Results 31 to 40 of about 9,275 (242)
Channels, 2022 The voltage-gated sodium channel isoform NaV1.7 is a critical player in the transmission of nociceptive information. This channel has been heavily implicated in human genetic pain disorders and is a validated pain target.
Jiahe Li +4 more
doaj +1 more source
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
Molecular Pain, 2012 Background Sodium channel Nav1.7 has emerged as a target of considerable interest in pain research, since loss-of-function mutations in SCN9A, the gene that encodes Nav1.7, are associated with a syndrome of congenital insensitivity to pain, gain-of ...
Black Joel A +3 more
doaj +1 more source
Identification and targeting of a unique NaV1.7 domain driving chronic pain
Proceedings of the National Academy of Sciences of the United States of America, 2023 Significance The voltage-gated sodium channel isoform 1.7 (NaV1.7) has been widely implicated in chronic pain. We have discovered a unique intracellular region of NaV1.7 that facilitates its regulation by intracellular auxiliary proteins and which can be
Kimberly Gomez +17 more
semanticscholar +1 more source
Frontiers in Cellular Neuroscience, 2021 Trigeminal sensory neurons of transgenic knock-in (KI) mice expressing the R192Q missense mutation in the α1A subunit of neuronal voltage-gated CaV2.1 Ca2+ channels, which leads to familial hemiplegic migraine type 1 (FHM1) in patients, exhibit a ...
Riffat Mehboob +5 more
doaj +1 more source
Global Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain. [PDF]
PLoS ONE, 2014 Clinical genetic studies have shown that loss of Nav1.7 function leads to the complete loss of acute pain perception. The global deletion is reported lethal in mice, however, and studies of mice with promoter-specific deletions of Nav1.7 have suggested ...
Jacinthe Gingras +13 more
doaj +1 more source
Structure of the saxiphilin:saxitoxin (STX) complex reveals a convergent molecular recognition strategy for paralytic toxins. [PDF]
, 2019 Dinoflagelates and cyanobacteria produce saxitoxin (STX), a lethal bis-guanidinium neurotoxin causing paralytic shellfish poisoning. A number of metazoans have soluble STX-binding proteins that may prevent STX intoxication.
Du Bois, J +4 more
core +2 more sources
The β3‐subunit modulates the effect of venom peptides ProTx‐II and OD1 on NaV1.7 gating
Journal of Cellular Physiology, 2023 The voltage‐gated sodium channel NaV1.7 is involved in various pain phenotypes and is physiologically regulated by the NaV‐β3‐subunit. Venom toxins ProTx‐II and OD1 modulate NaV1.7 channel function and may be useful as therapeutic agents and/or research ...
S. Salvage +6 more
semanticscholar +1 more source
eLife, 2022 The voltage-gated sodium NaV1.7 channel plays a key role as a mediator of action potential propagation in C-fiber nociceptors and is an established molecular target for pain therapy.
Phuong T Nguyen +16 more
doaj +1 more source
Extracellular signal-regulated kinases mediate the enhancing effects of inflammatory mediators on resurgent currents in dorsal root ganglion neurons [PDF]
, 2019 Previously we reported that a group of inflammatory mediators significantly enhanced resurgent currents in dorsal root ganglion neurons. To understand the underlying intracellular signaling mechanism, we investigated the effects of inhibition of ...
Cummins, Theodore R. +6 more
core +1 more source