Results 141 to 150 of about 9,275 (242)

Nav1.7 and Nav1.8: Role in the pathophysiology of pain

open access: yesMolecular Pain, 2019
Chronic pain is a significant unmet medical problem. Current research regarding sodium channel function in pathological pain is advancing with the hope that it will enable the development of isoform-specific sodium channel blockers, a promising treatment
S. Hameed
semanticscholar   +1 more source

Paroxysmal Extreme Pain Disorder (PEPD): clinical and genetic investigation [PDF]

open access: yes, 2012
Objectifs 1) Caractériser une famille avec PEPD aux plans clinique, généalogique et génétique. 2) Identifier la cause génétique de la maladie dans cette famille, et en démontrer la pathogénicité. Introduction Le "Paroxysmal Extreme Pain Disorder " (PEPD)
Stauffacher, M.
core  

Rescuing Abandoned Molecules as Nav1.7 and PCSK9 Inhibitors

open access: yesJournal of Advances in Medical and Pharmaceutical Sciences, 2016
Academic institutions have plentiful of unexploited compounds. A cost-effective repositioning strategy from abandoned molecules coming from different research projects was applied. This strategy was based on the creation of a 2D-database then the biological assaying following adherence to the the Lilly OIDD (Open Innovation Drug Discovery) program by ...
Amico G   +8 more
openaire   +2 more sources

Similar excitability through different sodium channels and implications for the analgesic efficacy of selective drugs

open access: yeseLife
Nociceptive sensory neurons convey pain-related signals to the CNS using action potentials. Loss-of-function mutations in the voltage-gated sodium channel NaV1.7 cause insensitivity to pain (presumably by reducing nociceptor excitability) but clinical ...
Yu-Feng Xie   +3 more
doaj   +1 more source

Conservation of alternative splicing in sodium channels reveals evolutionary focus on release from inactivation and structural insights into gating [PDF]

open access: yes, 2017
Voltage-gated sodium channels are critical for neuronal activity, and highly intolerant to variation. Even mutations that cause subtle changes in the activity these channels are sufficient to cause devastating inherited neurological diseases, such as ...
Liavas, A, Lignani, G, Schorge, S
core   +1 more source

Dendritikus sejt altípusok együttműködése fiziológiás és kóros állapotban = The interplay of dendritic cell subtypes in health and disease [PDF]

open access: yes, 2011
A dendritikus sejtek (DC) az immunfolyamatok fontos irányítói, melyek alapvető szerepet játszanak a központi és perifériás tolerancia és a gyulladásos folyamatok kiváltásában, fenntartásában és szabályozásában.
Benkő, Szilvia   +9 more
core  

Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation

open access: yesScientific Reports, 2018
Sodium channel Nav1.7 plays a central role in pain-signaling: gain-of-function Nav1.7 mutations usually cause severe pain and loss-of-function mutations produce insensitivity to pain.
Jianying Huang   +8 more
doaj   +1 more source

SUMOylation and calcium signalling: potential roles in the brain and beyond [PDF]

open access: yes, 2017
Small ubiquitin-like modi er (SUMO) conjugation (or SUMOylation) is a post-translational protein modi cation implicated in alterations to protein expression, localization and func- tion. Despite a number of nuclear roles for SUMO being well characterized,
Abeywardana   +176 more
core   +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

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