Results 21 to 30 of about 9,275 (242)
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 +9 more
doaj +1 more source
The Selective Nav1.7 Inhibitor, PF-05089771, Interacts Equivalently with Fast and Slow Inactivated Nav1.7 Channels [PDF]
Molecular Pharmacology, 2016 Voltage-gated sodium (Nav) channel inhibitors are used clinically as analgesics and local anesthetics. However, the absence of Nav channel isoform selectivity of current treatment options can result in adverse cardiac and central nervous system side effects, limiting their therapeutic utility.
Jonathan W, Theile +2 more
openaire +2 more sources
Differential Inhibition of Nav1.7 and Neuropathic Pain by Hybridoma-Produced and Recombinant Monoclonal Antibodies that Target Nav1.7 [PDF]
Neuroscience Bulletin, 2018 The voltage-gated Na+ channel subtype Nav1.7 is important for pain and itch in rodents and humans. We previously showed that a Nav1.7-targeting monoclonal antibody (SVmab) reduces Na+ currents and pain and itch responses in mice. Here, we investigated whether recombinant SVmab (rSVmab) binds to and blocks Nav1.7 similar to SVmab.
Sangsu Bang +14 more
openaire +2 more sources
Hierarchical CRMP2 posttranslational modifications control NaV1.7 function [PDF]
Proceedings of the National Academy of Sciences, 2016 SignificanceThe voltage-gated sodium channel NaV1.7 is important for electrogenesis in sensory neurons. Insertion within the membrane is required for function of NaV1.7. However, the mechanisms determining how NaV1.7 is trafficked to neuronal cell membranes are poorly understood. Here, we elucidate a signaling program involving a complex and intriguing
Erik T. Dustrude +5 more
openaire +2 more sources
NaV1.7 and pain: contribution of peripheral nerves [PDF]
Pain, 2017 Abstract The sodium channel NaV1.7 contributes to action potential (AP) generation and propagation. Loss-of-function mutations in patients lead to congenital indifference to pain, though it remains unclear where on the way from sensory terminals to central nervous system the signalling is disrupted.
Hoffmann, T. +8 more
openaire +4 more sources
Inhibition of the Nav1.7 Channel in the Trigeminal Ganglion Relieves Pulpitis Inflammatory Pain
Frontiers in Pharmacology, 2021 Pulpitis causes significant changes in the peripheral nervous system, which induce hyperalgesia. However, the relationship between neuronal activity and Nav1.7 expression following pulpal noxious pain has not yet been investigated in the trigeminal ...
Minjee Kwon +4 more
doaj +1 more source
CRMP2 Protein SUMOylation Modulates NaV1.7 Channel Trafficking [PDF]
Journal of Biological Chemistry, 2013 Voltage-gated sodium channel (NaV) trafficking is incompletely understood. Post-translational modifications of NaVs and/or auxiliary subunits and protein-protein interactions have been posited as NaV-trafficking mechanisms. Here, we tested if modification of the axonal collapsin response mediator protein 2 (CRMP2) by a small ubiquitin-like modifier ...
Erik T, Dustrude +4 more
openaire +2 more sources
Uncomfortably numb: how Nav1.7 mediates paclitaxel-induced peripheral neuropathy [PDF]
Brain, 2021 This scientific commentary refers to ‘Paclitaxel increases axonal localization and vesicular trafficking of Nav1.7’ by Akin et al. (doi: 10.1093/brain/awab113).
Elizabeth S Silagi, Rosalind A Segal
openaire +2 more sources
The neonatal splice variant of Nav1.5 potentiates in vitro invasive behaviour of MDA-MB-231 human breast cancer cells [PDF]
, 2007 Upregulation of functional voltage-gated Na+ channels (VGSCs) occurs in metastatic human breast cancer (BCa) in vitro and in vivo. The present study aimed to ascertain the specific involvement of the 'neonatal' splice variant of Nav1.5 (nNav1.5), thought
Brackenbury, William J. +3 more
core +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 +4 more
core +1 more source