Results 41 to 50 of about 3,773 (193)

Nav1.7 and other voltage-gated sodium channels as drug targets for pain relief [PDF]

, 2016
INTRODUCTION: Chronic pain is a massive clinical problem. We discuss the potential of subtype selective sodium channel blockers that may provide analgesia with limited side effects.
Emery, EC, Luiz, AP, Wood, JN
core   +1 more source

NaV1.9 Potentiates Oxidized Phospholipid-Induced TRP Responses Only under Inflammatory Conditions

Frontiers in Molecular Neuroscience, 2018
Oxidized phospholipids (OxPL) like oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC) were recently identified as novel proalgesic targets in acute and chronic inflammatory pain.
Corinna Martin, Corinna Martin, Carolin Stoffer, Milad Mohammadi, Milad Mohammadi, Julian Hugo, Julian Hugo, Enrico Leipold, Beatrice Oehler, Heike L. Rittner, Robert Blum   +10 more
doaj   +1 more source

Gain-of-function mutation in SCN11A causes itch and affects neurogenic inflammation and muscle function in Scn11a+/L799P mice.

PLoS ONE, 2020
Mutations in the genes encoding for voltage-gated sodium channels cause profound sensory disturbances and other symptoms dependent on the distribution of a particular channel subtype in different organs.
Matthias Ebbinghaus, Lorena Tuchscherr, Gisela Segond von Banchet, Lutz Liebmann, Volker Adams, Mieczyslaw Gajda, Christian A Hübner, Ingo Kurth, Hans-Georg Schaible   +8 more
doaj   +1 more source

Post-translational modifications of voltage-gated sodium channels in chronic pain syndromes. [PDF]

, 2015
In the peripheral sensory nervous system the neuronal expression of voltage-gated sodium channels (Navs) is very important for the transmission of nociceptive information since they give rise to the upstroke of the action potential (AP).
Abdulla, Abrahamsen, Abriel, Abriel, Abriel, Abriel, Akopian, Akopian, Akopian, Aley, Aley, Amaya, Arévalo, Bair, Basbaum, Battaini, Ben-Johny, Bendahhou, Beneski, Bennett, Bennett, Berta, Bierhaus, Bierhaus, Bird, Bird, Biswas, Black, Black, Black, Bongiorno, Bouhassira, Bretin, Brouwer, Brower, Brüggemann, Cachemaille, Campbell, Cang, Cantrell, Cantrell, Casals-Diaz, Catterall, Catterall, Cesare, Cesare, Chahine, Chatelier, Chattopadhyay, Chen, Chen, Cheng, Chi, Ciechanover, Coggeshall, Cohen, Costa, Costa, Coward, Coward, Cox, Cronin, Cummins, Cummins, Cummins, Cusdin, Daemen, Dascal, Decosterd, Deribe, Deschênes, Deval, Dib-Hajj, Dib-Hajj, Dib-Hajj, Dib-Hajj, Dib-Hajj, Dietrich, Dina, Dina, Djouhri, Dogrul, Dong, Duan, Dubin, Dustrude, Edinger, Ednie, England, Errington, Errington, Faber, Faber, Fahmi, Ferrari, Ferreira, Ferreira, Fertleman, Firsov, Fitzgerald, Fjell, Fotia, Fotia, Fukuoka, Fukuoka, Galan, Gasser, Gaudet, Gee, Gershon, Gold, Gold, Gold, Goldin, Gould, Gudes, Han, Heikamp, Henry, Herzog, Herzog, Hirade, Hiruma, Ho, Hockley, Hoeijmakers, Hoeijmakers, Huang, Hucho, Hudmon, Hunter, Ikeda, Inagaki, Isom, Isom, Isom, James, Jarecki, Jarvis, Ji, Ji, Jin, Joazeiro, Johnson, Johnson, Joshi, Julius, Kazarinova-Noyes, Kazen-Gillespie, Kerr, Khasar, Khasar, Khasar, Kim, Kispersky, Klugbauer, Kreegipuu, Kresge, Kress, Kretschmer, Kruger, Laedermann, Laedermann, Laedermann, Laedermann, Lai, Latremoliere, Leipold, Leo, Leung, Li, Liang, Liu, Liu, Liu, Liu, Liu, Lolignier, Lopez-Santiago, Lopez-Santiago, Lou, Luo, Luo, Maingret, Malhotra, Malhotra, Maltsev, Mann, Mao, Matzner, Matzner, Messner, Metzger, Millan, Minett, Mittmann, Moon, Moremen, Morgan, Mori, Murphy, Murray, Nagasako, Narayanan, Nassar, Nelson, Noda, Novella, Numann, Nuss, Obata, Olsson, Payandeh, Perry, Persson, Pertin, Petho, Pickart, Pierre, Pitchford, Plummer, Priest, Qu, Rang, Ranscht, Raymond, Recio-Pinto, Ren, Renganathan, Renganathan, Ritchie, Rossie, Rossier, Rush, Rush, Rush, Sadamasu, Sangameswaran, Sanna, Schaller, Schepelmann, Schild, Schirmeyer, Schmidt, Schmidt, Scholz, Shah, Shao, Shi, Shih, Smith, Smith, Snyder, Snyder, Solà, Souza, Stamboulian, Staub, Strickland, Stucky, Sun, Suter, Taiwo, Tan, Thakor, Theriault, Thornalley, Toledo-Aral, Toledo-Aral, Tong, Toth, Turk, Tyrrell, van Bemmelen, Vanoye, Vijayaragavan, Vijayaragavan, Vijayaragavan, von Hehn, Wada, Wada, Waechter, Wang, Waxman, Waxman, Waxman, Waxman, Way, Wells, Widmann, Woolf, Woolf, Woolf, Woolf, Woolf, Wu, Xu, Xu, Xu, Xu, Yan, Yanagita, Yanagita, Yang, Yeomans, Yin, Young, Yu, Yu, Yuhi, Zhang, Zhang, Zhang, Zhang, Zhou, Zhou, Zhuang, Zimmer, Zochodne   +318 more
core   +2 more sources

Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1 [PDF]

, 2017
Human intoxication with the seafood poison ciguatoxin, a dinoflagellate polyether that activates voltage-gated sodium channels (NaV), causes ciguatera, a disease characterised by gastrointestinal and neurological disturbances. We assessed the activity of
Brierley, S., Caldwell, A., Castro, J., Deuis, J., Erickson, A., Garcia-Caraballo, S., Grundy, L., Harrington, A., Inserra, M., Israel, M., Keramidas, A., Lewis, R., Maddern, J., Rychkov, G., Vetter, I., Zimmermann, K.   +15 more
core   +3 more sources

Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas [PDF]

, 2013
Background: Voltage-gated sodium channels Nav1.8 and Nav1.9 are expressed preferentially in small diameter sensory neurons, and are thought to play a role in the generation of ectopic activity in neuronal cell bodies and/or their axons following ...
Alison R Loescher, Bird, Emma V, Claire R Christmas, Emma V Bird, Fiona M Boissonade, Joel A Black, Keith G Smith, Peter P Robinson, Stephen G Waxman   +8 more
core   +2 more sources

E44Q mutation in NaV1.7 in a patient with infantile paroxysmal knee pain: electrophysiological analysis of voltage-dependent sodium current

Heliyon, 2021
Gain-of-function mutations in voltage-gated sodium channels (NaV1.7, NaV1.8, and NaV1.9) are known causes of inherited pain disorders. Identification and functional assessment of new NaV1.7 mutations could help elucidate the phenotypic spectrum of NaV1.7
Kiichi Takahashi, Takayoshi Ohba, Yosuke Okamoto, Atsuko Noguchi, Hiroko Okuda, Hatasu Kobayashi, Kouji H. Harada, Akio Koizumi, Kyoichi Ono, Tsutomu Takahashi   +9 more
doaj   +1 more source

Pharmacological modification of sodium channel Nav1.9 activity

, 2022
Published by RWTH Aachen University ...
openaire   +2 more sources

Spider venom-derived peptide induces hyperalgesia in Nav1.7 knockout mice by activating Nav1.9 channels

Nature Communications, 2020
Loss of function of Nav1.7 leads to congenital insensitivity to pain in humans. Here the authors found that activation of Nav1.9 can restore nociception in Nav1.7 knockout mice, revealed by a venom-derived peptide as a probe.
Xi Zhou, Tingbin Ma, Luyao Yang, Shuijiao Peng, Lulu Li, Zhouquan Wang, Zhen Xiao, Qingfeng Zhang, Li Wang, Yazhou Huang, Minzhi Chen, Songping Liang, Xianwei Zhang, Jing Yu Liu, Zhonghua Liu   +14 more
doaj   +1 more source

Pharmacogenetics of analgesic drugs [PDF]

, 2013
• Individual variability in pain perception and differences in the efficacy of analgesic drugs are complex phenomena and are partly genetically predetermined.
Branford, R, Cregg, R, Gubbay, A, Russo, G, Sato, H   +4 more
core   +1 more source