William A Catterall



  1. Levin M, Singh G, Zhang H, Uchida K, Kozel B, Stein P, et al. K(ATP) channel gain-of-function leads to increased myocardial L-type Ca(2+) current and contractility in Cantu syndrome. Proc Natl Acad Sci U S A. 2016;113:6773-8 pubmed publisher
    ..2 at Ser1928, suggesting enhanced protein kinase activity as a potential link between increased KATP current and CS cardiac pathophysiology. ..
  2. Gamal El Din T, Lenaeus M, Ramanadane K, Zheng N, Catterall W. Molecular dissection of multiphase inactivation of the bacterial sodium channel NaVAb. J Gen Physiol. 2018;: pubmed publisher
    ..These results have important implications for the sequence of conformational changes that lead to multiphase inactivation of NaVAb and other sodium channels. ..
  3. Catterall W, Zheng N. Deciphering voltage-gated Na(+) and Ca(2+) channels by studying prokaryotic ancestors. Trends Biochem Sci. 2015;40:526-34 pubmed publisher
    ..New insights into their voltage-dependent activation and inactivation, ion conductance, and ion selectivity provide realistic structural models for the function of these complex membrane proteins at the atomic level. ..
  4. Catterall W. Regulation of Cardiac Calcium Channels in the Fight-or-Flight Response. Curr Mol Pharmacol. 2015;8:12-21 pubmed
    ..2 channels serves as a signaling platform, mediating beat-to-beat physiological regulation of channel activity and up-regulation by β-adrenergic signaling in the fight-or-flight response. ..
  5. Nanou E, Catterall W. Calcium Channels, Synaptic Plasticity, and Neuropsychiatric Disease. Neuron. 2018;98:466-481 pubmed publisher
    ..This article reviews the molecular properties of calcium channels, considers their multiple roles in synaptic plasticity, and discusses their potential involvement in this wide range of neuropsychiatric diseases. ..
  6. Catterall W, Swanson T. Structural Basis for Pharmacology of Voltage-Gated Sodium and Calcium Channels. Mol Pharmacol. 2015;88:141-50 pubmed publisher
  7. Nanou E, Lee A, Catterall W. Control of Excitation/Inhibition Balance in a Hippocampal Circuit by Calcium Sensor Protein Regulation of Presynaptic Calcium Channels. J Neurosci. 2018;38:4430-4440 pubmed publisher
    ..Disruption of this regulation causes altered short-term plasticity and impaired balance of hippocampal excitatory to inhibitory circuits. ..
  8. Jiang D, Gamal El Din T, Ing C, Lu P, Pomès R, Zheng N, et al. Structural basis for gating pore current in periodic paralysis. Nature. 2018;557:590-594 pubmed publisher
    ..Our results reveal pathogenic mechanisms of periodic paralysis at the atomic level and suggest designs of drugs that may prevent ionic leak and provide symptomatic relief from hypokalaemic and normokalaemic periodic paralysis. ..
  9. Yu H, Yuan C, Westenbroek R, Catterall W. The AKAP Cypher/Zasp contributes to β-adrenergic/PKA stimulation of cardiac CaV1.2 calcium channels. J Gen Physiol. 2018;150:883-889 pubmed publisher
    ..2 channels. Other AKAPs may work cooperatively with Cypher/Zasp to give the full magnitude of β-adrenergic regulation of CaV1.2 channels observed in vivo. ..

