Recent progress in sodium channel modulators for pain.
暂无分享,去创建一个
Sharan K Bagal | Brian E Marron | S. Bagal | R. I. Storer | N. Swain | Nigel A Swain | M. Chapman | R Ian Storer | Mark L Chapman | Rebecca Prime | B. Marron | Rebecca Prime
[1] William A. Catterall,et al. Crystal structure of a voltage-gated sodium channel in two potentially inactivated states , 2012, Nature.
[2] M. Noda,et al. Structure and function of sodium channel. , 1987, Journal of receptor research.
[3] W. Catterall,et al. THE CRYSTAL STRUCTURE OF A VOLTAGE-GATED SODIUM CHANNEL , 2011, Nature.
[4] S. Dib-Hajj,et al. Gain-of-function Nav1.8 mutations in painful neuropathy , 2012, Proceedings of the National Academy of Sciences.
[5] John N. Wood,et al. SCN9A Mutations in Paroxysmal Extreme Pain Disorder: Allelic Variants Underlie Distinct Channel Defects and Phenotypes , 2006, Neuron.
[6] F. Blaney,et al. Structural Determinants of Drugs Acting on the Nav1.8 Channel* , 2009, Journal of Biological Chemistry.
[7] S. Dib-Hajj,et al. Sodium channels in normal and pathological pain. , 2010, Annual review of neuroscience.
[8] O. McManus. HTS assays for developing the molecular pharmacology of ion channels. , 2014, Current opinion in pharmacology.
[9] S. Dib-Hajj,et al. Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy , 2012, Annals of neurology.
[10] T. Cummins,et al. Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navβ4 peptide‐mediated resurgent sodium currents , 2011, The Journal of physiology.
[11] S. Dib-Hajj,et al. Two tetrodotoxin‐resistant sodium channels in human dorsal root ganglion neurons , 1999, FEBS letters.
[12] Clare London,et al. Characterization of a new class of potent inhibitors of the voltage-gated sodium channel Nav1.7. , 2007, Biochemistry.
[13] E. Campbell,et al. Atomic structure of a voltage-dependent K+ channel in a lipid membrane-like environment , 2007, Nature.
[14] B. Ding,et al. Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia , 2004, Journal of Medical Genetics.
[15] X. Zhang,et al. Gain-of-function mutations in SCN11A cause familial episodic pain. , 2013, American journal of human genetics.
[16] D. Henze,et al. Recent Advances Toward Pain Therapeutics , 2011 .
[17] B. Bean,et al. Role of Tetrodotoxin-Resistant Na+ Current Slow Inactivation in Adaptation of Action Potential Firing in Small-Diameter Dorsal Root Ganglion Neurons , 2003, The Journal of Neuroscience.
[18] A. Gibbs,et al. Analysis of the Structural and Molecular Basis of Voltage-sensitive Sodium Channel Inhibition by the Spider Toxin Huwentoxin-IV (μ-TRTX-Hh2a) , 2013, The Journal of Biological Chemistry.
[19] C. Gibbons,et al. Diagnosis and Treatment of Pain in Small-fiber Neuropathy , 2011, Current pain and headache reports.
[20] Michael P. Eastwood,et al. Atomic-level simulation of current–voltage relationships in single-file ion channels , 2013, The Journal of general physiology.
[21] Kresten Lindorff-Larsen,et al. Principles of conduction and hydrophobic gating in K+ channels , 2010, Proceedings of the National Academy of Sciences.
[22] James O. Jackson,et al. The Tarantula Toxins ProTx-II and Huwentoxin-IV Differentially Interact with Human Nav1.7 Voltage Sensors to Inhibit Channel Activation and Inactivation , 2010, Molecular Pharmacology.
[23] M. Hayden,et al. Treatment of Nav1.7-mediated pain in inherited erythromelalgia using a novel sodium channel blocker , 2012, PAIN.
[24] Martin Koltzenburg,et al. ProTx-II, a Selective Inhibitor of NaV1.7 Sodium Channels, Blocks Action Potential Propagation in Nociceptors , 2008, Molecular Pharmacology.
[25] Peter Nürnberg,et al. A de novo gain-of-function mutation in SCN11A causes loss of pain perception , 2013, Nature Genetics.
[26] W. Catterall,et al. Molecular mechanisms of neurotoxin action on voltage-gated sodium channels. , 2000, Biochimie.
[27] J. Schulz,et al. Butyl 2-(4-[1.1'-biphenyl]-4-yl-1H-imidazol-2-yl)ethylcarbamate, a potent sodium channel blocker for the treatment of neuropathic pain. , 2007, Bioorganic & medicinal chemistry letters.
[28] W. Catterall,et al. Common molecular determinants of local anesthetic, antiarrhythmic, and anticonvulsant block of voltage-gated Na+ channels. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[29] Cecilia Farre,et al. Renaissance of ion channel research and drug discovery by patch clamp automation. , 2010, Future medicinal chemistry.
[30] J. Wood,et al. GTP up‐regulated persistent Na+ current and enhanced nociceptor excitability require NaV1.9 , 2008, The Journal of physiology.
[31] M. D. de Groot,et al. Voltage sensor interaction site for selective small molecule inhibitors of voltage-gated sodium channels , 2013, Proceedings of the National Academy of Sciences.
[32] S. Waxman,et al. The roles of sodium channels in nociception: Implications for mechanisms of pain , 2007, PAIN.
[33] Markéta Bébarová,et al. Advances in patch clamp technique: towards higher quality and quantity. , 2012, General physiology and biophysics.
[34] S. Dib-Hajj,et al. Gain-of-function mutations in sodium channel Na(v)1.9 in painful neuropathy. , 2014, Brain : a journal of neurology.
[35] Hussain Jafri,et al. An SCN9A channelopathy causes congenital inability to experience pain , 2006, Nature.
[36] H. Takeshima,et al. Expression of functional sodium channels from cloned cDNA , 1986, Nature.
[37] Jeffrey J Clare,et al. Targeting ion channels for drug discovery. , 2010, Discovery medicine.
[38] M. D. de Groot,et al. Subtype‐selective targeting of voltage‐gated sodium channels , 2009, British journal of pharmacology.
[39] G. King,et al. Discovery of a selective NaV1.7 inhibitor from centipede venom with analgesic efficacy exceeding morphine in rodent pain models , 2013, Proceedings of the National Academy of Sciences.
[40] M. Bednarek,et al. Potency optimization of Huwentoxin-IV on hNav 1.7: A neurotoxin TTX-S sodium-channel antagonist from the venom of the Chinese bird-eating spider Selenocosmia huwena , 2013, Peptides.
[41] Xiao Mei Zheng,et al. Identification of a potent, state-dependent inhibitor of Nav1.7 with oral efficacy in the formalin model of persistent pain. , 2011, Journal of medicinal chemistry.
[42] H. Fozzard,et al. A structural model of the tetrodotoxin and saxitoxin binding site of the Na+ channel. , 1994, Biophysical journal.
[43] A. Wickenden,et al. Sodium channel inhibitor drug discovery using automated high throughput electrophysiology platforms. , 2009, Combinatorial chemistry & high throughput screening.
[44] J. W. Wolfe,et al. Local anesthetic systemic toxicity: update on mechanisms and treatment , 2011, Current opinion in anaesthesiology.