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phosphosite cbn pc11 biopax bel_lc signor biogrid lincs_drug tas hprd trrust ctd virhostnet phosphoelm drugbank omnipath | geneways tees isi trips rlimsp medscan sparser eidos reach
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SCN9A affects sodium atom
| 7
SCN9A activates sodium atom.
| 4
| 3
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"Knockout of Scn9a lowers Na + current by> 85%, disclosing a small Scn3a dependent component."
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"Recently, SCN9A gene variants (single amino acid substitutions) have been found in ~ 30% of a cohort of idiopathic SFN patients, producing gain-of-function changes in sodium channel Na (V) 1.7, which is preferentially expressed in small diameter peripheral axons."
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"In beta-cells, knockout of Scn9a lowers the Na + current by> 85%, unveiling a small Scn3a dependent component."
Mutated SCN9A activates sodium atom. 1 / 1
| 1
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"It is therefore conceivable that the SCN9A mutations described here also cause misfolding of the channel which leads to ER retention and hence defective cell surface localization of Na v 1.7."
SCN9A decreases the amount of sodium atom.
| 2
Mutated SCN9A decreases the amount of sodium atom. 2 / 2
| 2
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"These SCN9A mutations caused loss-of-function of Na v 1.7, and therefore the disorder was designated " channelopathy associated insensitivity to pain " (OMIM # 243000)."
reach
"These SCN9A mutations caused loss-of-function of Na v 1.7, and therefore the disorder was designated " channelopathy associated insensitivity to pain " (OMIM # 243000) [20,22,23]."
SCN9A inhibits sodium atom.
| 1
| 1
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"Loss-of-function mutations in SCN9A, which encodes Na V 1.7, a nociceptor specific voltage activated Na + channel, cause a dramatic loss of sensitivity to painful stimuli in humans and mice."
SCN9A affects NAV1
| 3 3
SCN9A binds NAV1.
| 3
| 3
sparser
"In addition, our results also showed that only the mouse forms of NaV1.6, NaV1.7 and NaV1.9 sodium channels were expressed in ND7/23 cells that was originally generated as a hybridoma of rat embryonic DRG and mouse neuroblastoma cell-line."
sparser
"In particular, Nav1.7 has recently emerged as a target of considerable interest, since loss-of-function mutations in SCN9A , the gene that encodes Nav1.7, are associated with congenital insensitivity to pain [ xref - xref ] and gain-of-function mutations have been linked to pain in erythromelalgia [ xref - xref ] and paroxysmal extreme pain disorder (PEPD) [ xref - xref ]."
sparser
"Sodium channel Nav1.7 has emerged as a target of considerable interest in pain research, since loss-of-function mutations in SCN9A , the gene that encodes Nav1.7, are associated with a syndrome of congenital insensitivity to pain, gain-of-function mutations are linked to the debiliting chronic pain conditions erythromelalgia and paroxysmal extreme pain disorder, and upregulated expression of Nav1.7 accompanies pain in diabetes and inflammation."
SCN9A activates NAV1.
| 2
SCN9A activates NAV1. 1 / 1
| 1
reach
"These preliminary findings reported herein, when combined with the previously reported efficacy of the active ingredient of TV-45070 in IEM patients where the mutations in the SCN9A gene are known to cause a gain-of-function of Nav1.7 channel, support the continued evaluation of the R1150W polymorphism in larger clinical studies in common disorders of pain."
Mutated SCN9A activates NAV1. 1 / 1
| 1
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"Due to the strong dependence of the action potential on Nav1.7 in nociceptive neuron cells, molecular alterations in Nav1.7 caused by SCN9A mutations can lead to nociceptive dysfunction."
SCN9A inhibits NAV1.
| 1
SCN9A inhibits NAV1. 1 / 1
| 1
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"Congenital insensitivity to pain (OMIM 243000) is an extremely rare disorder caused by loss-of-function mutations in SCN9A encoding Nav1.7."
SCN9A affects sodium(1+)
1 | 4
SCN9A activates sodium(1+).
| 3
| 3
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"The SCN9A sodium channel, if active, allows entry of sodium into the cells and then promotes plasma membrane depolarization."
reach
"SCN9A belongs to the sodium channel gene family and mediates the voltage dependent sodium ion permeability of excitable membranes."
reach
"Recently, SCN9A gene variants (single amino acid substitutions) have been found in ~ 30% of a cohort of idiopathic SFN patients, producing gain-of-function changes in sodium channel Na (V) 1.7, which is preferentially expressed in small diameter peripheral axons."
