William A Catterall

Summary

Publications

  1. ncbi request reprint Sodium channels, inherited epilepsy, and antiepileptic drugs
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280 email
    Annu Rev Pharmacol Toxicol 54:317-38. 2014
  2. pmc Voltage-gated calcium channels
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    Cold Spring Harb Perspect Biol 3:a003947. 2011
  3. ncbi request reprint Differential regulation of CaV2.1 channels by calcium-binding protein 1 and visinin-like protein-2 requires N-terminal myristoylation
    Alexandra P Few
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    J Neurosci 25:7071-80. 2005
  4. ncbi request reprint Neuromodulation of Na+ channel slow inactivation via cAMP-dependent protein kinase and protein kinase C
    Yuan Chen
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    Neuron 49:409-20. 2006
  5. pmc Autistic-like behaviour in Scn1a+/- mice and rescue by enhanced GABA-mediated neurotransmission
    Sung Han
    Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, Washington 98195, USA
    Nature 489:385-90. 2012
  6. pmc Ca2+-independent activation of Ca2+/calmodulin-dependent protein kinase II bound to the C-terminal domain of CaV2.1 calcium channels
    Venkat G Magupalli
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Biol Chem 288:4637-48. 2013
  7. ncbi request reprint Reduced sodium current in GABAergic interneurons in a mouse model of severe myoclonic epilepsy in infancy
    Frank H Yu
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    Nat Neurosci 9:1142-9. 2006
  8. pmc Cardiomyocytes from AKAP7 knockout mice respond normally to adrenergic stimulation
    Brian W Jones
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 109:17099-104. 2012
  9. pmc Sequential formation of ion pairs during activation of a sodium channel voltage sensor
    Paul G DeCaen
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 106:22498-503. 2009
  10. ncbi request reprint Ion permeation through a voltage- sensitive gating pore in brain sodium channels having voltage sensor mutations
    Stanislav Sokolov
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Neuron 47:183-9. 2005

Collaborators

Detail Information

Publications80

  1. ncbi request reprint Sodium channels, inherited epilepsy, and antiepileptic drugs
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280 email
    Annu Rev Pharmacol Toxicol 54:317-38. 2014
    ..The recent advances in understanding of disease mechanisms and sodium channel structure promise to yield improved therapeutic approaches...
  2. pmc Voltage-gated calcium channels
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    Cold Spring Harb Perspect Biol 3:a003947. 2011
    ..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...
  3. ncbi request reprint Differential regulation of CaV2.1 channels by calcium-binding protein 1 and visinin-like protein-2 requires N-terminal myristoylation
    Alexandra P Few
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    J Neurosci 25:7071-80. 2005
    ..Differential, myristoylation-dependent regulation of presynaptic Ca2+ channels by nCaBPs may provide a flexible mechanism for diverse forms of short-term synaptic plasticity...
  4. ncbi request reprint Neuromodulation of Na+ channel slow inactivation via cAMP-dependent protein kinase and protein kinase C
    Yuan Chen
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    Neuron 49:409-20. 2006
    ..Modulation of slow inactivation by neurotransmitters acting through G protein-coupled receptors, PKA, and PKC is a flexible mechanism of cellular plasticity controlling the firing behavior of central neurons...
  5. pmc Autistic-like behaviour in Scn1a+/- mice and rescue by enhanced GABA-mediated neurotransmission
    Sung Han
    Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, Washington 98195, USA
    Nature 489:385-90. 2012
    ..These results demonstrate a critical role for Na(V)1.1 channels in neuropsychiatric functions and provide a potential therapeutic strategy for cognitive deficit and autism-spectrum behaviours in Dravet's syndrome...
  6. pmc Ca2+-independent activation of Ca2+/calmodulin-dependent protein kinase II bound to the C-terminal domain of CaV2.1 calcium channels
    Venkat G Magupalli
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Biol Chem 288:4637-48. 2013
    ....
  7. ncbi request reprint Reduced sodium current in GABAergic interneurons in a mouse model of severe myoclonic epilepsy in infancy
    Frank H Yu
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    Nat Neurosci 9:1142-9. 2006
    ..Our results indicate that reduced sodium currents in GABAergic inhibitory interneurons in Scn1a+/- heterozygotes may cause the hyperexcitability that leads to epilepsy in patients with SMEI...
