Colin Nichols


Affiliation: Washington University School of Medicine
Country: USA


  1. Wang S, Lee S, Maksaev G, Fang X, Zuo C, Nichols C. Potassium channel selectivity filter dynamics revealed by single-molecule FRET. Nat Chem Biol. 2019;15:377-383 pubmed publisher
    ..This suggests differential ion selectivity in constrained versus dilated states, potentially providing a structural basis for this anomalous mole fraction effect. ..
  2. Nichols C, Lee S. Polyamines and potassium channels: A 25-year romance. J Biol Chem. 2018;293:18779-18788 pubmed publisher
    ..This Minireview will summarize current understanding of the relevance and molecular mechanisms of polyamine block and offer some ideas to try to help resolve the fundamental issue of the voltage dependence of polyamine block. ..
  3. Cheng W, D Avanzo N, Doyle D, Nichols C. Dual-mode phospholipid regulation of human inward rectifying potassium channels. Biophys J. 2011;100:620-628 pubmed publisher
    ..In conclusion, we utilized purified proteins in defined lipid membranes to quantitatively determine the phospholipid requirements for human Kir channel activity. ..
  4. Silva J, Cooper P, Nichols C. Modeling K,ATP--dependent excitability in pancreatic islets. Biophys J. 2014;107:2016-26 pubmed publisher
    ..The study highlights the importance of parameterization of detailed models of ?-cell excitability and suggests future experiments that will lead to improved characterization of ?-cell excitability and the control of insulin secretion. ..
  5. Nichols C, Remedi M. The diabetic ?-cell: hyperstimulated vs. hyperexcited. Diabetes Obes Metab. 2012;14 Suppl 3:129-35 pubmed publisher
    ..On the other hand, chronic inexcitability in vivo leads to systemic diabetes and consequential ?-cell death, even while [Ca(2+)](i) remains low. ..
  6. Cooper P, Sala Rabanal M, Lee S, Nichols C. Differential mechanisms of Cantú syndrome-associated gain of function mutations in the ABCC9 (SUR2) subunit of the KATP channel. J Gen Physiol. 2015;146:527-40 pubmed publisher
    ..The results indicate that these three CS mutations all lead to overactive K(ATP) channels, but at least two mechanisms underlie the observed gain of function: decreased ATP inhibition and enhanced MgADP activation. ..
  7. Nichols C. Adenosine Triphosphate-Sensitive Potassium Currents in Heart Disease and Cardioprotection. Card Electrophysiol Clin. 2016;8:323-35 pubmed publisher
  8. McClenaghan C, Hanson A, Sala Rabanal M, Roessler H, Josifova D, Grange D, et al. Cantu syndrome-associated SUR2 (ABCC9) mutations in distinct structural domains result in KATP channel gain-of-function by differential mechanisms. J Biol Chem. 2018;293:2041-2052 pubmed publisher
    ..They help link CS genotypes to phenotypes and shed light on the underlying molecular mechanisms, including consequences for inhibitory drug sensitivity, insights that may inform the development of therapeutic approaches to manage CS. ..
  9. Borschel W, Wang S, Lee S, Nichols C. Control of Kir channel gating by cytoplasmic domain interface interactions. J Gen Physiol. 2017;149:561-576 pubmed publisher
    ..2 partially rescues inactivating mutants from the phenotype. These results indicate that the stability of the intersubunit CD-I is a major determinant of the inactivation process in Kir6.2 and may control gating in other Kir channels. ..

More Information


  1. Cooper P, McClenaghan C, Chen X, Stary Weinzinger A, Nichols C. Conserved functional consequences of disease-associated mutations in the slide helix of Kir6.1 and Kir6.2 subunits of the ATP-sensitive potassium channel. J Biol Chem. 2017;292:17387-17398 pubmed publisher
    ..This raises the possibility that, at least for some CS mutations, sulfonylurea therapy may not prove to be successful and highlights the need for detailed pharmacogenomic analyses of CS mutations. ..
  2. Nichols C, Singh G, Grange D. KATP channels and cardiovascular disease: suddenly a syndrome. Circ Res. 2013;112:1059-72 pubmed publisher
    ..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. ..
  3. Levin M, Zhang H, Uchida K, Grange D, Singh G, Nichols C. Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome. Heart Rhythm. 2015;12:2316-24 pubmed publisher
    ..The primary electrophysiologic consequence of cardiac KATP GOF is on the conduction system, particularly the AV node, resulting in conduction abnormalities in CS patients who carry KATP GOF mutations. ..
  4. Lee S, Ren F, Zangerl Plessl E, Heyman S, Stary Weinzinger A, Yuan P, et al. Structural basis of control of inward rectifier Kir2 channel gating by bulk anionic phospholipids. J Gen Physiol. 2016;148:227-37 pubmed publisher
  5. Wang S, Borschel W, Heyman S, Hsu P, Nichols C. Conformational changes at cytoplasmic intersubunit interactions control Kir channel gating. J Biol Chem. 2017;292:10087-10096 pubmed publisher
    ..We conclude that the removal of stabilizing CD-I salt bridges results in a collapsed state of the Kir domain. ..
  6. Wang S, Brettmann J, Nichols C. Studying Structural Dynamics of Potassium Channels by Single-Molecule FRET. Methods Mol Biol. 2018;1684:163-180 pubmed publisher