| Nav1.7 is essential for nociceptor action potentials in the mouse in a manner independent of endogenous opioids. | Nav1.7 is essential for nociceptor action potentials in the mouse in a manner independent of endogenous opioids.
Deng L, Dourado M, Reese RM, Huang K, Shields SD, Stark KL, Maksymetz J, Lin H, Kaminker JS, Jung M, Foreman O, Tao J, Ngu H, Joseph V, Roose-Girma M, Tam L, Lardell S, Orrhult LS, Karila P, Allard J, Hackos DH. | 10/26/2023 |
| Nav1.7 gain-of-function mutation I228M triggers age-dependent nociceptive insensitivity and C-LTMR dysregulation. | Na(v)1.7 gain-of-function mutation I228M triggers age-dependent nociceptive insensitivity and C-LTMR dysregulation.
Wimalasena NK, Taub DG, Shim J, Hakim S, Kawaguchi R, Chen L, El-Rifai M, Geschwind DH, Dib-Hajj SD, Waxman SG, Woolf CJ., Free PMC Article | 05/8/2023 |
| Nav1.7 is required for normal C-low threshold mechanoreceptor function in humans and mice. | Nav1.7 is required for normal C-low threshold mechanoreceptor function in humans and mice.
Middleton SJ, Perini I, Themistocleous AC, Weir GA, McCann K, Barry AM, Marshall A, Lee M, Mayo LM, Bohic M, Baskozos G, Morrison I, Löken LS, McIntyre S, Nagi SS, Staud R, Sehlstedt I, Johnson RD, Wessberg J, Wood JN, Woods CG, Moqrich A, Olausson H, Bennett DL., Free PMC Article | 10/29/2022 |
| Selective optogenetic activation of NaV1.7-expressing afferents in NaV1.7-ChR2 mice induces nocifensive behavior without affecting responses to mechanical and thermal stimuli. | Selective optogenetic activation of NaV1.7-expressing afferents in NaV1.7-ChR2 mice induces nocifensive behavior without affecting responses to mechanical and thermal stimuli.
Maruta T, Hidaka K, Kouroki S, Koshida T, Kurogi M, Kage Y, Mizuno S, Shirasaka T, Yanagita T, Takahashi S, Takeya R, Tsuneyoshi I., Free PMC Article | 10/15/2022 |
| Examination of the contribution of Nav1.7 to axonal propagation in nociceptors. | Examination of the contribution of Nav1.7 to axonal propagation in nociceptors.
Goodwin G, McMurray S, Stevens EB, Denk F, McMahon SB. | 06/25/2022 |
| Two independent mouse lines carrying the Nav1.7 I228M gain-of-function variant display dorsal root ganglion neuron hyperexcitability but a minimal pain phenotype. | Two independent mouse lines carrying the Nav1.7 I228M gain-of-function variant display dorsal root ganglion neuron hyperexcitability but a minimal pain phenotype.
Chen L, Wimalasena NK, Shim J, Han C, Lee SI, Gonzalez-Cano R, Estacion M, Faber CG, Lauria G, Dib-Hajj SD, Woolf CJ, Waxman SG., Free PMC Article | 05/22/2021 |
| Nav1.7 and MGO-mediated activation of TRPA1 play key roles in itch and hypoalgesia in a murine model of type 1 diabetes. | The role of Na(v)1.7 and methylglyoxal-mediated activation of TRPA1 in itch and hypoalgesia in a murine model of type 1 diabetes.
Cheng RX, Feng Y, Liu D, Wang ZH, Zhang JT, Chen LH, Su CJ, Wang B, Huang Y, Ji RR, Hu J, Liu T., Free PMC Article | 07/11/2020 |
| data illustrated the therapeutic potential for 3'-O-methylorobol for histamine-dependent itching, and the small molecule inhibition of Nav1.7 may represent a useful strategy to develop novel therapeutics for itching. | 3'-O-Methylorobol Inhibits the Voltage-Gated Sodium Channel Nav1.7 with Anti-Itch Efficacy in A Histamine-Dependent Itch Mouse Model.
Zhang F, Wu Y, Xue S, Wang S, Zhang C, Cao Z., Free PMC Article | 04/11/2020 |
| This study demonstrated that nav1.7 contribution to peripheral nerves pain. | NaV1.7 and pain: contribution of peripheral nerves.
Hoffmann T, Sharon O, Wittmann J, Carr RW, Vyshnevska A, Col R, Nassar MA, Reeh PW, Weidner C. | 04/6/2019 |
| Nav1.7, known to regulate opioid receptor efficacy, interacts with the G protein-regulated inducer of neurite outgrowth (Gprin1), an opioid receptor-binding protein, demonstrating a physical and functional link between Nav1.7 and opioid signalling. | Mapping protein interactions of sodium channel Na(V)1.7 using epitope-tagged gene-targeted mice.
Kanellopoulos AH, Koenig J, Huang H, Pyrski M, Millet Q, Lolignier S, Morohashi T, Gossage SJ, Jay M, Linley JE, Baskozos G, Kessler BM, Cox JJ, Dolphin AC, Zufall F, Wood JN, Zhao J., Free PMC Article | 10/13/2018 |
| the NaV1.7 channel is an important mechanism underlying hyperalgesia | Antihyperalgesic effect by herpes vector-mediated knockdown of NaV1.7 sodium channels after skin incision.