  8. pmc Cardiomyocytes from AKAP7 knockout mice respond normally to adrenergic stimulation
    Brian W Jones
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 109:17099-104. 2012
    ..Immunoblot and RT-PCR revealed that only the long isoforms of AKAP7 were detectable in ventricular cardiomyocytes. The results indicate that AKAP7 is not required for regulation of Ca(2+) handling in mouse cardiomyocytes...
  9. pmc Sequential formation of ion pairs during activation of a sodium channel voltage sensor
    Paul G DeCaen
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 106:22498-503. 2009
    ..Our results directly demonstrate sequential ion pair formation that is an essential feature of the sliding helix model of voltage sensor function but is not compatible with the other widely discussed gating models...
  10. ncbi request reprint Ion permeation through a voltage- sensitive gating pore in brain sodium channels having voltage sensor mutations
    Stanislav Sokolov
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Neuron 47:183-9. 2005
    ..Paired substitutions of glutamine allow cation movement through the constriction when appropriately positioned by the gating movements of the S4 segment...
  11. pmc Autoinhibitory control of the CaV1.2 channel by its proteolytically processed distal C-terminal domain
    Joanne T Hulme
    Department of Pharmacology, Mailstop 357280, University of Washington, Seattle, 98195 7280, USA
    J Physiol 576:87-102. 2006
    ..2 channel function...
  12. ncbi request reprint International Union of Pharmacology. XLVIII. Nomenclature and structure-function relationships of voltage-gated calcium channels
    William A Catterall
    Department of Pharmacology, University of Washington, Mailstop 357280, Seattle, WA 98195 7280, USA
    Pharmacol Rev 57:411-25. 2005
    ..This article presents the molecular relationships and physiological functions of these calcium channel proteins and provides comprehensive information on their molecular, genetic, physiological, and pharmacological properties...
  13. pmc Functional roles of a C-terminal signaling complex of CaV1 channels and A-kinase anchoring protein 15 in brain neurons
    Misty R Marshall
    Department of Pharmacology, School of Medicine, University of Washington, Seattle, Washington 98195 7280, USA
    J Biol Chem 286:12627-39. 2011
    ..2 channels in vivo: increased functional expression, anchoring of AKAP15 and PKA, and initiation of excitation-transcription coupling...
  14. pmc The crystal structure of a voltage-gated sodium channel
    Jian Payandeh
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    Nature 475:353-8. 2011
    ..This structure provides the template for understanding electrical signalling in excitable cells and the actions of drugs used for pain, epilepsy and cardiac arrhythmia at the atomic level...
  15. ncbi request reprint Molecular determinants for modulation of persistent sodium current by G-protein betagamma subunits
    Massimo Mantegazza
    Department of Pharmacology, University of Washington School of Medicine, Seattle, Washington 98195 7280, USA
    J Neurosci 25:3341-9. 2005
    ....
  16. pmc Structural basis for Ca2+ selectivity of a voltage-gated calcium channel
    Lin Tang
    1 Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA 2 Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195, USA 3
    Nature 505:56-61. 2014
    ..The multi-ion selectivity filter of our CaVAb model establishes a structural framework for understanding the mechanisms of ion selectivity and conductance by vertebrate CaV channels. ..
  17. pmc Molecular determinants of CaV2.1 channel regulation by calcium-binding protein-1
    Alexandra P Few
    Department of Pharmacology, School of Medicine, University of Washington, Seattle, Washington 98195 7280, USA
    J Biol Chem 286:41917-23. 2011
    ..1 channels by CaBP1. These findings give insight into the molecular code by which CaS proteins differentially regulate Ca(V)2.1 channel function and provide diversity of form and function of short term synaptic plasticity...
  18. ncbi request reprint Mechanism of SNARE protein binding and regulation of Cav2 channels by phosphorylation of the synaptic protein interaction site
    Charles T Yokoyama
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Mol Cell Neurosci 28:1-17. 2005
    ..Our results support a bipartite model for the synprint site in which each SNARE-binding microdomain is controlled by a separate PKC and CaMKII phosphorylation site that regulates channel modulation by SNARE proteins...
  19. pmc Dopamine modulation of neuronal Na(+) channels requires binding of A kinase-anchoring protein 15 and PKA by a modified leucine zipper motif
    W Preston Few
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 104:5187-92. 2007
    ..Our results define the molecular mechanism by which G protein-coupled signaling pathways can rapidly and efficiently modulate neuronal excitability through local protein phosphorylation of Na(+) channels by specifically anchored PKA...
