Results 51 to 60 of about 3,773 (193)

Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability [PDF]

open access: yesJournal of Clinical Investigation, 2017
Voltage-gated sodium channel (NaV) mutations cause genetic pain disorders that range from severe paroxysmal pain to a congenital inability to sense pain. Previous studies on NaV1.7 and NaV1.8 established clear relationships between perturbations in channel function and divergent clinical phenotypes.
Jianying, Huang   +7 more
openaire   +2 more sources

Prostaglandin E2 Has No Effect on Two Components of Tetrodotoxin-Resistant Na+ Current in Mouse Dorsal Root Ganglion

open access: yesJournal of Pharmacological Sciences, 2007
One possible mechanism underlying inflammation-induced sensitization of the primary afferent neuron is the upregulation of tetrodotoxin-resistant (TTX-R) Na+ current by inflammatory mediators such as prostaglandins.
Taixing Zheng   +4 more
doaj   +1 more source

Computational design of peptides to target NaV1.7 channel with high potency and selectivity for the treatment of pain

open access: yeseLife, 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

Voltage-gated sodium channels: new targets in cancer therapy? [PDF]

open access: yes, 2006
Early detection and treatment of cancers have increased survival and improved clinical outcome. The development of metastases is often associated with a poor prognostic of survival. Finding early markers of metastasis and developing new therapies against
Besson, Pierre   +4 more
core   +2 more sources

Electrophysiological and Pharmacological Analyses of Nav1.9 Voltage-Gated Sodium Channel by Establishing a Heterologous Expression System

open access: yesFrontiers in Pharmacology, 2017
Nav1. 9 voltage-gated sodium channel is preferentially expressed in peripheral nociceptive neurons. Recent progresses have proved its role in pain sensation, but our understanding of Nav1.9, in general, has lagged behind because of limitations in ...
Xi Zhou   +16 more
doaj   +1 more source

Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families. [PDF]

open access: yesPLoS ONE, 2016
Painful peripheral neuropathy has been correlated with various voltage-gated sodium channel mutations in sensory neurons. Recently Nav1.9, a voltage-gated sodium channel subtype, has been established as a genetic influence for certain peripheral pain ...
Hiroko Okuda   +18 more
doaj   +1 more source

Decoding Pain: Next-Generation In Vitro Systems for Mechanistic Insights and Drug Discovery. [PDF]

open access: yesFASEB J
Developing an in vitro pain model that mimics essential features of the in vivo pain circuit requires careful consideration of multiple components and choices. These include selecting the cellular population for the model, choosing from the origin of nociceptors and other cells that are cultured, deciding between 3D or 2D dimensions, designing the ...
Khosrowshahi D, Lagae L, Bolander J.
europepmc   +2 more sources

Increased Activity of Nav1.9 Sodium Channels Causes Loss of Pain Perception [PDF]

open access: yesBiophysical Journal, 2014
Nociceptive sensory neurons transmit painful stimuli from the periphery to the central nervous system. Voltage-gated sodium (NaV) channels are instrumental for the generation of the corresponding electrical signals, but - so far - the sensory neuron-specific NaV1.9 only appeared to play a minor role.
Leipold, Enrico   +4 more
openaire   +1 more source

Neuronal voltage-gated sodium channel subtypes: Key roles in inflammatory and neuropathic pain [PDF]

open access: yes, 2006
Voltage-gated sodium channels (VGSCs) play an important role in neuronal excitability. Regulation of VGSC activity is a complex phenomenon that occurs at multiple levels in the cell, including transcriptional regulation, post-translational modification ...
Adams, D. J., Ekberg, J.
core   +1 more source

The insecticide deltamethrin enhances sodium channel slow inactivation of human Nav1.9, Nav1.8 and Nav1.7

open access: yesToxicology and Applied Pharmacology, 2021
Toxicology and applied pharmacology : TAP 428, 115676 (2021).
Bothe, Stefanie, Lampert, Angelika
openaire   +3 more sources

Home - About - Disclaimer - Privacy