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Original Paper

Mechanistic contributions of residues in the M1 transmembrane domain of the nicotinic receptor to channel gating

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Pages 39-50 | Received 25 Apr 2003, Published online: 09 Jul 2009

References

  • Akabas, M. H. and Karlin, A., 1995, Identification of acetylcholine receptor channel-lining residues in the M1 segment of the alpha- subunit. Biochemistry, 34, 12496–12500.
  • Akk, G., Sine, S. and Auerbach, A., 1996, Binding sites contribute unequallyto the gating of mouse nicotinic alpha D200N acetylcho- line receptors. Journal of Physiology, 496, 185 –196.
  • Auerbach, A. and Akk, G., 1998, Desensitization of mouse Nicotinic Acetylcholine Receptor channels. A two-gate mechanism. Journal of General Physiology, 112, 181 –197.
  • Blanton, M. P. and Cohen, J. B., 1994, Identifying the lipid -protein interface of the Torpedo nicotinic acetylcholine receptor: second- arystructure implications. Biochemistry, 33, 2859–2872.
  • Bouzat, C., Bren, N. and Sine, S. M., 1994, Structural basis of the different gating kinetics of fetal and adult acetylcholine receptors. Neuron, 13, 1395 -1402.
  • Bouzat, C., Roccamo, A. M., Garbus, I. and Barrantes, F. J., 1998, Mutations at lipid-exposed residues of the acetylcholine receptor affect its gating kinetics. Molecluar Pharmacology, 54, 146 –153. Bouzat, C., Barrantes, F. and Sine, S., 2000, Nicotinic receptor fourth transmembrane domain: hydrogen bonding by conserved threonine contributes to channel gating kinetics. Journal of General Physiology, 115, 663 –672.
  • Bouzat, C., Gumilar, F., Esandi, M. C and Sine, S. M., 2002, Subunit- selective contribution to channel gating of the M4 domain of the nicotinic receptor. Biophysics Journal, 82, 1920 -1929.
  • Croxen, R., Hatton, C., Shelley, C., Brydson, M., Chauplannaz, G., Oosterhuis, H., Vincent, A., Newsom-Davis, J., Colquhoun, D. and Beeson, D., 2002, Recessive inheritance and variable penetrance of slow-channel congenital myasthenic syndromes. Neurology, 59, 162 –168.
  • Cymes, G. D., Grosman, C. and Auerbach, A., 2002, Structure of the transition state of gating in the acetylcholine receptor channel pore: a F-value analysis. Biochemistry, 41, 5548–5555.
  • De Rosa, M. J., Rayes, D., Spitzmaul, G. and Bouzat, C., 2002, Nicotinic receptor M3 transmembrane domain: position 8? contrib- utes to channel gating. Molecular Pharmacology, 62, 406 –414.
  • Engel, A. G., Ohno, K., Milone, M., Wang, H. L., Nakano, S., Bouzat, C., Pruitt, J. N., Hutchinson, D. O., Brengman, J. M., Bren, N., Sieb, J. P. and Sine, S. M., 1996, New mutations in acetylcholine receptor subunit genes reveal heterogeneityin the slow-channel congenital myasthenic syndrome. Human Molecular Genetics, 5, 1217 -1227.
  • Engel, A. G., Ohno, K. and Sine, S. M., 2002, The spectrum of congenital myasthenic syndromes. Molecular Neurobiology, 26, 347 –367.
  • England, P. M., Zhang, Y., Dougherty, D. A. and Lester, H. A., 1999, Backbone mutations in transmembrane domains of a ligand-gated ion channel: implications for the mechanism of gating. Cell, 96, 89 –98.
  • Grosman, C. and Auerbach, A., 2000a, Asymmetric and independent contribution of the second transmembrane segment 12? residues to diliganded gating of acetylcholine receptor channels: a single- channel studywith choline as the agonist. Journal of General Physiology, 115, 637 –651.
  • Grosman, C. and Auerbach, A., 2000b, Kinetic, mechanistic, and structural aspects of unliganded gating of acetylcholine receptor channels: a single-channel studyof second transmembrane segment 12? mutants. Journal of General Physiology, 115, 621 –635.
  • Grosman, C. and Auerbach, A., 2001, The dissociation of acetylcho- line from open nicotinic receptor channels. Proceedings of the National Academy of Sciences (USA), 98, 14102–14107.
  • Grosman, C., Salamone, F. N., Sine, S. M. and Auerbach, A., 2000a, The extracellular linker of muscle acetylcholine receptor channels is a gating control element. Journal of General Physiology, 116, 327 –340.