  20. pmc Modulation of CaV2.1 channels by Ca2+/calmodulin-dependent protein kinase II bound to the C-terminal domain
    Xin Jiang
    Department of Pharmacology, University of Washington, Mailstop 357280, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 105:341-6. 2008
    ..This regulatory mechanism would be important in presynaptic nerve terminals, where Ca(V)2.1 channels initiate synaptic transmission and CaMKII has noncatalytic effects on presynaptic plasticity...
  21. ncbi request reprint Inhibition of sodium channel gating by trapping the domain II voltage sensor with protoxin II
    Stanislav Sokolov
    University of Washington School of Medicine Department of Pharmacology, Box 357280, Seattle, WA 98195 7280, USA
    Mol Pharmacol 73:1020-8. 2008
    ....
  22. pmc Phosphorylation sites required for regulation of cardiac calcium channels in the fight-or-flight response
    Ying Fu
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280
    Proc Natl Acad Sci U S A 110:19621-6. 2013
    ..Disruption of phosphorylation at those sites leads to impaired cardiac function in vivo, as indicated by reduced exercise capacity and cardiac hypertrophy. ..
  23. ncbi request reprint Modulation of CaV2.1 channels by the neuronal calcium-binding protein visinin-like protein-2
    Nathan J Lautermilch
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Neurosci 25:7062-70. 2005
    ..Differential regulation of CaV2.1 channels by CaM, VILIP-2, CaBP1, and other neurospecific Ca2+-binding proteins is a potentially important determinant of Ca2+ entry in neurotransmission...
  24. pmc Structural basis for gating charge movement in the voltage sensor of a sodium channel
    Vladimir Yarov-Yarovoy
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 109:E93-102. 2012
    ..We confirmed the validity of these structural models by comparing with a high-resolution structure of a NaChBac homolog and showing predicted molecular interactions of hydrophobic residues in the S4 segment in disulfide-locking studies...
  25. pmc Gating charge interactions with the S1 segment during activation of a Na+ channel voltage sensor
    Paul G DeCaen
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 108:18825-30. 2011
    ....
  26. pmc Sympathetic stimulation of adult cardiomyocytes requires association of AKAP5 with a subpopulation of L-type calcium channels
    C Blake Nichols
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Circ Res 107:747-56. 2010
    ..We hypothesized that scaffolding of cAMP signaling complexes by AKAP5 is required for efficient sympathetic stimulation of calcium transients...
  27. pmc Cooperative regulation of Ca(v)1.2 channels by intracellular Mg(2+), the proximal C-terminal EF-hand, and the distal C-terminal domain
    Sylvain Brunet
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    J Gen Physiol 134:81-94. 2009
    ..2 channels by Mg(i), the proximal C-terminal EF-hand, and the DCT, and suggest that conformational changes that regulate VDI are propagated from the DCT through the proximal C-terminal EF-hand to the channel-gating mechanism...
  28. ncbi request reprint Helical motion of an S4 voltage sensor revealed by gating pore currents
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, USA
    Channels (Austin) 4:75-7. 2010
    ..Their results provide strong support for a sliding helix or helical screw mechanism of gating charge movement...
  29. pmc Structure and function of the voltage sensor of sodium channels probed by a beta-scorpion toxin
    Sandrine Cestele
    Department of Pharmacology, University of Washington, Seattle, 98195 7280, USA
    J Biol Chem 281:21332-44. 2006
    ....
  30. pmc Beta-adrenergic-regulated phosphorylation of the skeletal muscle Ca(V)1.1 channel in the fight-or-flight response
    Michelle A Emrick
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 107:18712-7. 2010
    ....
  31. pmc Specific deletion of NaV1.1 sodium channels in inhibitory interneurons causes seizures and premature death in a mouse model of Dravet syndrome
    Christine S Cheah
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 109:14646-51. 2012
    ..Evidently, loss of Na(V)1.1 channels in forebrain GABAergic neurons is both necessary and sufficient to cause epilepsy and premature death in DS...
  32. pmc Mapping the interaction site for a β-scorpion toxin in the pore module of domain III of voltage-gated Na(+) channels
    Joel Z Zhang
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    J Biol Chem 287:30719-28. 2012
    ..Binding of α- and β-scorpion toxins to two distinct, pseudo-symmetrically organized receptor sites on Na(V) channels acts synergistically to modify channel gating and paralyze prey...
