Lengths of the C-terminus and interconnecting loops impact stability of spider-derived gating modifier toxins, Toxins, vol.9, pp.248-263, 2017. ,
The concise guide to pharmacology 2017/18: Voltage-gated ion channels, British Journal of Pharmacology, vol.174, pp.160-194, 2017. ,
Painful and painless channelopathies, Lancet Neurology, vol.13, issue.14, pp.70024-70033, 2014. ,
Mapping the interaction site for the tarantula toxin hainantoxin-IV (?-TRTX-Hn2a) in the voltage sensor module of domain II of voltagegated sodium channels, Peptides, vol.68, pp.148-156, 2015. ,
Sodium channel Na(v)1.6 is localized at nodes of ranvier, dendrites, and synapses, Proceedings of the National Academy of Sciences of the United States of America, vol.97, pp.5616-5620, 2000. ,
Dexamethasone influence on morphine-induced analgesia in outbred Swiss and inbred DBA/2J and C57BL/6 mice, Progress in Neuro-Psychopharmacology & Biological Psychiatry, vol.18, pp.779-792, 1994. ,
Identification and characterization of ProTx-III [mu-TRTX-Tp1a], a new voltage-gated sodium channel inhibitor from venom of the tarantula Thrixopelma pruriens, Molecular Pharmacology, vol.88, pp.291-303, 2015. ,
Modulatory features of the novel spider toxin mu-TRTX-Df1a isolated from the venom of the spider Davus fasciatus, British Journal of Pharmacology, vol.174, pp.2528-2544, 2017. ,
Sodium channels and pain: From toxins to therapies, British Journal of Pharmacology, vol.175, pp.2138-2157, 2018. ,
International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels, Pharmacological Reviews, vol.57, pp.397-409, 2005. ,
Niclosamide inhibits oxaliplatin neurotoxicity while improving colorectal cancer therapeutic response. Molecular Cancer Therapeutics, vol.16, pp.300-311, 2017. ,
URL : https://hal.archives-ouvertes.fr/cea-02121953
Intrathecal miR-96 inhibits Na V 1.3 expression and alleviates neuropathic pain in rat following chronic construction injury, Neurochemical Research, vol.39, pp.76-83, 2014. ,
Pathophysiological implication of CaV3.1 T-type Ca2+ channels in trigeminal neuropathic pain, Proceedings of the National Academy of Sciences of the United States of America, vol.113, pp.2270-2275, 2016. ,
An evaluation of 30 clinical drugs against the comprehensive in vitro proarrhythmia assay (CiPA) proposed ion channel panel, Journal Of Pharmacological And Toxicological Methods, vol.81, pp.251-262, 2016. ,
Analgesic effects of GpTx-1, PF-04856264 and CNV1014802 in a mouse model of Na V 1.7-mediated pain, Toxins, vol.8, pp.78-87, 2016. ,
The Na V 1.7 sodium channel: From molecule to man, Nature Reviews. Neuroscience, vol.14, pp.49-62, 2013. ,
Insensitivity to pain induced by a potent selective closed-state Na V 1.7 inhibitor, Scientific Reports, vol.7, 2017. ,
Global Na V 1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain, PLoS ONE, vol.9, 2014. ,
The Na V 1.7 channel subtype as an antinociceptive target for spider toxins in adult dorsal root ganglia neurons, Frontiers in Pharmacology, vol.9, 2018. ,
Direct evidence for high affinity blockade of Na V 1.6 channel subtype by huwentoxin-IV spider peptide, using multiscale functional approaches, Neuropharmacology, vol.133, pp.404-414, 2018. ,
Tetrodotoxin for moderate to severe cancerrelated pain: A multicentre, randomized, double-blind, placebocontrolled, parallel-design trial, Pain Research & Management, pp.1-7, 2017. ,
The IUPHAR/BPS Guide to pharmacology in 2018: Updates and expansion to encompass the new guide to immunopharmacology, Nucleic Acids Research, vol.46, pp.1091-1106, 2018. ,
Sodium channels and venom peptide pharmacology, Advances in Pharmacology, vol.79, pp.67-116, 2017. ,
Effects of membrane polarization and ischaemia on the excitability properties of human motor axons, Brain, vol.123, pp.2542-2551, 2000. ,
Animal research: Reporting in vivo experiments: The ARRIVE guidelines, British Journal of Pharmacology, vol.160, pp.1577-1579, 2010. ,
