Elimination of rapid potassium channel inactivation by phosphorylation of the inactivation gate
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[1] F Bezanilla,et al. Inactivation of the sodium channel. II. Gating current experiments , 1977, The Journal of general physiology.
[2] B. Hille. Ionic channels of excitable membranes , 2001 .
[3] E. R. Kandel,et al. Cyclic AMP-dependent protein kinase closes the serotonin-sensitive K+channels of Aplysia sensory neurones in cell-free membrane patches , 1985, Nature.
[4] K. F. Chan,et al. Autophosphorylation of rat brain Ca2+-activated and phospholipid-dependent protein kinase. , 1986, The Journal of biological chemistry.
[5] R. Eckert,et al. Voltage-activated calcium channels that must be phosphorylated to respond to membrane depolarization. , 1987, Proceedings of the National Academy of Sciences of the United States of America.
[6] R. Kass,et al. Regulation of a heart potassium channel by protein kinase A and C. , 1988, Science.
[7] P. Vassilev,et al. Identification of an intracellular peptide segment involved in sodium channel inactivation. , 1988, Science.
[8] E. Sigel,et al. Activation of protein kinase C differentially modulates neuronal Na+, Ca2+, and gamma-aminobutyrate type A channels. , 1988, Proceedings of the National Academy of Sciences of the United States of America.
[9] R. Nicoll,et al. The coupling of neurotransmitter receptors to ion channels in the brain. , 1988, Science.
[10] F. Conti,et al. Structural parts involved in activation and inactivation of the sodium channel , 1989, Nature.
[11] T. Tamaoki,et al. Calphostin C (UCN-1028C), a novel microbial compound, is a highly potent and specific inhibitor of protein kinase C. , 1989, Biochemical and biophysical research communications.
[12] Y. Nishizuka,et al. Modulation of ion channel activity: a key function of the protein kinase C enzyme family. , 1989, Pharmacological reviews.
[13] Modulation of a single ion channel by several different protein kinases. , 1990, Advances in second messenger and phosphoprotein research.
[14] R. Aldrich,et al. Voltage-dependent gating of Shaker A-type potassium channels in Drosophila muscle , 1990, The Journal of general physiology.
[15] T Hoshi,et al. Biophysical and molecular mechanisms of Shaker potassium channel inactivation , 1990, Science.
[16] F. Bezanilla,et al. Phosphorylation modulates potassium conductance and gating current of perfused giant axons of squid , 1990, The Journal of general physiology.
[17] Francisco Bezanilla,et al. Phosphorylation affects voltage gating of the delayed rectifier K+ channel by electrostatic interactions , 1990, Neuron.
[18] L. Salkoff,et al. K+ current diversity is produced by an extended gene family conserved in Drosophila and mouse. , 1990, Science.
[19] J. Woodgett,et al. Studies on the primary sequence requirements for PKC‐α, ‐β1 and ‐γ peptide substrates , 1990 .
[20] R. Aldrich,et al. Restoration of inactivation in mutants of Shaker potassium channels by a peptide derived from ShB , 1990, Science.
[21] Stefan H. Heinemann,et al. Regulation of fast inactivation of cloned mammalian IK(A) channels by cysteine oxidation , 1991, Nature.
[22] J. Ruppersberg,et al. Cloned neuronal Ik(A) channels reopen during recovery from inactivation , 1991, Nature.
[23] F. Sachs,et al. The ultrastructure of patch-clamped membranes: a study using high voltage electron microscopy , 1991, The Journal of cell biology.
[24] W. Catterall,et al. A phosphorylation site in the Na+ channel required for modulation by protein kinase C. , 1991, Science.
[25] R. MacKinnon. Determination of the subunit stoichiometry of a voltage-activated potassium channel , 1991, Nature.
[26] S. Demo,et al. The inactivation gate of the Shaker K+ channel behaves like an open-channel blocker , 1991, Neuron.
[27] L. Salkoff,et al. mShal, a subfamily of A-type K+ channel cloned from mammalian brain. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[28] N. Dascal,et al. Modulation of a Shaker potassium A‐channel by protein kinase C activation , 1991, FEBS letters.
[29] J. Ruppersberg,et al. Cloning and functional expression of a TEA‐sensitive A‐type potassium channel from rat brain , 1991, FEBS letters.
[30] I. Levitan,et al. Protein kinase activity closely associated with a reconstituted calcium-activated potassium channel. , 1991, Science.
[31] E. Krebs,et al. Consensus sequences as substrate specificity determinants for protein kinases and protein phosphatases. , 1991, The Journal of biological chemistry.
[32] W. Catterall,et al. Functional modulation of brain sodium channels by protein kinase C phosphorylation. , 1991, Science.
[33] B. Rudy,et al. Cloning of a human cDNA expressing a high voltage‐activating. Tea‐sensitive, type‐a K+ channel which maps to chromosome 1 band p21 , 1991, Journal of neuroscience research.
[34] Y. Jan,et al. Putative receptor for the cytoplasmic inactivation gate in the Shaker K+ channel , 1991, Nature.
[35] Leonard K. Kaczmarek,et al. The Neuron: Cell and Molecular Biology , 1991 .
[36] T. Abrams,et al. cAMP modulates multiple K+ currents, increasing spike duration and excitability in Aplysia sensory neurons. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[37] R. Huganir,et al. Phosphorylation of ligand‐gated ion channels: a possible mode of synaptic plasticity , 1992, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[38] R. North,et al. An amino acid mutation in a potassium channel that prevents inhibition by protein kinase C. , 1992, Science.
[39] A. L. Goldin,et al. Preparation of RNA for injection into Xenopus oocytes. , 1992, Methods in enzymology.
[40] Walter Stühmer,et al. Electrophysiological recording from Xenopus oocytes. , 1992, Methods in enzymology.
[41] E R Kandel,et al. Modulation of a transient K+ current in the pleural sensory neurons of Aplysia by serotonin and cAMP: implications for spike broadening. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[42] A L Goldin,et al. A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[43] J. Ruppersberg,et al. Characterization of a Shaw‐related potassium channel family in rat brain. , 1992, The EMBO journal.
[44] A. L. Goldin,et al. Amino acid residues required for fast Na(+)-channel inactivation: charge neutralizations and deletions in the III-IV linker. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[45] R. Aldrich,et al. Energetics of Shaker K channels block by inactivation peptides , 1993, The Journal of general physiology.
[46] W. Catterall,et al. Voltage-dependent potentiation of L-type Ca2+ channels due to phosphorylation by cAMP-dependent protein kinase , 1993, Nature.
[47] R. MacKinnon,et al. Functional stoichiometry of Shaker potassium channel inactivation. , 1993, Science.
[48] S. Slater,et al. Inhibition of protein kinase C by alcohols and anaesthetics , 1993, Nature.
[49] R. Aldrich,et al. Interactions of amino terminal domains of Shaker K channels with a pore blocking site studied with synthetic peptides , 1993, The Journal of general physiology.
[50] Ming Li,et al. Convergent regulation of sodium channels by protein kinase C and cAMP-dependent protein kinase. , 1993, Science.
[51] B. Rudy,et al. Differential expression of Shaw-related K+ channels in the rat central nervous system , 1994, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[52] R. Huganir,et al. Regulation of GABAA receptor function by protein kinase C phosphorylation , 1994, Neuron.
[53] R. Aldrich,et al. Shaker potassium channel gating. I: Transitions near the open state , 1994, The Journal of general physiology.
[54] R. Aldrich,et al. Regulation of Shaker K+ channel inactivation gating by the cAMP-dependent protein kinase , 1994, Neuron.