  33. pmc Structure-function map of the receptor site for β-scorpion toxins in domain II of voltage-gated sodium channels
    Joel Z Zhang
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Biol Chem 286:33641-51. 2011
    ..These results provide new molecular insights into the voltage sensor-trapping model of toxin action and further define the molecular requirements for the development of antagonists that can prevent or reverse toxicity of scorpion toxins...
  34. pmc Depolarization-activated gating pore current conducted by mutant sodium channels in potassium-sensitive normokalemic periodic paralysis
    Stanislav Sokolov
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 105:19980-5. 2008
    ....
  35. ncbi request reprint Reduced sodium current in Purkinje neurons from Nav1.1 mutant mice: implications for ataxia in severe myoclonic epilepsy in infancy
    Franck Kalume
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Neurosci 27:11065-74. 2007
    ..Loss of these channels in Purkinje neurons of mutant mice and SMEI patients may be sufficient to cause their ataxia and related functional deficits...
  36. ncbi request reprint Gating pore current in an inherited ion channelopathy
    Stanislav Sokolov
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    Nature 446:76-8. 2007
    ..A survey of other ion channelopathies reveals numerous examples of mutations that would be expected to cause gating pore current, raising the possibility of a broader impact of gating pore current in ion channelopathies...
  37. pmc Localization of sodium channel subtypes in mouse ventricular myocytes using quantitative immunocytochemistry
    Ruth E Westenbroek
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA Electronic address
    J Mol Cell Cardiol 64:69-78. 2013
    ....
  38. ncbi request reprint Distinct subcellular localization of different sodium channel alpha and beta subunits in single ventricular myocytes from mouse heart
    Sebastian K G Maier
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Circulation 109:1421-7. 2004
    ..Voltage-gated sodium channels composed of pore-forming alpha and auxiliary beta subunits are responsible for the rising phase of the action potential in cardiac muscle, but their localizations have not yet been clearly defined...
  39. pmc Na(V)1.1 channels are critical for intercellular communication in the suprachiasmatic nucleus and for normal circadian rhythms
    Sung Han
    Program in Neurobiology and Behavior, University of Washington, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 109:E368-77. 2012
    ..Heterozygous loss of Na(V)1.1 channels is the underlying cause for severe myoclonic epilepsy of infancy; the circadian deficits that we report may contribute to sleep disorders in severe myoclonic epilepsy of infancy patients...
  40. pmc Reversed voltage-dependent gating of a bacterial sodium channel with proline substitutions in the S6 transmembrane segment
    Yong Zhao
    Department of Pharmacology, Mail Stop 357280, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 101:17873-8. 2004
    ..Native hyperpolarization-activated gating of hyperpolarization- and cyclic nucleotide-gated (HCN) channels in animals and KAT channels in plants may involve bending at analogous S6 amino acid residues...
  41. pmc Molecular determinants of Ca(2+)/calmodulin-dependent regulation of Ca(v)2.1 channels
    Amy Lee
    Department of Pharmacology, University of Washington School of Medicine, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 100:16059-64. 2003
    ..This multifaceted mechanism allows positive regulation of Cav2.1 in response to local Ca2+ increases (CDF) and negative regulation during more global Ca2+ increases (CDI)...
  42. pmc Phosphorylation of serine 1928 in the distal C-terminal domain of cardiac CaV1.2 channels during beta1-adrenergic regulation
    Joanne T Hulme
    Department of Pharmacology, University of Washington, Mailstop 357280, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 103:16574-9. 2006
    ..Our results correlate phosphorylation of S1928 with beta1-adrenergic functional up-regulation of cardiac calcium channels in the presence of BAPTA in intact ventricular myocytes...
  43. ncbi request reprint A gating hinge in Na+ channels; a molecular switch for electrical signaling
    Yong Zhao
    Department of Pharmacology, Box 357280, University of Washington, Seattle, WA 98105, USA
    Neuron 41:859-65. 2004
    ..Our results fit a model in which concerted bending at glycine 219 in the S6 segments of NaChBac serves as a gating hinge. This gating motion may be conserved in most members of this large ion channel protein family...
