pmc The diabetic β-cell: hyperstimulated vs. hyperexcited
    C G Nichols
    Department of Cell Biology and Physiology and Center for Investigation of Membrane Excitability Diseases, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes Obes Metab 14:129-35. 2012
  3. ncbi request reprint beta-cell hyperexcitability: from hyperinsulinism to diabetes
    C G Nichols
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes Obes Metab 9:81-8. 2007
  4. pmc Congenital hyperinsulinism and glucose hypersensitivity in homozygous and heterozygous carriers of Kir6.2 (KCNJ11) mutation V290M mutation: K(ATP) channel inactivation mechanism and clinical management
    Karen J Loechner
    Department of Pediatrics, University of North Carolina School of Medicine, Chapel Hill, USA
    Diabetes 60:209-17. 2011
  5. ncbi request reprint Regulation of KATP channel expression and activity by the SUR1 nucleotide binding fold 1
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Channels (Austin) 1:315-23. 2007
  6. ncbi request reprint Random assembly of SUR subunits in K(ATP) channel complexes
    Wayland W L Cheng
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Channels (Austin) 2:34-8. 2008
  7. ncbi request reprint An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetes
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Diabetes 56:328-36. 2007
  8. ncbi request reprint Differential nucleotide regulation of KATP channels by SUR1 and SUR2A
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Mol Cell Cardiol 39:491-501. 2005
  9. pmc Functional clustering of mutations in the dimer interface of the nucleotide binding folds of the sulfonylurea receptor
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 283:30322-9. 2008
  10. ncbi request reprint A mutation in the TMD0-L0 region of sulfonylurea receptor-1 (L225P) causes permanent neonatal diabetes mellitus (PNDM)
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 56:1357-62. 2007

Research Grants

  1. SUR1 (ABCC8) AND ATRIAL KATP CHANNELS
    Colin G Nichols; Fiscal Year: 2011
  2. Rectification & Block of Ion Channel Currents
    Colin Nichols; Fiscal Year: 2006
  3. ATP-SENSITIVE POTASSIUM CHANNELS IN THE HEART
    Colin Nichols; Fiscal Year: 2005
  4. Metabolism-excitation coupling in the heart
    Colin Nichols; Fiscal Year: 2005
  5. Electrical Control of Insulin Secretion
    Colin Nichols; Fiscal Year: 2007
  6. RECTIFICATION AND BLOCK OF ION CHANNEL CURRENTS
    Colin G Nichols; Fiscal Year: 2011
  7. Electrical Control of Insulin Secretion
    Colin G Nichols; Fiscal Year: 2010
  8. ATP-SENSITIVE POTASSIUM CHANNELS IN THE HEART
    Colin G Nichols; Fiscal Year: 2010
  9. RECTIFICATION AND BLOCK OF ION CHANNEL CURRENTS
    Colin G Nichols; Fiscal Year: 2010
  10. SUR1 (ABCC8) AND ATRIAL KATP CHANNELS
    Colin G Nichols; Fiscal Year: 2010

Collaborators

Detail Information

Publications63

  1. pmc KATP channels and cardiovascular disease: suddenly a syndrome
    Colin G Nichols
    Center for the Investigation of Membrane Excitability Diseases and Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Circ Res 112:1059-72. 2013
    ..This realization of previously unconsidered consequences provides significant insight into the roles of the KATP channel in the cardiovascular system and suggests novel therapeutic possibilities...
  2. pmc The diabetic β-cell: hyperstimulated vs. hyperexcited
    C G Nichols
    Department of Cell Biology and Physiology and Center for Investigation of Membrane Excitability Diseases, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes Obes Metab 14:129-35. 2012
    ..On the other hand, chronic inexcitability in vivo leads to systemic diabetes and consequential β-cell death, even while [Ca(2+)](i) remains low...
  3. ncbi request reprint beta-cell hyperexcitability: from hyperinsulinism to diabetes
    C G Nichols
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes Obes Metab 9:81-8. 2007
    ..The causes of the overcompensation and diabetic susceptibility are poorly understood but may have broader implications for the progression of hyperinsulinism and type 2 diabetes in humans...
