Results 1 to 10 of about 9,275 (242)

An approach to targeting Nav1.7 for pain sensations [PDF]

open access: yesThe Journal of Clinical Investigation
Pain is a serious medical condition with current treatments remaining limited by side effects. The Nav1.7 voltage-gated sodium channel is a crucial determinant of nociceptor excitability and a promising target for nonaddictive analgesics.
Theodore R. Cummins
doaj   +4 more sources

Histone lactylation regulates DOCK4 to control heat nociception and supports Dynein-mediated Nav1.7 trafficking [PDF]

open access: yesNature Communications
Heat nociception involves thermosensors like transient receptor potential channel V1 in dorsal root ganglion (DRG) neurons, but their loss only partially impairs heat sensing, suggesting other mechanisms.
Man-Xiu Xie   +12 more
doaj   +3 more sources

Analgesic Effects of GpTx-1, PF-04856264 and CNV1014802 in a Mouse Model of NaV1.7-Mediated Pain [PDF]

open access: yesToxins, 2016
Loss-of-function mutations of NaV1.7 lead to congenital insensitivity to pain, a rare condition resulting in individuals who are otherwise normal except for the inability to sense pain, making pharmacological inhibition of NaV1.7 a promising therapeutic ...
Jennifer R. Deuis   +12 more
doaj   +4 more sources

Subtype-Selective Small Molecule Inhibitors Reveal a Fundamental Role for Nav1.7 in Nociceptor Electrogenesis, Axonal Conduction and Presynaptic Release. [PDF]

open access: yesPLoS ONE, 2016
Human genetic studies show that the voltage gated sodium channel 1.7 (Nav1.7) is a key molecular determinant of pain sensation. However, defining the Nav1.7 contribution to nociceptive signalling has been hampered by a lack of selective inhibitors.
Aristos J Alexandrou   +27 more
doaj   +2 more sources

A Review of the Therapeutic Targeting of SCN9A and Nav1.7 for Pain Relief in Current Human Clinical Trials

open access: yesJournal of Pain Research, 2023
Anton Dormer,1 Mahesh Narayanan,1 Jerome Schentag,1 Daniel Achinko,1 Elton Norman,1 James Kerrigan,2 Gary Jay,2 William Heydorn2 1Research and Development, Pepvax, Inc, Silver Spring, MD, USA; 2Research and Development, Navintus, Inc, Princeton, NJ ...
Dormer A   +7 more
doaj   +2 more sources

Ectopic expression of Nav1.7 in spinal dorsal horn neurons induced by NGF contributes to neuropathic pain in a mouse spinal cord injury model

open access: yesFrontiers in Molecular Neuroscience, 2023
Neuropathic pain (NP) induced by spinal cord injury (SCI) often causes long-term disturbance for patients, but the mechanisms behind remains unclear. Here, our study showed SCI-induced ectopic expression of Nav1.7 in abundant neurons located in deep and ...
Yan Fu   +10 more
doaj   +2 more sources

Preclinical Animal Models to Investigate the Role of Na<sub>v</sub>1.7 Ion Channels in Pain. [PDF]

open access: yesLife (Basel)
Chronic pain is a maladaptive neurological disease that remains a major global healthcare problem. Voltage-gated sodium channels (Navs) are major drivers of the excitability of sensory neurons, and the Nav subtype 1.7 (Nav1.7) has been shown to be ...
Yogi A   +3 more
europepmc   +2 more sources

The Plant Alkaloid Harmaline Blocks the Voltage-Gated Sodium Channel Na<sub>v</sub>1.7: A Study Using an Automated Patch-Clamp. [PDF]

open access: yesInt J Mol Sci
The voltage-gated sodium channel Nav1.7 is essential for pain perception and is an interesting target for the development of pain-relieving substances.
Eisfeld J   +6 more
europepmc   +2 more sources

Compartment-specific regulation of NaV1.7 in sensory neurons after acute exposure to TNF-α

open access: yesCell Reports
Summary: Tumor necrosis factor α (TNF-α) is a major pro-inflammatory cytokine, important in many diseases, that sensitizes nociceptors through its action on a variety of ion channels, including voltage-gated sodium (NaV) channels. We show here that TNF-α
Sidharth Tyagi   +11 more
doaj   +2 more sources

Therapeutic targeting of voltage-gated sodium channel NaV1.7 for cancer metastasis

open access: yesFrontiers in Pharmacology
This review focuses on the expression and function of voltage-gated sodium channel subtype NaV1.7 in various cancers and explores its impact on the metastasis driving cell functions such as proliferation, migration, and invasiveness.
Piyasuda Pukkanasut   +5 more
doaj   +2 more sources

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