The image on the left is immunohistochemistry of paraffin-embedded Human liver cancer tissue using CSB-PA260136(SCN9A Antibody) at dilution 1/20, on the right is treated with synthetic peptide. (Original magnification: ×200)
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Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-sensitive Na(+) channel isoform. Plays a role in pain mechanisms, especially in the development of inflammatory pain.
This study demonstrated that the higher expression Nav1.7 in human Dorsal Root Ganglion Neurons. PMID: 28424991
cross-talk between distinct CRMP2 posttranslational modifications is a key factor in determining NaV1.7 trafficking and localization PMID: 27940916
Hereditary Small fiber neuropathy has been described with pathogenic mutations in sodium channels [Nav1.7 (mostly), which lead to hyperexcitability of dorsal root ganglions. These gain-of-function mutations result in degeneration of small fibers. PMID: 28639956
Genetic polymorphisms of SCN9A are associated with protection for severe neuropathy induced by oxaliplatin in digestive cancer. PMID: 28103821
the results of this study provide mechanistic evidence for a time-dependent increase in intracellular [Ca2+]i and energetic compromise in the neurites of dorsal root ganglia neurons expressing G856D mutant Nav1.7 channels. PMID: 27821467
the FGF13/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals PMID: 28162808
This study showed that gain-of-function attributes at the channel level and differential effects of physiologically relevant thermal stimuli on the excitability of DRG neurons expressing mutant and WT Nav1.7 channels, suggesting a cellular mechanism for warmth-triggered pain episodes in Erythromelalgia patients. PMID: 27413160
The four congenital insensitivity to pain families, while not closely related, belong to the same ethnic group and clan, and the SCN9A mutation may be specific, if not unique to this group PMID: 27747863
A novel Nav1.9 mutation, p.Arg222His, was identified in patients with early-onset pain in distal extremities including joints and gastrointestinal disturbances, but was absent from an asymptomatic blood relative. PMID: 27503742
Gain-of-function mutation of a voltage-gated sodium channel NaV1.7 associated with peripheral pain and impaired limb development PMID: 28381558
Results indicate that Nav 1.7 promotes gastric cancer progression through MACC1-mediated upregulation of NHE1. PMID: 27529686
This is the first study to demonstrate that binding of ProTx-II to the lipid membrane is directly linked to its potency as an hNaV1.7 channel inhibitor. PMID: 27311819
report the engineering of highly potent and selective inhibitors of the Nav1.7 channel based on tarantula ceratotoxin-1 (CcoTx1). We utilized a combination of directed evolution, saturation mutagenesis, chemical modification, and rational drug design to obtain higher potency and selectivity to the Nav1.7 channel PMID: 27129258
Mutant cycle analysis with modified saxitoxins reveals specific interactions critical to attaining high-affinity inhibition of human NaV1.7. PMID: 27162340
Postoperative pain was affected by SCN9A genetic variability in gynecological surgical patients. PMID: 26752484
Patients with the SCN9A mutation with inherited erythromelalgia were characterized for the pain phenotype among individuals. PMID: 26920677
These findings provided evidence that the variability of basal pain sensitivity was associated with SCN9A polymorphisms in the general population. PMID: 26168879
Nav1.7 deletion has profound effects on gene expression, leading to an upregulation of enkephalin precursor Penk mRNA and met-enkephalin protein in sensory neurons. PMID: 26634308
Association of SCN9A variants with neuropathic pain and pain severity suggests a role of SCN9A in the disease etiology of neuropathic pain PMID: 25585270
We report the case of a 6-year-old girl with a SCN9A mutation who presented with both gain of function and loss of function phenotypes, including congenital corneal anesthesia. PMID: 26486037
the activity of mutant Nav1.7 channels in smooth muscle cells of skin vasculature and innervating sensory and sympathetic fibers contribute to the skin reddening PMID: 25957174
The co-segregation of the I739V variant in the affected members of the family provides evidence, for the first time, that paroxysmal itch can be related to a mutation in sodium channel gene. PMID: 24820863
Novel SCN9A mutations altering Nav1.7 channel activation were found families with inherited erythromelalgia, paroxysmal extreme pain disorder and congenital insensitivity to pain. PMID: 25995458