  4. pmc Congenital hyperinsulinism and glucose hypersensitivity in homozygous and heterozygous carriers of Kir6.2 (KCNJ11) mutation V290M mutation: K(ATP) channel inactivation mechanism and clinical management
    Karen J Loechner
    Department of Pediatrics, University of North Carolina School of Medicine, Chapel Hill, USA
    Diabetes 60:209-17. 2011
    ..In this study, we sought to identify the mechanistic basis of K(ATP)-induced HI in two probands and to characterize the clinical course...
  5. ncbi request reprint Regulation of KATP channel expression and activity by the SUR1 nucleotide binding fold 1
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Channels (Austin) 1:315-23. 2007
    ....
  6. ncbi request reprint Random assembly of SUR subunits in K(ATP) channel complexes
    Wayland W L Cheng
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Channels (Austin) 2:34-8. 2008
    ..The data demonstrate clearly that SUR1 and SUR2A subunits associate randomly, and suggest that heteromeric channels will occur in native tissues...
  7. ncbi request reprint An ATP-binding mutation (G334D) in KCNJ11 is associated with a sulfonylurea-insensitive form of developmental delay, epilepsy, and neonatal diabetes
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Diabetes 56:328-36. 2007
    ....
  8. ncbi request reprint Differential nucleotide regulation of KATP channels by SUR1 and SUR2A
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Mol Cell Cardiol 39:491-501. 2005
    ..SUR2A-containing channels, which may in turn contribute to physiological differences, observed at the tissue level, between pancreatic and cardiac K(ATP) channels...
  9. pmc Functional clustering of mutations in the dimer interface of the nucleotide binding folds of the sulfonylurea receptor
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 283:30322-9. 2008
    ..Overall, the data support the idea that SUR1 NBFs assemble as heterodimers and that this interaction is functionally critical...
  10. ncbi request reprint A mutation in the TMD0-L0 region of sulfonylurea receptor-1 (L225P) causes permanent neonatal diabetes mellitus (PNDM)
    Ricard Masia
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 56:1357-62. 2007
    ....
  11. pmc Diazoxide maintenance of myocyte volume and contractility during stress: evidence for a non-sarcolemmal K(ATP) channel location
    Angela D Sellitto
    Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St Louis, MO 63110, USA
    J Thorac Cardiovasc Surg 140:1153-9. 2010
    ..2 subunits in the atria. This study was performed to localize the mechanism of diazoxide by direct probing of sarcolemmal adenosine triphosphate-sensitive potassium channel current and by genetic deletion of channel subunits...
  12. ncbi request reprint Sarcolemmal K(ATP) channels: what do we really know?
    Thomas P Flagg
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Mol Cell Cardiol 39:61-70. 2005
    ..However, the true physiological determinants of sarcolemmal K(ATP) activity remain elusive, we still await full illumination of the role of the channel in the intact heart...
  13. pmc Differential structure of atrial and ventricular KATP: atrial KATP channels require SUR1
    Thomas P Flagg
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Circ Res 103:1458-65. 2008
    ....
  14. pmc Differential K(ATP) channel pharmacology in intact mouse heart
    Alexey V Glukhov
    Department of Biomedical Engineering, Washington University, St Louis, MO 63130, USA
    J Mol Cell Cardiol 48:152-60. 2010
    ....
  15. pmc Molecular biology of K(ATP) channels and implications for health and disease
    Alejandro Akrouh
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    IUBMB Life 61:971-8. 2009
    ..Continuing studies of channel physiology and pathology will bring new insights to the molecular basis of K(ATP) channel function, leading to a better understanding of the role that K(ATP) channels play in both health and disease...
  16. ncbi request reprint Functional characterization of a prokaryotic Kir channel
    Decha Enkvetchakul
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 279:47076-80. 2004
    ..1 is inhibited by extraliposomal acid (pKa approximately 6). This characterization of KirBac1.1 activity now paves the way for further correlation of structure and function in this model Kir channel...