  44. pmc Disulfide locking a sodium channel voltage sensor reveals ion pair formation during activation
    Paul G DeCaen
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 105:15142-7. 2008
    ..Our results demonstrate voltage-dependent formation of an ion pair during activation of the voltage sensor in real time and suggest that this interaction catalyzes S4 movement and channel activation...
  45. pmc Functional properties and differential neuromodulation of Na(v)1.6 channels
    Yuan Chen
    Department of Pharmacology, Mailstop 357280, University of Washington, Seattle, WA 98195, USA
    Mol Cell Neurosci 38:607-15. 2008
    ..The unique properties of Na(V)1.6 channels, together with the resurgent currents that they conduct in neurons, make these channels well-suited to provide the driving force for sustained repetitive firing, a crucial property of neurons...
  46. ncbi request reprint Specific modulation of Na+ channels in hippocampal neurons by protein kinase C epsilon
    Yuan Chen
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Neurosci 25:507-13. 2005
    ..Overall, our data from four experimental approaches indicate that anchored PKCepsilon is the isozyme responsible for PKC-mediated reduction of peak Na+ currents in mouse hippocampal neurons...
  47. pmc Sites of proteolytic processing and noncovalent association of the distal C-terminal domain of CaV1.1 channels in skeletal muscle
    Joanne T Hulme
    Department of Pharmacology, University of Washington, Mailstop 357280, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 102:5274-9. 2005
    ..1 channels in skeletal muscle cells...
  48. pmc Ion permeation and block of the gating pore in the voltage sensor of NaV1.4 channels with hypokalemic periodic paralysis mutations
    Stanislav Sokolov
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    J Gen Physiol 136:225-36. 2010
    ..4 gating pores, define voltage-dependent and voltage-independent block by divalent and trivalent cations, respectively, and provide initial support for the concept that guanidine-based gating pore blockers could be therapeutically useful...
  49. ncbi request reprint Molecular mechanism of convergent regulation of brain Na(+) channels by protein kinase C and protein kinase A anchored to AKAP-15
    Angela R Cantrell
    Department of Pharmacology, University of Washington, Seattle 98195 7280, USA
    Mol Cell Neurosci 21:63-80. 2002
    ..This convergent regulation provides a novel mechanism by which information from multiple signaling pathways may be integrated at the cellular level in the hippocampus and throughout the central nervous system...
  50. pmc A gating charge interaction required for late slow inactivation of the bacterial sodium channel NavAb
    Tamer M Gamal El-Din
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    J Gen Physiol 142:181-90. 2013
    ....
  51. pmc Synergistic GABA-enhancing therapy against seizures in a mouse model of Dravet syndrome
    John C Oakley
    Department of Neurology, University of Washington, Seattle, Washington, USA
    J Pharmacol Exp Ther 345:215-24. 2013
    ..The synergistic actions of clonazepam and tiagabine gave enhanced seizure protection and reduced toxicity, suggesting that combination therapy may be well tolerated and effective for seizures in DS...
  52. pmc Sudden unexpected death in a mouse model of Dravet syndrome
    Franck Kalume
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Clin Invest 123:1798-808. 2013
    ..These results have important implications for prevention of SUDEP in DS patients...
  53. pmc Calcium channels and short-term synaptic plasticity
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Biol Chem 288:10742-9. 2013
    ..Emerging evidence reviewed here points to this mode of regulation of Ca(V)2.1 channels as a major contributor to short-term synaptic plasticity of neurotransmission and its diversity among synapses...
  54. pmc Beta-adrenergic regulation requires direct anchoring of PKA to cardiac CaV1.2 channels via a leucine zipper interaction with A kinase-anchoring protein 15
    Joanne T Hulme
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 100:13093-8. 2003
    ....
  55. pmc Asynchronous Ca2+ current conducted by voltage-gated Ca2+ (CaV)-2.1 and CaV2.2 channels and its implications for asynchronous neurotransmitter release
    Alexandra P Few
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 109:E452-60. 2012
    ....
  56. ncbi request reprint International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels
    William A Catterall
    Department of Pharmacology, University of Washington, Mailstop 357280, Seattle, WA 98195 7280
    Pharmacol Rev 57:397-409. 2005
    ..This article presents the molecular relationships and physiological roles of these sodium channel proteins and provides comprehensive information on their molecular, genetic, physiological, and pharmacological properties...