SCN9A inhibits sodium(1+).
| 1
Mutated SCN9A inhibits sodium(1+). 1 / 1
| 1
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"XREF_BIBR In contrast to gain of function mutations in PE, functional studies have shown that SCN9A mutations in PEPD impair the fast inactivation of sodium channels leading to a persistent sodium current."
SCN9A increases the amount of sodium(1+).
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SCN9A increases the amount of sodium(1+). 1 / 1
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signor
"Voltage-gated Na1 channels (NaV channels) drive the rapid upstroke of action potentials in cardiac and skeletal muscle and in most neurons, thereby serving as initiators of electrical activity in excitable tissue. Nine genes encode a family of homologous of NaV channel pore-forming a subunits. While channels are open, Na1 ions flux through the central pore down an electrochemical gradient, further depolarizing the membrane and triggering an action potential."
NFkappaB affects SCN9A
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NFkappaB increases the amount of SCN9A.
| 3
NFkappaB increases the amount of SCN9A. 3 / 3
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"To assess whether the increase in SCN9A levels induced by an oncogenic stress and by NF-kappaB transcription factors resulted in changes in the plasma membrane potential, we conducted two different approaches."
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"Interestingly, SCN9A levels were upregulated during OIS by the NF-kappaB transcription factors."
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"We determined that the increased expression of SCN9A induced by NF-kappaB transcription factors during OIS resulted in plasma membrane depolarization."
NFkappaB inhibits SCN9A.
| 1
| 1
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"We examined whether or not the inhibition of NF-kappaB transcription factors, either by constitutively expressing a stabilized version of IKBA (mIKBA), a well-known inhibitor of NF-kappaB, or by knocking down the expression of RELA, the main subunit of the NF-kappaB transcription factors, blocked the induction of SCN9A during OIS."
NFkappaB activates SCN9A.
| 1
| 1
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"2.2 NF-kappaB transcription factors mediate the induction of SCN9A during OIS."
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Transcriptionally active hsa-miR-6885-3p decreases the amount of SCN9A. 4 / 4
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biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-548o-3p decreases the amount of SCN9A. 4 / 4
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biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-548c-3p decreases the amount of SCN9A. 4 / 4
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biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-532-3p decreases the amount of SCN9A. 4 / 4
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biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-3977 decreases the amount of SCN9A. 4 / 4
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biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-188-3p decreases the amount of SCN9A. 4 / 4
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biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
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Transcriptionally active hsa-miR-1323 decreases the amount of SCN9A. 4 / 4
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biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
SCN9A affects CD59
| 4
SCN9A activates CD59. 4 / 4
| 4
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"SCN9A driven CIP is typically considered to be an immutable phenomenon, with patients suffering from lifelong painlessness accompanied by a lack of ability to smell."
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"Intriguingly, the clinical features of the CIP patients do not entirely match with previously reported CIP caused by variants in SCN9A."
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"To date, thirteen rare SCN9A alleles causing CIP have been reported, all leading to loss-of-function mutations occurring in coding regions of the gene [XREF_BIBR, XREF_BIBR]."
reach
"CIP is caused by mutations in the SCN9A gene encoding for the Na1.7 channel."
MiR-30b affects SCN9A
| 3
MiR-30b activates SCN9A.
| 2
MiR-30b activates SCN9A. 2 / 2
| 2
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"Based on bioinformatics analysis using TargetScan software, we determined that miR-30b directly targets SCN9A To investigate the roles of Nav1.7 and miR-30b in neuropathic pain, we examined changes in the expression of Nav1.7 in the dorsal root ganglion by miR-30b over-expression or knockdown in rats with spared nerve injury."
reach
"Based on bioinformatics analysis using TargetScan software, we determined that miR-30b directly targets SCN9A."