  17. pmc Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance
    Dennis T Villareal
    Department of Medicine, Washington University School of Medicine, St Louis, Missouri, USA
    Diabetes 58:1869-78. 2009
    ..To avoid confounding effects of hyperglycemia, insulin secretion and action were studied in subjects with the variant who had normal glucose tolerance...
  18. pmc KirBac1.1: it's an inward rectifying potassium channel
    Wayland W L Cheng
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Gen Physiol 133:295-305. 2009
    ....
  19. pmc The role of the cytoplasmic pore in inward rectification of Kir2.1 channels
    Harley T Kurata
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Gen Physiol 130:145-55. 2007
    ..The data highlight a "long-pore" effect in Kir channels, and emphasize the importance of considering blocker permeation when assessing the effects of mutations on apparent blocker affinity...
  20. ncbi request reprint Gating dependence of inner pore access in inward rectifier K(+) channels
    L Revell Phillips
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, Saint Louis, MO 63110, USA
    Neuron 37:953-62. 2003
    ....
  21. pmc Molecular basis of inward rectification: polyamine interaction sites located by combined channel and ligand mutagenesis
    Harley T Kurata
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    J Gen Physiol 124:541-54. 2004
    ..The data provide a coherent explanation of classical strong rectification as the result of polyamine block in the inner cavity and selectivity filter...
  22. pmc Hyperinsulinism and diabetes: genetic dissection of beta cell metabolism-excitation coupling in mice
    Maria Sara Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Metab 10:442-53. 2009
    ....
  23. ncbi request reprint Alchemy in the soup: transforming metabolic signals to excitability
    Colin G Nichols
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Sci STKE 2007:pe59. 2007
    ..Recent studies have begun to delineate the roles of K(ATP) channels in multiple tissues and the far-reaching consequences of aberrant K(ATP) channel activity and disturbed sensing of cell metabolism...
  24. pmc DEND mutation in Kir6.2 (KCNJ11) reveals a flexible N-terminal region critical for ATP-sensing of the KATP channel
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Biophys J 95:4689-97. 2008
    ..The results reveal an important feature of the noncanonical ATP-sensing mechanism of K(ATP) channels...
  25. ncbi request reprint Transgenic overexpression of SUR1 in the heart suppresses sarcolemmal K(ATP)
    Thomas P Flagg
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 S Euclid Avenue, Box 8228, St Louis, MO 63110, USA
    J Mol Cell Cardiol 39:647-56. 2005
    ..2 suppresses the functional expression of K(ATP) from optimized dimeric SUR1-Kir6.2. Thus, the graded effect of SUR1 expression in the intact heart appears to demonstrate an in vivo requirement for 1:1 expression ratio of Kir6.2 and SURx...
  26. pmc Chronic antidiabetic sulfonylureas in vivo: reversible effects on mouse pancreatic beta-cells
    Maria Sara Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri, United States of America
    PLoS Med 5:e206. 2008
    ....
  27. doi request reprint Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K(ATP)-induced neonatal diabetes mellitus
    Maria Sara Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Cell Metab 9:140-51. 2009
    ....
  28. pmc Structural and functional determinants of conserved lipid interaction domains of inward rectifying Kir6.2 channels
    Catherine A Cukras
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Gen Physiol 119:581-91. 2002
    ..Together with systematic mutation of conserved charges, the results define critical determinants of a conserved domain that underlies phospholipid interaction in Kir channels...
  29. pmc Cardiac sarcolemmal K(ATP) channels: Latest twists in a questing tale!
    Haixia Zhang
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    J Mol Cell Cardiol 48:71-5. 2010
    ..This topical review focuses on these new findings and considers their implications...
  30. pmc Molecular mechanisms of EAST/SeSAME syndrome mutations in Kir4.1 (KCNJ10)
    Monica Sala-Rabanal
    Department of Cell Biology and Physiology, Washington University, St Louis, Missouri 63110, USA
    J Biol Chem 285:36040-8. 2010
    ..These results provide an explanation for the molecular defects that underlie the EAST/SeSAME syndrome...