Isolation, synthesis and characterization of omega-TRTX-Cc1a, a novel tarantula venom peptide that selectively targets L-type Cav channels, Biochemical Pharmacology, vol.89, pp.276-286, 2014. ,
Rational engineering defines a molecular switch that is essential for activity of spider-venom peptides against the analgesics target Na V 1.7, Molecular Pharmacology, vol.88, pp.1002-1010, 2015. ,
Spider-venom peptides that target voltage-gated sodium channels: pharmacological tools and potential therapeutic leads, Toxicon, vol.60, pp.478-491, 2012. ,
Assessment of nerve excitability in toxic and metabolic neuropathies, Journal of the Peripheral Nervous System, vol.13, pp.7-26, 2008. ,
Voltage-gated sodium channels: Structure, function, pharmacology, and clinical indications, Journal of Medicinal Chemistry, vol.58, pp.7093-7118, 2015. ,
Structure-activity relationships of hainantoxin-IV and structure determination of active and inactive sodium channel blockers, The Journal of Biological Chemistry, vol.279, pp.37734-37740, 2004. ,
A positively charged surface patch is important for hainantoxin-IV binding to voltage-gated sodium channels, Journal of Peptide Science, vol.18, pp.643-649, 2012. ,
Structure and function of hainantoxin-III, a selective antagonist of neuronal tetrodotoxin-sensitive voltage-gated sodium channels isolated from the Chinese bird spider Ornithoctonus hainana, The Journal of Biological Chemistry, vol.288, pp.20392-20403, 2013. ,
Isolation and characterization of hainantoxin-IV, a novel antagonist of tetrodotoxin-sensitive sodium channels from the Chinese bird spider Selenocosmia hainana, Cellular and Molecular Life Sciences, vol.60, pp.972-978, 2003. ,
Analysis of the structural and molecular basis of voltage-sensitive sodium channel inhibition by the spider toxin huwentoxin-IV (mu-TRTX-Hh2a), The Journal of Biological Chemistry, vol.288, pp.22707-22720, 2013. ,
Sex differences in pain and pain inhibition: Multiple explanations of a controversial phenomenon, Nature Reviews. Neuroscience, vol.13, pp.859-866, 2012. ,
Pharmacological characterization of potent and selective Na V 1.7 inhibitors engineered from Chilobrachys jingzhao tarantula venom peptide JzTx-V, PLoS ONE, vol.13, 2018. ,
Engineering potent and selective analogues of GpTx-1, a tarantula venom peptide antagonist of the Na V 1.7 sodium channel, Journal of Medicinal Chemistry, vol.58, pp.2299-2314, 2015. ,
Single residue substitutions that confer voltagegated sodium ion channel subtype selectivity in the Na V 1.7 inhibitory peptide GpTx-1, Journal of Medicinal Chemistry, vol.59, pp.2704-2717, 2016. ,
Selective spider toxins reveal a role for the Na V 1.1 channel in mechanical pain, Nature, vol.534, pp.494-499, 2016. ,
Function and solution structure of huwentoxin-IV, a potent neuronal tetrodotoxin (TTX)-sensitive sodium channel antagonist from Chinese bird spider Selenocosmia huwena, The Journal of Biological Chemistry, vol.277, pp.47564-47571, 2002. ,
Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons, The Journal of Physiology, vol.579, pp.1-14, 2007. ,
Spider-venom peptides as therapeutics, Toxins, vol.2, pp.2851-2871, 2010. ,
Involvement of voltagegated calcium channels in inflammation and inflammatory pain, Biological & Pharmaceutical Bulletin, vol.41, pp.1127-1134, 2018. ,
Engineering highly potent and selective microproteins against Na V 1.7 sodium channel for treatment of pain, 2016. ,
, The Journal of Biological Chemistry, vol.291, pp.13974-13986
Na V 1.7 as a pain target-From gene to pharmacology, Pharmacology & Therapeutics, vol.172, pp.73-100, 2017. ,
Regulating excitability of peripheral afferents: Emerging ion channel targets, Nature Neuroscience, vol.17, pp.153-163, 2014. ,
Tarantula huwentoxin-IV inhibits neuronal sodium channels by binding to receptor site 4 and trapping the domain II voltage sensor in the closed configuration, The Journal of Biological Chemistry, vol.283, pp.27300-27313, 2008. ,