MiR-30b decreases the amount of SCN9A.
| 1
MiR-30b decreases the amount of SCN9A. 1 / 1
| 1
reach
"Our data indicate that miR-30b can inhibit Nav1.7 expression by preventing SCN9A transcription in DRGs."
| 3
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sparser
"For example, one study suggested that the SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism was associated with severe symptoms of FM. xref "
sparser
"The SCN9A gene, which encodes the Nav1.7 voltage-gated sodium channel, is associated with different abnormal pathophysiological conditions, such as human pain sensitivity xref , xref ."
Sodium_channels activates SCN9A.
| 1
sparser
"We previously demonstrated that veratridine-induced NaV1.7 sodium channel activation caused intracellular calcium elevation, catecholamine secretion and tau dephosphorylation in adrenal chromaffin cells."
SCN9A affects EGFP
| 3
| 3
sparser
"As a control, cells were also transfected with the empty pN1EGFP vector (EGFP)."
sparser
"The PCR product was digested with XhoI and BglII and ligated into the XhoI‐BamHI digested pN1EGFP expression plasmid (Clontech)."
sparser
"As controls, cells were transfected with the empty pN1EGFP vector or mock transfected."
NAV1 affects SCN9A
| 3
| 3
sparser
"In addition, our results also showed that only the mouse forms of NaV1.6, NaV1.7 and NaV1.9 sodium channels were expressed in ND7/23 cells that was originally generated as a hybridoma of rat embryonic DRG and mouse neuroblastoma cell-line."
sparser
"In particular, Nav1.7 has recently emerged as a target of considerable interest, since loss-of-function mutations in SCN9A , the gene that encodes Nav1.7, are associated with congenital insensitivity to pain [ xref - xref ] and gain-of-function mutations have been linked to pain in erythromelalgia [ xref - xref ] and paroxysmal extreme pain disorder (PEPD) [ xref - xref ]."
sparser
"Sodium channel Nav1.7 has emerged as a target of considerable interest in pain research, since loss-of-function mutations in SCN9A , the gene that encodes Nav1.7, are associated with a syndrome of congenital insensitivity to pain, gain-of-function mutations are linked to the debiliting chronic pain conditions erythromelalgia and paroxysmal extreme pain disorder, and upregulated expression of Nav1.7 accompanies pain in diabetes and inflammation."
EGFP affects SCN9A
| 3
| 3
sparser
"As a control, cells were also transfected with the empty pN1EGFP vector (EGFP)."
sparser
"The PCR product was digested with XhoI and BglII and ligated into the XhoI‐BamHI digested pN1EGFP expression plasmid (Clontech)."
sparser
"As controls, cells were transfected with the empty pN1EGFP vector or mock transfected."
Neoline affects SCN9A
| 2
| 2
eidos
"Like GJG and PA , neoline could inhibit Nav1.7 VGSC current ."
eidos
"In the present study , we investigated whether GJG , PA , and neoline could inhibit Nav1.7 voltage-gated sodium channel ( VGSC ) current and whether neoline could ameliorate mechanical hyperalgesia in diabetic mice ."
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Transcriptionally active hsa-miR-4263 decreases the amount of SCN9A. 2 / 2
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biopax:mirtarbase
No evidence text available
biopax:mirtarbase
No evidence text available
TNF affects SCN9A
2 |
TNF increases the amount of SCN9A.
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Transcriptionally active TNF increases the amount of SCN9A. 1 / 1
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signor
"TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels."
TNF activates SCN9A.
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TNF activates SCN9A. 1 / 1
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signor
"TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels."
SCN9A affects pyraclofos
| 2
| 2
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"The age of onset of the symptoms has been correlated with Na+ channel voltage activation produced by pathogenic SCN9A variants."
reach
"For example, several missense SNPs in the SCN9A gene increase activity of its protein product voltage gated sodium Nav1.7 and are associated with primary erythromelalgia, paroxysmal extreme pain disorder and osteoarthritic pain [XREF_BIBR - XREF_BIBR]."
SCN9A affects channel mRNA
| 2
SCN9A inhibits channel mRNA.
| 1
Mutated SCN9A inhibits channel mRNA. 1 / 1
| 1
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"Mutation of the SCN9A truncates the channel protein or impairs splicing signals to prevent the production of channel mRNA [XREF_BIBR]."
