Results 91 to 100 of about 9,275 (242)

Nuclear Factor-kappaB Gates Nav1.7 Channels in DRG Neurons via Protein-Protein Interaction

open access: yesiScience, 2019
Summary: It is well known that nuclear factor-kappaB (NF-κB) regulates neuronal structures and functions by nuclear transcription. Here, we showed that phospho-p65 (p-p65), an active form of NF-κB subunit, reversibly interacted with Nav1.7 channels in ...
Man-Xiu Xie   +8 more
doaj   +1 more source

Case Report: Mutant SCN9A Susceptible to Charcot Neuroarthropathy in a Patient With Congenital Insensitivity to Pain

open access: yesFrontiers in Neuroscience, 2021
Charcot neuroarthropathy is a systemic disease with pathological changes in the musculoskeletal system, which leads to fractures, dislocations, and deformities involving multiple bones and joints, particularly those of the feet.
Xiao-hui Xie   +7 more
doaj   +1 more source

Evaluation of behavior in transgenic mouse models to understand human congenital pain conditions [PDF]

open access: yes, 2018
BACKGROUND: Containing a brain for signal processing and decision making, and a peripheral component for sensation and response, the nervous system provides higher organisms a powerful method of interacting with their environment.
Bullock, Daniel
core  

Voltage-gated sodium channels potentiate the invasive capacities of human non-small-cell lung cancer cell lines. [PDF]

open access: yes, 2007
Ionic channel activity is involved in fundamental cellular behaviour and participates in cancerous features such as proliferation, migration and invasion which in turn contribute to the metastatic process.
Barascu, Aurélia   +9 more
core   +3 more sources

Loss-of-function mutations in sodium channel Nav1.7 cause anosmia [PDF]

open access: yesNature, 2011
Loss of function of the gene SCN9A, encoding the voltage-gated sodium channel Na(v)1.7, causes a congenital inability to experience pain in humans. Here we show that Na(v)1.7 is not only necessary for pain sensation but is also an essential requirement for odour perception in both mice and humans.
Jan, Weiss   +12 more
openaire   +2 more sources

The role of disulfide bond replacements in analogues of the Tarantula toxin ProTx-II and their effects on inhibition of the voltage-gated sodium ion channel Nav1.7 [PDF]

open access: yes, 2017
Spider venom toxins, such as Protoxin-II (ProTx-II), have recently received much attention as selective Nav1.7 channel blockers, with potential to be developed as leads for the treatment of chronic nocioceptive pain.
Cryar, Adam   +12 more
core   +2 more sources

Depletion of membrane cholesterol modifies structure, dynamic and activation of Nav1.7

open access: yesbioRxiv
Cholesterol is a major component of plasma membranes and unsurprisingly plays a significant role in actively regulating the functioning of several membrane proteins in humans.
Simone Albani   +5 more
semanticscholar   +1 more source

Elucidating molecular mechanisms of protoxin-II state-specific binding to the human NaV1.7 channel

open access: yesThe Journal of General Physiology, 2023
NaV1.7, a voltage-gated sodium channel, plays a crucial role in pain perception and is specifically targeted by PTx2, which serves as a template for designing pain therapeutics. In this study, Ngo et al.
K. Ngo   +8 more
semanticscholar   +1 more source

Burn Selection: How Fire Injury Shaped Human Evolution

open access: yesBioEssays, Volume 48, Issue 2, February 2026.
Intentional fire use exposed humans and their ancestors to high‐temperature burn injury, a risk rare in other species, bringing major survival benefits and technologies but also repeated exposure to extreme heat. The Burn Selection Hypothesis reframes this cost of fire mastery as a unique selective pressure, which shaped our evolution.
Joshua Cuddihy   +9 more
wiley   +1 more source

Genetics update: monogenetics, polygene disorders and the quest for modifying genes [PDF]

open access: yes, 2018
The genetic channelopathies are a broad collection of diseases. Many ion channel genes demonstrate wide phenotypic pleiotropy, but nonetheless concerted efforts have been made to characterise genotype-phenotype relationships.
Symonds, Joseph D., Zuberi, Sameer M.
core   +1 more source

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