  31. pmc Ligand-induced closure of inward rectifier Kir6.2 channels traps spermine in the pore
    L Revell Phillips
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    J Gen Physiol 122:795-804. 2003
    ..The results incontrovertibly demonstrate that spermine is trapped in channels that are closed by ATP, and implicate the M2 helix bundle crossing, or somewhere lower, as the probable location of the gate...
  32. pmc Blocker protection by short spermine analogs: refined mapping of the spermine binding site in a Kir channel
    Harley T Kurata
    Department of Cell Biology and Physiology, Center for Computational Biology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Biophys J 95:3827-39. 2008
    ..These data support the validity of a blocker protection approach for mapping polyamine-binding sites in a Kir pore, and confirm that spermine binds stably at a deep site in the inner cavity of strongly rectifying Kir channels...
  33. pmc The G53D mutation in Kir6.2 (KCNJ11) is associated with neonatal diabetes and motor dysfunction in adulthood that is improved with sulfonylurea therapy
    Joseph C Koster
    Washington University School of Medicine, Department of Cell Biology and Physiology, Box 8228, St Louis, MO 63110, USA
    J Clin Endocrinol Metab 93:1054-61. 2008
    ..2 mutations. There are two reports of improved neurological features in SU-treated DEND patients but no report of such improvement in adulthood...
  34. ncbi request reprint Diabetes and insulin secretion: the ATP-sensitive K+ channel (K ATP) connection
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 54:3065-72. 2005
    ....
  35. ncbi request reprint Arrhythmia susceptibility and premature death in transgenic mice overexpressing both SUR1 and Kir6.2[DeltaN30,K185Q] in the heart
    Thomas P Flagg
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 S Euclid Avenue, St Louis, MO 63110, USA
    Am J Physiol Heart Circ Physiol 293:H836-45. 2007
    ..2[DeltaN30,K185Q] in the myocardium specifically, the results highlight the critical differential activation of SUR1 versus SUR2A, and indicate that expression of hyperactive K(ATP) in the heart is likely to be proarrhythmic...
  36. ncbi request reprint Expression of ATP-insensitive KATP channels in pancreatic beta-cells underlies a spectrum of diabetic phenotypes
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Ave, St Louis, MO 63110, USA
    Diabetes 55:2957-64. 2006
    ..The data demonstrate that a range of phenotypes can be expected for a reduction in ATP sensitivity of beta-cell K(ATP) channels and provide models for the corollary neonatal diabetes in humans...
  37. ncbi request reprint C-terminal determinants of Kir4.2 channel expression
    WADE L PEARSON
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 S Euclid Ave, St Louis, Missouri, 63110, USA
    J Membr Biol 213:187-93. 2006
    ..These data demonstrate novel determinants of Kir4.2 channel expression...
  38. pmc The polyamine binding site in inward rectifier K+ channels
    Harley T Kurata
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Gen Physiol 127:467-80. 2006
    ..These data provide physical constraints on the spermine binding site, demonstrating that spermine stably binds at a deep site beyond the "rectification controller" residue, near the extracellular entrance to the channel...
  39. ncbi request reprint Role of the sarcolemmal adenosine triphosphate-sensitive potassium channel in hyperkalemic cardioplegia-induced myocyte swelling and reduced contractility
    Sandip M Prasad
    Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Ann Thorac Surg 81:148-53. 2006
    ..To examine whether the mitochondrial or sarcolemmal KATP channel might be involved, volume and contractility in isolated myocytes from wild-type mice and mice lacking the sarcolemmal KATP channel (Kir6.2-/-) were evaluated...
  40. ncbi request reprint KATP channels as molecular sensors of cellular metabolism
    Colin G Nichols
    Department of Cell Biology and Physiology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA
    Nature 440:470-6. 2006
    ..In parallel, the uncovering of disease-causing mutations of K(ATP) has led to an explanation of the molecular basis of disease and, in turn, to a better understanding of the structural basis of channel function...