SCN9A activates channel mRNA.
| 1
Mutated SCN9A activates channel mRNA. 1 / 1
| 1
reach
"Mutation of the SCN9A truncates the channel protein or impairs splicing signals to prevent the production of channel mRNA [XREF_BIBR]."
| 2
SCN9A inhibits cell migration.
| 1
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"TTX and SCN9A siRNA significantly inhibited cell migration (P < 0.01, respectively) and horseradish peroxidase uptake (P < 0.01, respectively)."
SCN9A activates cell migration.
| 1
reach
"SCN9A silencing inhibited cell migration, while not affecting cell proliferation."
| 2
sparser
"For example, one study suggested that the SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism was associated with severe symptoms of FM. xref "
sparser
"The SCN9A gene, which encodes the Nav1.7 voltage-gated sodium channel, is associated with different abnormal pathophysiological conditions, such as human pain sensitivity xref , xref ."
SCN9A affects NUP85
| 2
SCN9A inhibits NUP85.
| 1
SCN9A inhibits NUP85. 1 / 1
| 1
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"As the NUP85-SEH1 interaction is structurally very similar to the NUP145C-SEC13 pair, it is also conceivable that the loss of NENA causes a partial displacement of NUP85 by NUP145-SEC13, which in turn could lead to the increased degradation of NUP85."
SCN9A binds NUP85.
| 1
| 1
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"Additionally, positive interaction of L. japonicus NUP85 and NENA (SEH1) in yeast-two-hybrid analysis is consistent with the arrangement of the homologous proteins in the S. cerevisiae NUP84 complex."
SCN9A affects MAVS
| 2
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sparser
"The pEGFP-STAT1 and pN1-IPS-1 plasmids were constructed by PCR amplification of STAT1 and IPS-1 genes from the full-length cDNA clones (ATCC IMAGE clone ID 3627218 and ID 5751684, respectively), and subsequently cloned into pEGFP-N1 vector."
sparser
"HEK293T cells were seeded in 24-well plates and transfected with various combinations of plasmids DNA: the pEFneo-RIG-I, pEFneo-MDA5, pN1-IPS-1, pEFneo-TBK1, pEFneo-IKKɛ, pcDNA3-TRIF, or pCAGGS-IRF3 was mixed with a plasmid encoding the PRRSV protein (or empty pCAGGS), luciferase reporter plasmid and pSV40-RL."
SCN9A affects ITCH
| 2
SCN9A activates ITCH. 2 / 2
| 2
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"An SCN9A variant, known to cause pain, is now found to cause itch."
reach
"We describe a kindred characterized by paroxysmal itch caused by a variant in SCN9A gene encoding for the Nav1.7 sodium channel."
NOVA proteins affects SCN9A
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NOVA proteins increases the amount of SCN9A.
| 1
NOVA proteins increases the amount of SCN9A. 1 / 1
| 1
reach
"Depletion of the NOVA proteins causes exon 17a skipping and increases SCN9A protein expression in the Nova1/2 null mice."
NOVA proteins decreases the amount of SCN9A.
| 1
NOVA proteins decreases the amount of SCN9A. 1 / 1
| 1
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"Thus, by having opposite effects on NMD inducing exons, the NOVA proteins stimulate Dlg3 expression and inhibit Scn9a expression."
NEDD4L affects SCN9A
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NEDD4L ubiquitinates SCN9A.
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NEDD4L ubiquitinates SCN9A. 1 / 1
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signor
"The control of Nav density at the cell membrane is crucial to ensuring normal neuronal excitability. Navs are subject to posttranslational modifications that may influence their cell membrane availability. Ubiquitylation is a key process that orchestrates the internalization and subsequent degradation or recycling of Navs. This is accomplished by ubiquitin protein ligases, such as NEDD4-2 (neuronal precursor cell expressed developmentally downregulated-4 type 2)."
NEDD4L decreases the amount of SCN9A.
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NEDD4L decreases the amount of SCN9A. 1 / 1
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signor
"The control of Nav density at the cell membrane is crucial to ensuring normal neuronal excitability. Navs are subject to posttranslational modifications that may influence their cell membrane availability. Ubiquitylation is a key process that orchestrates the internalization and subsequent degradation or recycling of Navs. This is accomplished by ubiquitin protein ligases, such as NEDD4-2 (neuronal precursor cell expressed developmentally downregulated-4 type 2)."