  • Grosman, C., Zhou, M. and Auerbach, A., 2000b, Mapping the conformational wave of acetylcholine receptor channel gating. Nature, 403, 773 –776.
  • Hamill, O. P., Marty, A., Neher, E., Sakmann, B. and Sigworth, F. J., 1981, Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches. Pflu¨ gers Archiv, 391, 85 –100.
  • Hatton, C. J., Shelley, C., Brydson, M., Beeson, D. and Colquhoun, D., 2003, Properties of the human muscle nicotinic receptor, and of the slow-channel myasthenic syndrome mutant (L221F, inferred from maximum likelihood fits. Journal of Physiology, 547, 729 –760.
  • Jackson, M. B., 1986, Kinetics of unliganded acetylcholine receptor channel gating. Biophysics Journal, 49, 663 –672.
  • Lo, D. C., Pinkham, J. L. and Stevens, C. F., 1991, Role of a key cysteine residue in the gating of the acetylcholine receptor. Neuron, 6, 31 –40.
  • Milone, M., Wang, H. L., Ohno, K., Fukudome, T., Pruitt, J. N., Bren, N., Sine, S. M. and Engel, A. G., 1997, Slow-channel myasthenic syndrome caused by enhanced activation, desensitization, and agonist binding affinityattributable to mutation in the M2 domain of the acetylcholine receptor alpha subunit. Journal of Neu- roscience, 17, 5651 -5665.
  • Ohno, K., Hutchinson, D. O., Milone, M., Brengman, J. M., Bouzat, C., Sine, S. M. and Engel, A. G., 1995, Congenital myasthenic syndrome caused by prolonged acetylcholine receptor channel openings due to a mutation in the M2 domain of the epsilon subunit. Proceedings of the National Academy of Sciences (USA), 92, 758 –762.
  • Ortells, M. O. and Lunt, G. G., 1995, Evolutionaryhistory of the ligand-gated ion-channel superfamilyof receptors. Trends in Neurosciences, 18, 121 –127.
  • Prince, R. J. and Sine, S. M., 1998, The ligand binding domains of the nicotinic acetylcholine receptor. In F. J. Barrantes, ed. The Nicotinic Acetylcholine Receptor: Current Views and Future Trends (Springer Verlag, Austin, TX), pp. 31 –59.
  • Qin, F., Auerbach, A. and Sachs, F., 1996, Estimating single-channel kinetic parameters from idealized patch-clamp data containing missed events. Biophysics Journal, 70, 264 –280.
  • Salamone, F. N., Zhou, M. and Auerbach, A., 1999, A re-examina- tion of adult mouse nicotinic acetylcholine receptor channel activation kinetics. Journal of Physiology, 516, 315 –330.
  • Sigworth, F. J. and Sine, S. M., 1987, Data transformations for improved displayand fitting of single-channel dwell time histo- grams. Biophysics Journal, 52, 1047 -1054.
  • Sine, S. M., 1993, Molecular dissection of subunit interfaces in the acetylcholine receptor: identification of residues that determine curare selectivity. Proceedings of the National Academy of Sciences (USA), 90, 9436–9440.
  • Sine, S. M., Ohno, K., Bouzat, C., Auerbach, A., Milone, M., Pruitt, J. N. and Engel, A. G., 1995, Mutation of the acetylcholine receptor alpha subunit causes a slow- channel myasthenic syndrome by enhancing agonist binding affinity. Neuron, 15, 229 –239.
  • Tamamizu, S., Todd, A. P. and McNamee, M. G., 1995, Mutations in the M1 region of the nicotinic acetylcholine receptor alter the sensitivityto inhibition by quinacrine. Cell Molecular Neurobiol- ogy, 15, 427 –438.
  • Unwin, N., 1995, Acetylcholine receptor channel imaged in the open state. Nature, 373, 37 –43.
  • Vicente-Agullo, F., Rovira, J. C., Sala, S., Sala, F., Rodriguez-Ferrer, C., Campos-Caro, A., Criado, M. and Ballesta, J. J., 2001, Multiple roles of the conserved keyresidue arginine 209 in neuronal nicotinic receptors. Biochemistry, 40, 8300 -8306.
  • Wang, H. L., Auerbach, A., Bren, N., Ohno, K., Engel, A. G. and Sine, S. M., 1997, Mutation in the M1 domain of the acetylcholine receptor alpha subunit decreases the rate of agonist dissociation. Journal of General Physiology, 109, 757 –766.
  • Zhang, H. and Karlin, A., 1997, Identification of acetylcholine receptor channel-lining residues in the M1 segment of the beta- subunit. Biochemistry, 36, 15856–15864.
  • Zhou, M., Engel, A. G. and Auerbach, A., 1999, Serum choline activates mutant acetylcholine receptors that cause slow channel congenital myasthenic syndromes. Proceedings of the National Academy of Sciences (USA), 96, 10466–10471.

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