  41. ncbi request reprint Direct modulation of Kir channel gating by membrane phosphatidylinositol 4,5-bisphosphate
    Decha Enkvetchakul
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 280:35785-8. 2005
    ..The data exclude the possibility of indirect modulation via cytoskeletal or other intermediary elements and establish a direct interaction of the channel with PIP2 in the membrane...
  42. pmc Control of inward rectifier K channel activity by lipid tethering of cytoplasmic domains
    Decha Enkvetchakul
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Gen Physiol 130:329-34. 2007
    ..This study establishes a critical role of the slide-helix in Kir channel gating, and directly demonstrates that physical interaction of soluble domains with the membrane can control ion channel activity...
  43. ncbi request reprint ATP and sulfonylurea sensitivity of mutant ATP-sensitive K+ channels in neonatal diabetes: implications for pharmacogenomic therapy
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 54:2645-54. 2005
    ..These results have important implications for the use of insulinotropic SU drugs as an alternative therapy to insulin injections...
  44. pmc Muscle KATP channels: recent insights to energy sensing and myoprotection
    Thomas P Flagg
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Physiol Rev 90:799-829. 2010
    ..As yet, few human diseases have been correlated with altered muscle K(ATP) activity, but genetically modified animals give important insights to likely pathological roles of aberrant channel activity in different muscle types...
  45. pmc Human FXYD2 G41R mutation responsible for renal hypomagnesemia behaves as an inward-rectifying cation channel
    Qun Sha
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Am J Physiol Renal Physiol 295:F91-9. 2008
    ....
  46. doi request reprint Ca2+-independent alterations in diastolic sarcomere length and relaxation kinetics in a mouse model of lipotoxic diabetic cardiomyopathy
    Thomas P Flagg
    Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St Louis, MO 63110, USA
    Circ Res 104:95-103. 2009
    ....
  47. ncbi request reprint ATP-sensitive K+ channel signaling in glucokinase-deficient diabetes
    Maria S Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 54:2925-31. 2005
    ..The results have implications for understanding and therapy of glucokinase-related diabetes...
  48. ncbi request reprint Diet-induced glucose intolerance in mice with decreased beta-cell ATP-sensitive K+ channels
    Maria S Remedi
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Diabetes 53:3159-67. 2004
    ....
  49. pmc Direct and specific activation of human inward rectifier K+ channels by membrane phosphatidylinositol 4,5-bisphosphate
    Nazzareno D'Avanzo
    Department of Cell Biology and Physiology and the Center for Investigation of Membrane Excitability Diseases, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 285:37129-32. 2010
    ..This raises the interesting hypothesis that PIP(2) activation of eukaryotic channels reflects an evolutionary adaptation of the channel to the appearance of PIP(2) in the eukaryotic cell membrane...
  50. pmc Impaired contractile function and calcium handling in hearts of cardiac-specific calcineurin b1-deficient mice
    Paul J Schaeffer
    Departments of Medicine, Washington University School of Medicine, Center for Cardiovascular Research, St Louis, Missouri, USA
    Am J Physiol Heart Circ Physiol 297:H1263-73. 2009
    ..These results define a novel mouse model of cardiac-specific Cn deficiency and demonstrate novel links between Cn signaling, postnatal growth of the heart, pathological ventricular remodeling, and excitation-contraction coupling...
  51. ncbi request reprint Remodeling of excitation-contraction coupling in transgenic mice expressing ATP-insensitive sarcolemmal KATP channels
    Thomas P Flagg
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA
    Am J Physiol Heart Circ Physiol 286:H1361-9. 2004
    ..Collectively, the data demonstrate that a compensatory increase in I(Ca) counteracts a mild activation of ATP-insensitive K(ATP) channels to maintain the action potential duration and elevate the inotropic state of TG hearts...
  52. pmc HIV protease inhibitors acutely impair glucose-stimulated insulin release
    Joseph C Koster
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Diabetes 52:1695-700. 2003
    ..Thus, together with peripheral insulin resistance, beta-cell dysfunction likely contributes to altered glucose homeostasis associated with highly active antiretroviral therapy...