MT1L affects Meltf, NT5C3A, SCN9A, and SERPINE2
| 2
sparser
"Association Between Mortality of Those With PNI and MTF."
sparser
"Association Between Mortality of Those With PNI and MTF."
MAVS affects SCN9A
| 2
| 2
sparser
"The pEGFP-STAT1 and pN1-IPS-1 plasmids were constructed by PCR amplification of STAT1 and IPS-1 genes from the full-length cDNA clones (ATCC IMAGE clone ID 3627218 and ID 5751684, respectively), and subsequently cloned into pEGFP-N1 vector."
sparser
"HEK293T cells were seeded in 24-well plates and transfected with various combinations of plasmids DNA: the pEFneo-RIG-I, pEFneo-MDA5, pN1-IPS-1, pEFneo-TBK1, pEFneo-IKKɛ, pcDNA3-TRIF, or pCAGGS-IRF3 was mixed with a plasmid encoding the PRRSV protein (or empty pCAGGS), luciferase reporter plasmid and pSV40-RL."
LVI affects NT5C3A, SCN9A, and SERPINE2
| 2
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sparser
"In our study, high c-Myc nuclear expression of the overall tumor was significantly associated with sarcomatoid variant, PNI, LVI, lymph node metastasis, distant metastasis and advanced stage grouping, while there was no significant association with gender, age, tumor diameter, divergent differentiation, bilharziasis, necrosis, pathological tumor stage (pT) and recurrence."
sparser
"In our study, high c-Myc nuclear expression of the overall tumor was significantly associated with sarcomatoid variant, PNI, LVI, lymph node metastasis, distant metastasis and advanced stage grouping, while there was no significant association with gender, age, tumor diameter, divergent differentiation, bilharziasis, necrosis, pathological tumor stage (pT) and recurrence."
FGF14 affects SCN9A
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FGF14 inhibits SCN9A.
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FGF14 inhibits SCN9A. 1 / 1
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signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
FGF14 binds SCN9A.
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1 |
signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
FGF13 affects SCN9A
2 | 1
FGF13 inhibits SCN9A.
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FGF13 inhibits SCN9A. 1 / 1
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signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
FGF13 binds SCN9A.
1 | 1
1 | 1
signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
FGF12 affects SCN9A
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FGF12 inhibits SCN9A.
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FGF12 inhibits SCN9A. 1 / 1
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signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
FGF12 binds SCN9A.
1 |
1 |
signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
FGF11 affects SCN9A
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FGF11 inhibits SCN9A.
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FGF11 inhibits SCN9A. 1 / 1
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signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
FGF11 binds SCN9A.
1 |
1 |
signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
ERVK-10 affects SCN9A
| 2
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sparser
"In the current study, we examine how RT may mechanistically inhibit PNI in the context of this new paradigm, emphasizing the importance of considering the dynamic interactions occurring between cancer cells and the nerve microenvironment."
sparser
"In the current study, we elucidate a novel mechanism of how RT may inhibit PNI through the interruption of paracrine interactions between cancer cells and nerves."
| 2 1
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reach
"The recombinant human PN1 currents exhibited rapid activation and inactivation kinetics and were blocked by TTX with a half-maximal inhibitory concentration (IC50) of 32.6 nM."
Recognition process affects SCN9A
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Recognition process activates SCN9A. 1 / 1
| 1
reach
"Activated by the NF recognition process, a secondary messenger causes calcium oscillations in the nucleus responsible by nuclear membranes proteins such as POLLUX, CASTOR, and nuclear pore (NUP85, NUP133, and NENA) XREF_BIBR."
Pain affects SCN9A
| 1
| 1
reach
"SCN9A channelopathy associated autosomal recessive Congenital Indifference to Pain."
P65 affects SCN9A
| 1
SCN9A binds p65. 1 / 1
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sparser
"P-p65 could bind with SCN9A proximal promoter region for primer 2, primer 7, primer 8, primer 9."
MiR-30b-5p affects SCN9A
| 1
MiR-30b-5p activates SCN9A. 1 / 1
| 1
reach
"Finally, Scn9a is modulated by miR-30b-5p, miR-130a-3p, miR-134-5p, and miR-465-5p."