Eisenried A, Klukinov M, Yeomans DC, Tzabazis AZ. | 04/7/2018 |
| Voltage-gated sodium channel Nav1.7 controls the efficacy and balance of heterotrimeric guanine nucleotide-binding protein-coupled receptor (GPCR)-mediated pro- and antinociceptive intracellular signaling. | Synergistic regulation of serotonin and opioid signaling contributes to pain insensitivity in Nav1.7 knockout mice.
Isensee J, Krahé L, Moeller K, Pereira V, Sexton JE, Sun X, Emery E, Wood JN, Hucho T., Free PMC Article | 11/11/2017 |
| the FGF13/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals | FGF13 Selectively Regulates Heat Nociception by Interacting with Na(v)1.7.
Yang L, Dong F, Yang Q, Yang PF, Wu R, Wu QF, Wu D, Li CL, Zhong YQ, Lu YJ, Cheng X, Xu FQ, Chen L, Bao L, Zhang X. | 08/26/2017 |
| this paper shows that Nav1.7, by coupling with CRMP1, mediates the axonal retrograde signaling of Sema3A in axonal guidance | A functional coupling between CRMP1 and Na(v)1.7 for retrograde propagation of Semaphorin3A signaling.
Yamane M, Yamashita N, Hida T, Kamiya Y, Nakamura F, Kolattukudy P, Goshima Y. | 05/6/2017 |
| Experiments show that integration of synaptic inputs over time by Nav1.7 is critical for body weight regulation and reveal a mechanism for synaptic control of circuits regulating long term homeostatic functions. | Near-Perfect Synaptic Integration by Nav1.7 in Hypothalamic Neurons Regulates Body Weight.
Branco T, Tozer A, Magnus CJ, Sugino K, Tanaka S, Lee AK, Wood JN, Sternson SM., Free PMC Article | 01/14/2017 |
| Nav1.7 deletion has profound effects on gene expression, leading to an upregulation of enkephalin precursor Penk mRNA and met-enkephalin protein in sensory neurons. | Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7.
Minett MS, Pereira V, Sikandar S, Matsuyama A, Lolignier S, Kanellopoulos AH, Mancini F, Iannetti GD, Bogdanov YD, Santana-Varela S, Millet Q, Baskozos G, MacAllister R, Cox JJ, Zhao J, Wood JN., Free PMC Article | 07/2/2016 |
| Global Nav1.7 knockouts showed no defects in mechanical sensitivity or overall movement yet were completely insensitive to painful tactile, thermal, and chemical stimuli and were anosmic. | Global Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain.
Gingras J, Smith S, Matson DJ, Johnson D, Nye K, Couture L, Feric E, Yin R, Moyer BD, Peterson ML, Rottman JB, Beiler RJ, Malmberg AB, McDonough SI., Free PMC Article | 05/2/2015 |
| Sodium channel Nav1.7, encoded by SCN9A, is expressed in DRG neurons and regulates their excitability. | Depolarized inactivation overcomes impaired activation to produce DRG neuron hyperexcitability in a Nav1.7 mutation in a patient with distal limb pain.
Huang J, Yang Y, Dib-Hajj SD, van Es M, Zhao P, Salomon J, Drenth JP, Waxman SG., Free PMC Article | 01/10/2015 |
| a novel regulatory mechanism that utilizes CRMP2 SUMOylation to choreograph NaV1.7 trafficking. | CRMP2 protein SUMOylation modulates NaV1.7 channel trafficking.
Dustrude ET, Wilson SM, Ju W, Xiao Y, Khanna R., Free PMC Article | 11/16/2013 |
| Behavioural deficits in Nav1.7/Nav1.8 knockout mice reflects a failure of action potential propagation in a mechanosensitive set of sensory neurons rather than a loss of primary transduction currents. | Sodium channels and mammalian sensory mechanotransduction.
Raouf R, Rugiero F, Kiesewetter H, Hatch R, Hummler E, Nassar MA, Wang F, Wood JN., Free PMC Article | 10/27/2012 |
| Deleting SCN9A in both sensory and sympathetic neurons abolishes pain sensations. | Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons.
Minett MS, Nassar MA, Clark AK, Passmore G, Dickenson AH, Wang F, Malcangio M, Wood JN., Free PMC Article | 07/28/2012 |
| These results demonstrate increased expression levels of Nav1.7, Nav1.8, and perhaps Nav1.1 in the dorsal root ganglia in mice with a heterozygous mutation of the Nf1 gene | Dorsal root ganglia isolated from Nf1+/- mice exhibit increased levels of mRNA expression of voltage-dependent sodium channels.
Hodgdon KE, Hingtgen CM, Nicol GD. | 07/21/2012 |
| Nav1.7 is the dominant sodium channel in rat and mouse olfactory sensory neurons. | Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons.
Ahn HS, Black JA, Zhao P, Tyrrell L, Waxman SG, Dib-Hajj SD., Free PMC Article | 09/17/2011 |
| Na(v)1.7 is not only necessary for pain sensation but is also an essential requirement for odour perception in both mice and humans | Loss-of-function mutations in sodium channel Nav1.7 cause anosmia.
Weiss J, Pyrski M, Jacobi E, Bufe B, Willnecker V, Schick B, Zizzari P, Gossage SJ, Greer CA, Leinders-Zufall T, Woods CG, Wood JN, Zufall F., Free PMC Article | 06/18/2011 |
| contrast to the highly significant role for Nav1.7 in determining inflammatory pain thresholds, the development of neuropathic pain does not require the presence of either Nav1.7 or Nav1.8 alone or in combination | Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8.
Nassar MA, Levato A, Stirling LC, Wood JN., Free PMC Article | 01/21/2010 |