More Information


  1. Fu Y, Westenbroek R, Scheuer T, Catterall W. Basal and β-adrenergic regulation of the cardiac calcium channel CaV1.2 requires phosphorylation of serine 1700. Proc Natl Acad Sci U S A. 2014;111:16598-603 pubmed publisher
    ..As a consequence, blocking PKA phosphorylation at this site impairs cardiovascular physiology in vivo, leading to reduced exercise capacity in the fight-or-flight response and development of cardiac hypertrophy. ..
  2. Nanou E, Sullivan J, Scheuer T, Catterall W. Calcium sensor regulation of the CaV2.1 Ca2+ channel contributes to short-term synaptic plasticity in hippocampal neurons. Proc Natl Acad Sci U S A. 2016;113:1062-7 pubmed publisher
    ..Evidently, regulation of CaV2.1 channels by CaS proteins is required for normal short-term plasticity and normal encoding of information in native hippocampal synapses. ..
  3. Nanou E, Scheuer T, Catterall W. Calcium sensor regulation of the CaV2.1 Ca2+ channel contributes to long-term potentiation and spatial learning. Proc Natl Acad Sci U S A. 2016;113:13209-13214 pubmed
    ..Thus, regulation of CaV2.1 channels by calcium sensor proteins is required for normal short-term synaptic plasticity, LTP, and spatial learning and memory in mice. ..
  4. Nanou E, Yan J, Whitehead N, Kim M, Froehner S, Scheuer T, et al. Altered short-term synaptic plasticity and reduced muscle strength in mice with impaired regulation of presynaptic CaV2.1 Ca2+ channels. Proc Natl Acad Sci U S A. 2016;113:1068-73 pubmed publisher
    ..1 channels by CaS proteins is essential for normal synaptic plasticity at the neuromuscular junction and for muscle strength, endurance, and motor coordination in mice in vivo. ..
  5. Yang L, Dai D, Yuan C, Westenbroek R, Yu H, West N, et al. Loss of ?-adrenergic-stimulated phosphorylation of CaV1.2 channels on Ser1700 leads to heart failure. Proc Natl Acad Sci U S A. 2016;113:E7976-E7985 pubmed
    ..Our results demonstrate that normal regulation of CaV1.2 channels by phosphorylation of Ser1700 in cardiomyocytes is required for cardiovascular homeostasis and normal physiological regulation in vivo. ..
  6. Catterall W. Forty Years of Sodium Channels: Structure, Function, Pharmacology, and Epilepsy. Neurochem Res. 2017;42:2495-2504 pubmed publisher
    ..It has been rewarding for me to use our developing knowledge of sodium channels to help understand the pathophysiology and to suggest potential therapeutic approaches for this devastating childhood disease. ..
  7. Catterall W. Voltage-gated calcium channels. Cold Spring Harb Perspect Biol. 2011;3:a003947 pubmed publisher
    ..This article presents the molecular relationships and physiological functions of these Ca(2+) channel proteins and provides information on their molecular, genetic, physiological, and pharmacological properties. ..
  8. Lenaeus M, Gamal El Din T, Ing C, Ramanadane K, Pomès R, Zheng N, et al. Structures of closed and open states of a voltage-gated sodium channel. Proc Natl Acad Sci U S A. 2017;114:E3051-E3060 pubmed publisher
    ..These two structures allow completion of a closed-open-inactivated conformational cycle in a single voltage-gated sodium channel and give insight into the structural basis for state-dependent binding of sodium channel-blocking drugs. ..
  9. Kaplan J, Stella N, Catterall W, Westenbroek R. Cannabidiol attenuates seizures and social deficits in a mouse model of Dravet syndrome. Proc Natl Acad Sci U S A. 2017;114:11229-11234 pubmed publisher
    ..Our study provides essential preclinical evidence needed to build a sound scientific basis for increased medicinal use of CBD. ..
  10. Catterall W. Finding Channels. J Biol Chem. 2015;290:28357-73 pubmed publisher
  11. Brunet S, Emrick M, Sadilek M, Scheuer T, Catterall W. Phosphorylation sites in the Hook domain of CaVβ subunits differentially modulate CaV1.2 channel function. J Mol Cell Cardiol. 2015;87:248-56 pubmed publisher
    ..These results reveal a new dimension of regulation of Ca(V)1.2 channels through phosphorylation of the Hook domains of their β subunits. ..
  12. Rubinstein M, Han S, Tai C, Westenbroek R, Hunker A, Scheuer T, et al. Dissecting the phenotypes of Dravet syndrome by gene deletion. Brain. 2015;138:2219-33 pubmed publisher
    ..These results show that multiple disease traits can arise from similar functional deficits in specific interneuron types. ..
  13. Rubinstein M, Westenbroek R, Yu F, Jones C, Scheuer T, Catterall W. Genetic background modulates impaired excitability of inhibitory neurons in a mouse model of Dravet syndrome. Neurobiol Dis. 2015;73:106-17 pubmed publisher
    ..This mild impairment of excitability of interneurons leads to a milder disease phenotype in 129/SvJ mice, similar to Genetic Epilepsy with Febrile Seizures Plus in humans. ..
  14. Tai C, Abe Y, Westenbroek R, Scheuer T, Catterall W. Impaired excitability of somatostatin- and parvalbumin-expressing cortical interneurons in a mouse model of Dravet syndrome. Proc Natl Acad Sci U S A. 2014;111:E3139-48 pubmed publisher
    ..These major functional deficits are likely to contribute synergistically to the pathophysiology of Dravet syndrome. ..