Pharmacological activity and NMR solution structure of the leech peptide HSTX-I.

[1]  S. Dib-Hajj,et al.  A 49-residue sequence motif in the C terminus of Nav1.9 regulates trafficking of the channel to the plasma membrane , 2019, The Journal of Biological Chemistry.

[2]  David L. Bennett,et al.  The Role of Voltage-Gated Sodium Channels in Pain Signaling. , 2019, Physiological reviews.

[3]  Zuqin Yang,et al.  Naja atra venom peptide reduces pain by selectively blocking the voltage-gated sodium channel Nav1.8 , 2019, The Journal of Biological Chemistry.

[4]  D. Craik,et al.  Where cone snails and spiders meet: design of small cyclic sodium‐channel inhibitors , 2018, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[5]  D. A. Armstrong,et al.  Prediction of disulfide dihedral angles using chemical shifts† †Electronic supplementary information (ESI) available. See DOI: 10.1039/c8sc01423j , 2018, Chemical science.

[6]  Min Zhang,et al.  Novel Sodium Channel Inhibitor From Leeches , 2018, Front. Pharmacol..

[7]  S. Dib-Hajj,et al.  Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability , 2017, The Journal of clinical investigation.

[8]  I. Vetter,et al.  NaV1.7 as a pain target - From gene to pharmacology. , 2017, Pharmacology & therapeutics.

[9]  Jingze Liu,et al.  A Novel Toxin from Haplopelma lividum Selectively Inhibits the NaV1.8 Channel and Possesses Potent Analgesic Efficacy , 2016, Toxins.

[10]  Alex Gutteridge,et al.  Pharmacological reversal of a pain phenotype in iPSC-derived sensory neurons and patients with inherited erythromelalgia , 2016, Science Translational Medicine.

[11]  D. Craik,et al.  Development of a O-Conotoxin Analogue with Improved Lipid Membrane Interactions and Potency for the Analgesic Sodium Channel NaV1.8 , 2016 .

[12]  I. Vetter,et al.  The thermal probe test: A novel behavioral assay to quantify thermal paw withdrawal thresholds in mice , 2016, Temperature.

[13]  J. Deuis.  Using toxins to elucidate the role of voltage-gated sodium channels in pain , 2016 .

[14]  S. Dib-Hajj,et al.  Human Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons. , 2015, Journal of neurophysiology.

[15]  Peter J Bungay,et al.  A novel selective and orally bioavailable Nav1.8 channel blocker, PF‐01247324, attenuates nociception and sensory neuron excitability , 2015, British journal of pharmacology.

[16]  S. Heinemann,et al.  Heterologous expression of NaV1.9 chimeras in various cell systems , 2015, Pflügers Archiv - European Journal of Physiology.

[17]  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.

[18]  G. Cao,et al.  A Tarantula-Venom Peptide Antagonizes the TRPA1 Nociceptor Ion Channel by Binding to the S1–S4 Gating Domain , 2014, Current Biology.

[19]  A. Bax,et al.  Protein backbone and sidechain torsion angles predicted from NMR chemical shifts using artificial neural networks , 2013, Journal of Biomolecular NMR.

[20]  I. Vetter,et al.  Isolation, characterization and total regioselective synthesis of the novel μO-conotoxin MfVIA from Conus magnificus that targets voltage-gated sodium channels. , 2012, Biochemical pharmacology.

[21]  John Gilchrist,et al.  Animal Toxins Can Alter the Function of Nav1.8 and Nav1.9 , 2012, Toxins.

[22]  Muriel Amsalem,et al.  Nav1.9 Channel Contributes to Mechanical and Heat Pain Hypersensitivity Induced by Subacute and Chronic Inflammation , 2011, PloS one.

[23]  R. D'Hooge,et al.  Exploring the role of nociceptor-specific sodium channels in pain transmission using Nav1.8 and Nav1.9 knockout mice , 2010, Behavioural Brain Research.

[24]  Michael Zhao,et al.  TRPA1 mediates formalin-induced pain , 2007, Proceedings of the National Academy of Sciences.

[25]  R. Carr,et al.  Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures , 2007, Nature.

[26]  Matthew S. Johnson,et al.  A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat , 2007, Proceedings of the National Academy of Sciences.

[27]  Jack Snoeyink,et al.  Nucleic Acids Research Advance Access published April 22, 2007 MolProbity: all-atom contacts and structure validation for proteins and nucleic acids , 2007 .

[28]  D. Yoshikami,et al.  Synthetic muO-conotoxin MrVIB blocks TTX-resistant sodium channel NaV1.8 and has a long-lasting analgesic activity. , 2006, Biochemistry.

[29]  A. M. Rush,et al.  A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[30]  M. Lazdunski,et al.  Four Novel Tarantula Toxins as Selective Modulators of Voltage-Gated Sodium Channel Subtypes , 2006, Molecular Pharmacology.

[31]  Miron Livny,et al.  RECOORD: A recalculated coordinate database of 500+ proteins from the PDB using restraints from the BioMagResBank , 2005, Proteins.

[32]  S. Dib-Hajj,et al.  The Presence and Role of the Tetrodotoxin-Resistant Sodium Channel Nav1.9 (NaN) in Nociceptive Primary Afferent Neurons , 2002, The Journal of Neuroscience.

[33]  S. Dib-Hajj,et al.  NaN/Nav1.9: a sodium channel with unique properties , 2002, Trends in Neurosciences.

[34]  S G Waxman,et al.  A Novel Persistent Tetrodotoxin-Resistant Sodium Current In SNS-Null And Wild-Type Small Primary Sensory Neurons , 1999, The Journal of Neuroscience.

[35]  R J Read,et al.  Crystallography & NMR system: A new software suite for macromolecular structure determination. , 1998, Acta crystallographica. Section D, Biological crystallography.

[36]  R. Hodges,et al.  1H, 13C and 15N random coil NMR chemical shifts of the common amino acids. I. Investigations of nearest-neighbor effects , 1995, Journal of biomolecular NMR.

[37]  S. Abram.  A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat , 2008 .

[38]  B D Sykes,et al.  1H, 13C and 15N random coil NMR chemical shifts of the common amino acids. I. Investigations of nearest-neighbor effects , 1995, Journal of biomolecular NMR.

[39]  H. Fozzard,et al.  A structural model of the tetrodotoxin and saxitoxin binding site of the Na+ channel. , 1994, Biophysical journal.