Results 51 to 60 of about 9,275 (242)

Sodium Channels and Mammalian Sensory Mechanotransduction [PDF]

open access: yes, 2012
Background: Members of the degenerin/epithelial (DEG/ENaC) sodium channel family are mechanosensors in C elegans, and Nav1.7 and Nav1.8 voltage-gated sodium channel knockout mice have major deficits in mechanosensation.
Edith Hummler   +7 more
core   +4 more sources

Long-lasting analgesia via targeted in situ repression of NaV1.7 in mice

open access: yesScience Translational Medicine, 2021
In situ genome targeting of NaV1.7 via CRISPRs and zinc fingers enables genomically scarless, durable, and nonaddictive management of pain. Repressing pain LATER Opioids are the current standard of care for the treatment of chronic pain.
Ana M. Moreno   +18 more
semanticscholar   +1 more source

Voltage‐gated sodium channel 1.7 expression decreases in dorsal root ganglia in a spinal nerve ligation neuropathic pain model

open access: yesKaohsiung Journal of Medical Sciences, 2019
The role of the voltage‐gated sodium channel 1.7 (Nav1.7) is unclear in models of neuropathic pain induced by nerve injury. In the present study, we measured expression levels of Nav1.7 in two distinct neuropathic pain models: spinal nerve ligation (SNL)
Ming Li   +8 more
doaj   +1 more source

Post-translational modifications of voltage-gated sodium channels in chronic pain syndromes. [PDF]

open access: yes, 2015
In the peripheral sensory nervous system the neuronal expression of voltage-gated sodium channels (Navs) is very important for the transmission of nociceptive information since they give rise to the upstroke of the action potential (AP).
Abdulla   +318 more
core   +2 more sources

Pain-causing stinging nettle toxins target TMEM233 to modulate NaV1.7 function

open access: yesNature Communications, 2023
Voltage-gated sodium channels function as multiprotein signaling complexes. Here, authors show that the dispanin TMEM233 is essential for activity of stinging nettle toxins and that co-expression of TMEM233 modulates the gating properties of Na_V1.7 ...
S. Jami   +39 more
semanticscholar   +1 more source

NaV1.7 as a pain target – From gene to pharmacology [PDF]

open access: yesPharmacology & Therapeutics, 2017
Na(V)1.7, a subtype of the voltage-gated sodium channel family that is highly expressed in peripheral sensory neurons, remains one of the most promising targets for the treatment of pain. However, despite compelling genetic evidence supporting a key role for Na(V)1.7 in regulating excitability of peripheral sensory neurons, the development of truly ...
Vetter, Irina   +7 more
openaire   +3 more sources

Estradiol upregulates voltage-gated sodium channel 1.7 in trigeminal ganglion contributing to hyperalgesia of inflamed TMJ.

open access: yesPLoS ONE, 2017
BackgroundTemporomandibular disorders (TMDs) have the highest prevalence in women of reproductive age. The role of estrogen in TMDs and especially in TMDs related pain is not fully elucidated.
Rui-Yun Bi   +5 more
doaj   +1 more source

Deletion of annexin 2 light chain p11 in nociceptors causes deficits in somatosensory coding and pain behavior [PDF]

open access: yes, 2006
The S100 family protein p11 (S100A10, annexin 2 light chain) is involved in the trafficking of the voltage-gated sodium channel Na(V)1.8, TWIK-related acid-sensitive K+ channel (TASK-1), the ligand-gated ion channels acid-sensing ion channel 1a (ASIC1a ...
Baker, MD   +8 more
core   +1 more source

Nav1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis

open access: yesNature
Osteoarthritis (OA) is the most common joint disease. Currently there are no effective methods that simultaneously prevent joint degeneration and reduce pain1.
W. Fu   +26 more
semanticscholar   +1 more source

A mini-review: Bridging the gap between autism spectrum disorder and pain comorbidities

open access: yesCanadian Journal of Pain, 2020
Background Pain is a complex neurobiological response with a multitude of causes; however, patients with autism spectrum disorder (ASD) often report chronic pain with no known etiology.
Chad O. Brown   +2 more
doaj   +1 more source

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