NaN, a novel voltage-gated Na channel, is expressed preferentially in peripheral sensory neurons and down-regulated after axotomy.
about
Phyla- and Subtype-Selectivity of CgNa, a Na Channel Toxin from the Venom of the Giant Caribbean Sea Anemone Condylactis GiganteaFibroblast growth factor 14 is an intracellular modulator of voltage-gated sodium channelsA single sodium channel mutation produces hyper- or hypoexcitability in different types of neuronsReplicate high-density rat genome oligonucleotide microarrays reveal hundreds of regulated genes in the dorsal root ganglion after peripheral nerve injuryTwo tetrodotoxin-resistant sodium channels in human dorsal root ganglion neuronsSodium currents of large (Abeta-type) adult cutaneous afferent dorsal root ganglion neurons display rapid recovery from inactivation before and after axotomyFibroblast growth factor homologous factor 1B binds to the C terminus of the tetrodotoxin-resistant sodium channel rNav1.9a (NaN)Expression of background potassium channels in rat DRG is cell-specific and down-regulated in a neuropathic pain modelVoltage-gated Na+ channels in neuropathic pain.Nav1.9 channel contributes to mechanical and heat pain hypersensitivity induced by subacute and chronic inflammation.Voltage-gated sodium channel expression in mouse DRG after SNI leads to re-evaluation of projections of injured fibers.Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas.Increase of sodium channels (nav 1.8 and nav 1.9) in rat dorsal root ganglion neurons exposed to autologous nucleus pulposus.Sodium channels and pain.A comparison of the potential role of the tetrodotoxin-insensitive sodium channels, PN3/SNS and NaN/SNS2, in rat models of chronic pain.Tetrodotoxin-resistant Na+ currents and inflammatory hyperalgesiaTranscriptional and posttranslational plasticity and the generation of inflammatory painDiversity of mammalian voltage-gated sodium channels.Reduced thermal sensitivity and Nav1.8 and TRPV1 channel expression in sensory neurons of aged mice.The neuron as a dynamic electrogenic machine: modulation of sodium-channel expression as a basis for functional plasticity in neurons.The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways.Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.Pathobiology of visceral pain: molecular mechanisms and therapeutic implications. II. Genetic approaches to pain therapy.Antisense-mediated knockdown of Na(V)1.8, but not Na(V)1.9, generates inhibitory effects on complete Freund's adjuvant-induced inflammatory pain in rat.An in vivo tethered toxin approach for the cell-autonomous inactivation of voltage-gated sodium channel currents in nociceptors.Parathyroid hormone 2 receptor is a functional marker of nociceptive myelinated fibers responsible for neuropathic pain.Tetrodotoxin (TTX) as a therapeutic agent for pain.Characterization of Na+ and Ca2+ channels in zebrafish dorsal root ganglion neurons.Single-cell analysis of sodium channel expression in dorsal root ganglion neuronsMultiple roles for NaV1.9 in the activation of visceral afferents by noxious inflammatory, mechanical, and human disease-derived stimuli.Inhibition of tetrodotoxin-resistant sodium current in dorsal root ganglia neurons mediated by D1/D5 dopamine receptorsIon channelopathies in functional GI disorders.Are voltage-gated sodium channels on the dorsal root ganglion involved in the development of neuropathic pain?The roles of sodium channels in nociception: Implications for mechanisms of painMolecular and functional remodeling of electrogenic membrane of hypothalamic neurons in response to changes in their inputNav1.7 is the predominant sodium channel in rodent olfactory sensory neurons.μ-Conotoxins that differentially block sodium channels NaV1.1 through 1.8 identify those responsible for action potentials in sciatic nervemuO-conotoxin MrVIB selectively blocks Nav1.8 sensory neuron specific sodium channels and chronic pain behavior without motor deficitsNavβ subunits modulate the inhibition of Nav1.8 by the analgesic gating modifier μO-conotoxin MrVIBSensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis
P2860
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P2860
NaN, a novel voltage-gated Na channel, is expressed preferentially in peripheral sensory neurons and down-regulated after axotomy.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
NaN, a novel voltage-gated Na ...... down-regulated after axotomy.
@ast
NaN, a novel voltage-gated Na ...... down-regulated after axotomy.
@en
type
label
NaN, a novel voltage-gated Na ...... down-regulated after axotomy.
@ast
NaN, a novel voltage-gated Na ...... down-regulated after axotomy.
@en
prefLabel
NaN, a novel voltage-gated Na ...... down-regulated after axotomy.
@ast
NaN, a novel voltage-gated Na ...... down-regulated after axotomy.
@en
P2093
P2860
P356
P1476
NaN, a novel voltage-gated Na ...... down-regulated after axotomy.
@en
P2093
P2860
P304
P356
10.1073/PNAS.95.15.8963
P407
P577
1998-07-01T00:00:00Z