  53. pmc Acute sulfonylurea therapy at disease onset can cause permanent remission of KATP-induced diabetes
    Maria Sara Remedi
    Department of Cell Biology and Physiology, and Center for the Investigation of Membrane Excitability Diseases, Washington University School of Medicine, St Louis, Missouri, USA
    Diabetes 60:2515-22. 2011
    ..Interestingly, K(ATP) mutations may underlie remitting-relapsing, transient, or permanent forms of the disease in different patients, but the reason for the different outcomes is unknown...
  54. pmc Differential roles of blocking ions in KirBac1.1 tetramer stability
    Shizhen Wang
    Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, St Louis, MO 63104, USA
    J Biol Chem 284:2854-60. 2009
    ..This stabilization was additive with the effect of Ba(2+), consistent with both ions simultaneously occupying the channel: Ba(2+) at the selectivity filter entrance and Cd(2+) coordinated by I138C side chains in the inner cavity...
  55. ncbi request reprint Activation of adenosine triphosphate-sensitive potassium channels by acyl coenzyme A esters involves multiple phosphatidylinositol 4,5-bisphosphate-interacting residues
    Jocelyn E Manning Fox
    Department of Pharmacology, University of Alberta, Edmonton, Alberta, Canada T6G 2H7
    Mol Endocrinol 18:679-86. 2004
    ..2. We propose a model in which these residues mediate both direct electrostatic interactions and allosteric modulations of open state stability...
  56. doi request reprint Role of sulfonylurea receptor type 1 subunits of ATP-sensitive potassium channels in myocardial ischemia/reperfusion injury
    John W Elrod
    Department of Medicine and Pathology, Albert Einstein College of Medicine, New York, NY, USA
    Circulation 117:1405-13. 2008
    ..The aim of this study, therefore, was to examine the role of SUR1 in myocardial infarction...
  57. ncbi request reprint Polyamine permeation and rectification of Kir4.1 channels
    Yuri V Kucheryavykh
    Department of Biochemistry, Universidad Central del Caribe, School of Medicine, Bayamon, Puerto Rico
    Channels (Austin) 1:172-8. 2007
    ..This leads us to propose that spermine 'punchthrough' may be significant in Kir4 channels, and that this may be a major contributor to the weak rectification observed under physiological conditions...
  58. ncbi request reprint Molecular basis of ion selectivity, block, and rectification of the inward rectifier Kir3.1/Kir3.4 K(+) channel
    Katherine M Dibb
    School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom
    J Biol Chem 278:49537-48. 2003
    ..The latter effect occurs because polyamines now permeate rather than block the channel, to the remarkable extent that large polyamine currents can be measured...
  59. pmc Critical role of gap junction coupled KATP channel activity for regulated insulin secretion
    Jonathan V Rocheleau
    Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee, USA
    PLoS Biol 4:e26. 2006
    ..Control via coupling lessens the effects of cell-cell variation and provides resistance to defects in excitability that would otherwise lead to a profound diabetic state, such as occurs in persistent neonatal diabetes mellitus...
  60. pmc A difference in inward rectification and polyamine block and permeation between the Kir2.1 and Kir3.1/Kir3.4 K+ channels
    Samy M Y Makary
    Division of Cardiovascular and Endocrine Sciences, University of Manchester, Manchester Incubator Building, Manchester M13 9XX, UK
    J Physiol 568:749-66. 2005
    ..This suggests that Kir3.1/Kir3.4 exhibits weaker inward rectification than Kir2.1 because of the difference in the balance of polyamine block and permeation of the two channels...
  61. pmc Disruption of sarcolemmal ATP-sensitive potassium channel activity impairs the cardiac response to systolic overload
    Xinli Hu
    Cardiovascular Division, Department of Medicine, Universityof Minnesota Medical School, Minneapolis, MN 55455, USA
    Circ Res 103:1009-17. 2008
    ..These data indicate that K(ATP) channels facilitate the cardiac response to stress by regulating PGC-1alpha and its target genes, at least partially through the FOXO1 pathway...