The tarantula toxins ProTx-II and huwentoxin-IV differentially interact with human Na V 1.7 voltage sensors to inhibit channel activation and inactivation, Molecular Pharmacology, vol.78, pp.1124-1134, 2010. ,
From identification to functional characterization of cyriotoxin-1a, an antinociceptive toxin from the spider Cyriopagopus schioedtei, Br J Pharmacol, vol.176, pp.1298-1314, 2019. ,
, Supporting information for: From identification to functional characterization of cyriotoxin-1a, an antinociceptive toxin from Cyriopagopus schioedtei spider
, UMR CNRS/Université Paris-Sud 9197, Université Paris-Saclay, F-91198 Gif sur Yvette, France. ? Sanofi R & D, Integrated Drug Discovery -Synthetic Molecular Design, vol.6, p.8
, each consisting of a 50-ms step to the voltage of the peak current of the current-voltage relationship for each channel, were applied at 10 Hz (50-ms interpulse interval). The current signal was sampled at 10 kHz. Currents were leak-subtracted based on the estimate of current evoked during the -10 mV step at the start of the voltage pulse protocol. Pre-and postcompound sodium current amplitudes were measured automatically from the leak-subtracted traces by the IonWorks software through averaging a 10 ms current during the initial holding period at -90 mV (baseline current) and subtracting this from the peak of the current response for each of the eight voltage steps, pre-and post-compound responses were evoked by a voltage train as follows: after a 10-sec period holding at -120 mV, ten pulses
Venom fractions and sub-fractions, as well as CyrTx-1a, were diluted in the extracellular medium supplemented with bovine serum albumin (0.1%), to give the final concentrations indicated in the text. The times of incubation varied between ~2 and ~7 min to achieve steady-state effects. The experiments were carried out at room temperature (20-22°C). The hNa V -overexpressing HEK-293 cells were maintained at a holding potential of either -90 mV (hNa V 1.5) or -100 mV (other hNa V channel subtypes). Currents were elicited at a frequency of 0.2 Hz (at least 4.78-s interpulse interval) by 20-ms test-pulses to -20 mV (hNa V 1.1, 1.2, 1.4, and 1.7), -10 mV (hNa V 1.3), -40 mV (hNa V 1.5), -15 mV (hNa V 1.6) or +10 mV (hNa V 1.8), preceded by 200-ms (hNa V 1.5) or 40-ms (hNa V 1.7) pulses to -120 mV, or not (hNa V 1.1, 1.2, 1.3, 1.4 and 1.6). The hCa V -overexpressing CHO cells were maintained at a holding potential of -50 mV (hCa V 1.2) or -100 mV (hCa V 3.1 and 3.2), and currents were elicited at a frequency of 0.05 Hz (at least 19.5-s interpulse interval) by 200-ms test-pulses to +0 mV (hCa V 1.2) or by 500-ms test-pulses to -20 mV (hCa V 3.1 and 3.2). The hK V 11.1-overexpressing CHO cells were maintained at a holding potential of -80 mV, Filters were set to a pre-scan seal resistance of 40 M?, pre-scan hNa V 1.7 current amplitude of 200 pA, and post-scan seal resistance of 40 M?. Cells that did not meet these criteria were discarded from the measurements. Dividing the post-scan current amplitude by the respective pre-scan current amplitude for each well assessed the degree of inhibition of the hNa V 1.7 current. Secondary screening for hit confirmation, as well as rapid selectivity check, were also performed on an automated patch-clamp system, the QPatch HTX (Sophion Bioscience, Denmark) recording currents in whole-cell configuration, allowing both signal acquisition and data analyses, vol.4, pp.2312-2321, 2018. ,
Transforming TRP channel drug discovery using mediumthroughput electrophysiological assays, J. Biomol. Screen, vol.19, pp.468-477, 2014. ,
Direct evidence for high affinity blockade of NaV1.6 channel subtype by huwentoxin-IV spider peptide, using multiscale functional approaches, Neuropharmacology, vol.133, pp.404-414, 2018. ,
Cellular HTS assays for pharmacological characterization of Na(V)1.7 modulators, Assay Drug Dev. Technol, vol.6, pp.167-179, 2008. ,