NaV1.7 is expressed in both dorsal root ganglion neurons and pancreatic beta cells.Vulnerability of dorsal root ganglia neurons due to NaV1.7 mutations increases risk of neuropathy. PMID: 25008557
Our study demonstrates an example of predicting the treatment effect of mexiletine in patients suffering from a specific gain-of-function mutation in NaV1.7 PMID: 24866741
Nav1.7 mutations are associated with pain syndromes including erythromelalgia. PMID: 25575597
The novel p.L1612P Nav1.7 mutation expands the paroxysmal extreme pain disorder spectrum with a unique combination of clinical symptoms and electrophysiological properties PMID: 25285947
PKC can increase sodium resurgent currents through phosphorylation of a conserved Serine residue located in the domain III-IV linker of hNav1.7 PMID: 25240195
Sodium channel Nav1.7, encoded by SCN9A, is expressed in DRG neurons and regulates their excitability. PMID: 25209274
Recent studies have shown that mutations in the SCN9A gene are the cause of a subgroup of idiopathic small fiber neuropathies and that polymorphisms of SCN9A are associated with an increase in susceptibility to pain. PMID: 24202110
This study show a linear correlation between the level of Nav1.7 conductance and current threshold in DRG neurons. PMID: 24401712
EGF/EGFR-mediated upregulation of Nav1.7 is necessary for invasive behaviour in these cells. PMID: 23986482
A working link between nociception and olfaction via Nav1.7 in the gain-of-function direction. PMID: 23874707
persistent and resurgent currents are likely to determine whether a mutation in Nav1.7 leads to IEM or PEPD. PMID: 24311784
This study demonstrated that a variant of NaV1.7 associated with painful neuropathy depolarizes resting membrane potential and produces an enhanced inward current during interspike intervals, thereby contributing to DRG neuron hyperexcitability PMID: 23850641
Role of the SCN9A mutations in genetic epilepsy with febrile seizures plus and Dravet syndrome PMID: 23895530
2 gain-of-function mutations in the 4th domain of Nav1.7, A1746G & W1538R, caused hyperpolarization and affected age of erythromelalgia onset. PMID: 23292638
Data indicate that micro-SLPTX-Ssm6a, a unique 46-residue peptide from centipede venom, potently inhibits NaV1.7. PMID: 24082113
a novel regulatory mechanism that utilizes CRMP2 SUMOylation to choreograph NaV1.7 trafficking. PMID: 23836888
More patients have suffered dyskinesis pain. A 3448 (C/T) mutation of SCN9A gene may be related to pathogenesis of pain in Parkinsonism. PMID: 23450472
A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockers. PMID: 23383113
Structural and functional demonstration of the importance of radial tuning of the sodium channel S6 helix for the channel activation. PMID: 23536180
Patients carrying the SCN9A 3312Tallele presented with lower postoperative pain sensitivity in the presence of a similar surgical pain stimulus PMID: 23364568
We identified a novel homozygous mutation in SCN9A from 2 Japanese families with autosomal recessive hereditary sensory and autonomic neuropathy type IId. PMID: 23596073
We also found a splicing junction variant of SCN91 in all 19 patients WITH enital insensitivity to pain PMID: 23129781
In small-fiber neuropathy, [isoleucine]228[methionine] variant Nav1.7 channel contributes to impaired regeneration and degeneration of sensory axons. PMID: 23280954
Structural modelling reveals that Na(v)1.7-S241T is ~2.4 A apart from V400M in the folded channel, and thermodynamic analysis demonstrates energetic coupling of V400M and S241T during activation. PMID: 23149731
These data strongly suggest that pain perception in at least a subset of patients with interstitial cystitis/bladder pain syndrome is influenced by the rs6746030 polymorphism in the SCN9A voltage-gated sodium channel. PMID: 23102778
Splicing can change the way that Na(V) channels interact with beta subunits. PMID: 22911851
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相關(guān)疾病:
Primary erythermalgia (PERYTHM); Indifference to pain, congenital, autosomal recessive (CIP); Paroxysmal extreme pain disorder (PEPD); Generalized epilepsy with febrile seizures plus 7 (GEFS+7); Febrile seizures, familial, 3B (FEB3B)
Expressed strongly in dorsal root ganglion, with only minor levels elsewhere in the body, smooth muscle cells, MTC cell line and C-cell carcinoma. Also expressed in vagus nerves within the head and neck region. Isoform 1 is expressed preferentially in the