  57. pmc NaV1.1 channels and epilepsy
    William A Catterall
    University of Washington, Department of Pharmacology, SJ 30, Seattle, WA 98195 7280, USA
    J Physiol 588:1849-59. 2010
    ..1 channels, in which mild impairment predisposes to febrile seizures, intermediate impairment leads to GEFS+ epilepsy, and severe or complete loss of function leads to the intractable seizures and comorbidities of SMEI...
  58. pmc Modulation of CaV1.2 channels by Mg2+ acting at an EF-hand motif in the COOH-terminal domain
    Sylvain Brunet
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    J Gen Physiol 126:311-23. 2005
    ..2 channels, and reveal a potentially important role of Mg(i) binding to the COOH-terminal EF-hand in regulating Ca(2+) influx in physiological and pathophysiological states...
  59. pmc Mapping the receptor site for alpha-scorpion toxins on a Na+ channel voltage sensor
    Jinti Wang
    Department of Pharmacology, School of Medicine, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 108:15426-31. 2011
    ..This model defines the structure of the resting state of a voltage sensor of Na(+) channels and reveals its mode of interaction with a gating modifier toxin...
  60. ncbi request reprint Ca(v)1.3 channels produce persistent calcium sparklets, but Ca(v)1.2 channels are responsible for sparklets in mouse arterial smooth muscle
    Manuel F Navedo
    Department of Physiology and Biophysics, University of Washington, Box 357290, Seattle, WA 98195, USA
    Am J Physiol Heart Circ Physiol 293:H1359-70. 2007
    ..We conclude that although Ca(v)1.3 channels can produce Ca(2+) sparklets, Ca(v)1.2 channels underlie I(Ca), Ca(2+) sparklets, and hence dihydropyridine-sensitive Ca(2+) influx in mouse arterial myocytes...
  61. pmc Temperature- and age-dependent seizures in a mouse model of severe myoclonic epilepsy in infancy
    John C Oakley
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 106:3994-9. 2009
    ....
  62. pmc Deletion of the distal C terminus of CaV1.2 channels leads to loss of beta-adrenergic regulation and heart failure in vivo
    Ying Fu
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Biol Chem 286:12617-26. 2011
    ..2 channels is required in vivo for normal vascular regulation, cell-surface expression of CaV1.2 channels in cardiac myocytes, and β-adrenergic stimulation of L-type Ca2+ currents in the heart...
  63. ncbi request reprint Mice lacking sodium channel beta1 subunits display defects in neuronal excitability, sodium channel expression, and nodal architecture
    Chunling Chen
    Department of Pharmacology, The University of Michigan, Ann Arbor, Michigan 48109 0632, USA
    J Neurosci 24:4030-42. 2004
    ....
  64. ncbi request reprint Voltage-gated ion channels and gating modifier toxins
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Toxicon 49:124-41. 2007
    ..The voltage-sensor trapping mechanism may be a common mode of action for polypeptide gating modifier toxins acting on all of the voltage-gated ion channels...
  65. pmc Crystal structure of a voltage-gated sodium channel in two potentially inactivated states
    Jian Payandeh
    Department of Pharmacology, University of Washington, Seattle, Washington 98195, USA
    Nature 486:135-9. 2012
    ..These potential inactivated-state structures provide new insights into Na(V) channel gating and novel avenues to drug development and therapy for a range of debilitating Na(V) channelopathies...
  66. ncbi request reprint Regulation of Na(v)1.2 channels by brain-derived neurotrophic factor, TrkB, and associated Fyn kinase
    Misol Ahn
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Neurosci 27:11533-42. 2007
    ..These results indicate that Fyn kinase is associated with sodium channels in brain neurons and can modulate Na(V)1.2 channels by tyrosine phosphorylation after activation of TrkB/p75 signaling by BDNF...
  67. ncbi request reprint Sodium channel beta4, a new disulfide-linked auxiliary subunit with similarity to beta2
    Frank H Yu
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Neurosci 23:7577-85. 2003
    ..This novel, disulfide-linked beta subunit is likely to affect both protein-protein interactions and physiological function of multiple sodium channel alpha subunits...
  68. ncbi request reprint Sites and molecular mechanisms of modulation of Na(v)1.2 channels by Fyn tyrosine kinase
    Daniel Beacham
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Neurosci 27:11543-51. 2007
    ..2 channels are expressed in brain neurons...