  62. doi request reprint Complex rectification of Müller cell Kir currents
    Yuriy V Kucheryavykh
    Department of Biochemistry, Universidad Central del Caribe, School of Medicine, Bayamon, PR
    Glia 56:775-90. 2008
    ..Increase in [K+]in would then lead to relief of "slow block," further promoting K+-influx...
  63. ncbi request reprint International Union of Pharmacology. LIV. Nomenclature and molecular relationships of inwardly rectifying potassium channels
    Yoshihiro Kubo
    Division of Biophysics and Neurobiology, Department of Molecular Physiology, National Institute for Physiological Sciences, Nishigoh naka 38, Myodaiji, Okazaki, Aichi 444 8585, Japan
    Pharmacol Rev 57:509-26. 2005

Research Grants46

  1. SUR1 (ABCC8) AND ATRIAL KATP CHANNELS
    Colin G Nichols; Fiscal Year: 2011
    ....
  2. Rectification & Block of Ion Channel Currents
    Colin Nichols; Fiscal Year: 2006
    ..The work will provide information that will form the background to the development of rational therapies for cardiac arrhythmias, epilepsy and other disorders of cell excitability through modulation of Kir channel activity. ..
  3. ATP-SENSITIVE POTASSIUM CHANNELS IN THE HEART
    Colin Nichols; Fiscal Year: 2005
    ..The work will provide information that will ultimately underlie the development of rational therapies for the treatment of cardiac ischemia and arrhythmias. ..
  4. Metabolism-excitation coupling in the heart
    Colin Nichols; Fiscal Year: 2005
    ..The work will provide information that will ultimately underlie the development of rational therapies for the treatment of cardiac ischemia and arrhythmias. ..
  5. Electrical Control of Insulin Secretion
    Colin Nichols; Fiscal Year: 2007
    ..The results of this project will provide mechanistic information that may impact the development of new treatment approaches to both diabetes and hyperinsulinemia. ..
  6. RECTIFICATION AND BLOCK OF ION CHANNEL CURRENTS
    Colin G Nichols; Fiscal Year: 2011
    ....
  7. Electrical Control of Insulin Secretion
    Colin G Nichols; Fiscal Year: 2010
    ..The project makes use of these animals to understand the disease process in a way that is impossible in humans, and thereby helps us to develop appropriate therapies to treat the disease. ..
  8. ATP-SENSITIVE POTASSIUM CHANNELS IN THE HEART
    Colin G Nichols; Fiscal Year: 2010
    ..The results of the proposed experiments will bring detailed insight to the structural and mechanistic basis of KATP channel function and the role of differential SUR isoforms in cardiac function. ..
  9. RECTIFICATION AND BLOCK OF ION CHANNEL CURRENTS
    Colin G Nichols; Fiscal Year: 2010
    ....
  10. SUR1 (ABCC8) AND ATRIAL KATP CHANNELS
    Colin G Nichols; Fiscal Year: 2010
    ....
  11. Electrical Control of Insulin Secretion
    Colin Nichols; Fiscal Year: 2009
    ..The results of this project will provide mechanistic information that may impact the development of new treatment approaches to both diabetes and hyperinsulinemia. ..
  12. SUR1 (ABCC8) AND ATRIAL KATP CHANNELS
    Colin Nichols; Fiscal Year: 2009
    ....
  13. ATP-SENSITIVE POTASSIUM CHANNELS IN THE HEART
    Colin Nichols; Fiscal Year: 1993
    ..The work should therefore lay the foundations for more rational therapies for myocardial diseases involving metabolic compromise...
  14. RECTIFICATION AND BLOCK OF ION CHANNEL CURRENTS
    Colin Nichols; Fiscal Year: 2002
    ..The work will therefore provide information that may ultimately underlie the development of rational therapies for the treatment of cardiac arrhythmias, epilepsy and other disorders of cell excitability. ..
  15. ATP-SENSITIVE POTASSIUM CHANNELS IN THE HEART
    Colin Nichols; Fiscal Year: 2000
    ..The work will provide information that will ultimately underlie the development of rational therapies for the treatment of cardiac ischemia and arrhythmias. ..