  69. doi request reprint Calcium channel regulation and presynaptic plasticity
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Neuron 59:882-901. 2008
    ..We propose that presynaptic Ca(2+) channels serve as the regulatory node in a dynamic, multilayered signaling network that exerts short-term control of neurotransmission in response to synaptic activity...
  70. ncbi request reprint Regulation of cardiac ion channels by signaling complexes: role of modified leucine zipper motifs
    Joanne T Hulme
    Department of Pharmacology, University of Washington, Box 357280, Seattle, WA 98195 7280, USA
    J Mol Cell Cardiol 37:625-31. 2004
    ..This review will summarize the recent advances made on the regulation of cardiac ion channels by these macromolecular signaling complexes in the normal and diseased heart...
  71. pmc Convergent regulation of skeletal muscle Ca2+ channels by dystrophin, the actin cytoskeleton, and cAMP-dependent protein kinase
    Barry D Johnson
    Department of Pharmacology, University of Washington, Box 357280, Seattle, WA 98195 7280, USA
    Proc Natl Acad Sci U S A 102:4191-6. 2005
    ....
  72. pmc Signaling complexes of voltage-gated sodium and calcium channels
    William A Catterall
    Department of Pharmacology, Box 357280, University of Washington, Seattle, WA 98195 7280, United States
    Neurosci Lett 486:107-16. 2010
    ..These localized signaling complexes are essential for normal function and regulation of electrical excitability, synaptic transmission, and excitation-contraction coupling...
  73. pmc An unexpected requirement for brain-type sodium channels for control of heart rate in the mouse sinoatrial node
    Sebastian K G Maier
    Department of Pharmacology, University of Washington, Seattle, WA 98195, USA
    Proc Natl Acad Sci U S A 100:3507-12. 2003
    ..Our results demonstrate an important contribution of TTX-sensitive brain-type Na(+) channels to SA nodal automaticity in mouse heart and suggest that they may also contribute to SA nodal function and dysfunction in human heart...
  74. pmc Ion channel voltage sensors: structure, function, and pathophysiology
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, WA 98195 7280, USA
    Neuron 67:915-28. 2010
    ..The emerging structural model for voltage sensor function opens the way to development of a new generation of ion-channel drugs that act on voltage sensors rather than blocking the pore...
  75. pmc Molecular mechanism of calcium channel regulation in the fight-or-flight response
    Matthew D Fuller
    Department of Pharmacology, University of Washington, Box 357280, Seattle, WA 98195 7280, USA
    Sci Signal 3:ra70. 2010
    ..Our results define a conceptual framework for Ca(V)1.2 channel regulation and identify sites of phosphorylation that regulate channel activity...
  76. pmc Inherited neuronal ion channelopathies: new windows on complex neurological diseases
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Neurosci 28:11768-77. 2008
    ..Overall, these experiments indicate that imbalance in the activity of excitatory and inhibitory neurons is an important underlying cause of these diseases...
  77. pmc Insights into pathophysiology and therapy from a mouse model of Dravet syndrome
    John C Oakley
    Department of Pharmacology Neurology, University of Washington, Seattle, Washington 98195 7280, USA
    Epilepsia 52:59-61. 2011
    ..A mechanistic understanding of hyperexcitability, seizures, and comorbidities such as ataxia has led to novel strategies for treatment...
  78. ncbi request reprint Functional role of a C-terminal Gbetagamma-binding domain of Ca(v)2.2 channels
    Bin Li
    Department of Pharmacology, University of Washington, Box 357280, Seattle, WA 98195 7280, USA
    Mol Pharmacol 66:761-9. 2004
    ..C-terminal binding of Gbetagamma may influence the physiological responsiveness of Ca(2+) channels to low-level G protein activation...
  79. ncbi request reprint Overview of molecular relationships in the voltage-gated ion channel superfamily
    Frank H Yu
    Department of Pharmacology, Campus Box 357280, University of Washington, Seattle, WA 98195 7280, USA
    Pharmacol Rev 57:387-95. 2005
  80. ncbi request reprint Regulation of sodium and calcium channels by signaling complexes
    William A Catterall
    Department of Pharmacology, University of Washington, Seattle, Washington 98195 7280, USA
    J Recept Signal Transduct Res 26:577-98. 2006
    ..These localized signaling complexes are essential for normal function and regulation of electrical excitability, synaptic transmission, and excitation-contraction coupling...