1 |
Transcriptionally active hsa-miR-335-5p decreases the amount of SCN9A. 1 / 1
1 |
biopax:mirtarbase
No evidence text available
Antagonist affects SCN9A
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sparser
"MMP1 silencing with shRNA or treatment with either a PAR1 or an NK1R antagonist inhibited PNI."
UL83 affects SCN9A
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reach
"P-p65 could bind with SCN9A proximal promoter region for primer 2, primer 7, primer 8, primer 9."
TIPN affects SCN9A
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SCN9A binds TIPN. 1 / 1
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reach
"Our aim was to determine the association between TIPN and SCN9A and SCN10A polymorphisms."
SOCS3 affects SCN9A
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sparser
"We observed that low expression of SOCS3 and pN1 in tumors was associated with a poor prognosis independent of other clinical covariates, and the pTNM stage I was associated with a better prognosis compared to pTNM stage IIB (Table  xref )."
SCN9A affects resistance ethionamide treatment
| 1
SCN9A inhibits resistance ethionamide treatment. 1 / 1
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eidos
"Because EthA is natively repressed by EthR , resistance to ethionamide treatment is common ."
SCN9A affects release
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SCN9A inhibits release. 1 / 1
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sparser
"Albeit catecholamines (NE and DA) are not necessary for the analgesic effect of the exercise mice with PNI, once again increased TNF-α levels after PNI could inhibit NE release and exercise could counteract this reduction."
SCN9A affects production
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SCN9A activates production. 1 / 1
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sparser
"PNI activates de novo colony-stimulating factor 1 (CSF1) production in injured sensory neurons, which is transported to the spinal cord and binds to CSF1 receptors on microglia [ xref ]."
| 1
reach
"Indeed, the SCN9A promoter in human PCa PC-3 cells was shown to be activated by NGF [XREF_BIBR]."
SCN9A affects phase
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SCN9A activates phase. 1 / 1
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eidos
"Recently , Bennett et al. further refined the contribution of Nav1.7 to AP generation47 , proposing that Nav1.7 also contributes to the rising phase , consistent with our finding of a slight decrease in AP amplitude when Nav1.7 is knocked out ( Supplementary Table1 ) ."
SCN9A affects peroxidase
| 1
| 1
reach
"TTX and SCN9A siRNA significantly inhibited cell migration (P < 0.01, respectively) and horseradish peroxidase uptake (P < 0.01, respectively)."
SCN9A affects pain
| 1
| 1
reach
"SCN9A channelopathy associated autosomal recessive Congenital Indifference to Pain."
SCN9A affects p65
| 1
SCN9A binds p65. 1 / 1
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sparser
"P-p65 could bind with SCN9A proximal promoter region for primer 2, primer 7, primer 8, primer 9."
| 1
Mutated SCN9A activates localization. 1 / 1
| 1
reach
"It is therefore conceivable that the SCN9A mutations described here also cause misfolding of the channel which leads to ER retention and hence defective cell surface localization of Na v 1.7."
SCN9A affects lidocaine
| 1
| 1
reach
"An example of inherited drug-resistance is demonstrated by the p. 395N> K mutation in the SCN9A gene, which produces an increased resistance to lidocaine."
SCN9A affects growth
| 1
SCN9A inhibits growth. 1 / 1
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sparser
"PNI did not inhibit the growth of normal fibroblasts and also did not inhibit the growth of HT-1080 cells that were seeded onto plastic dishes rather than onto ECM."
SCN9A affects functions
| 1
SCN9A inhibits functions. 1 / 1
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sparser
"Tetrodotoxin or synthetic small interfering RNA targeted for SCN8A and SCN9A inhibited metastatic functions (endocytosis and invasion), but failed to inhibit proliferation in PC-3 cells."
SCN9A affects epsP
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SCN9A activates epsP. 1 / 1
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"Scn9a deletion in AGRP, POMC, or paraventricular hypothalamic neurons reduced EPSP duration, synaptic integration, and altered body weight in mice."
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"The SCN9A channel and plasma membrane depolarization promote cellular senescence through Rb pathway."
SCN9A affects calcium(2+)
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"Taken together, our work delineates a new pathway, which involves the NF-kappaB transcription factor, SCN9A expression, plasma membrane depolarization, increased calcium, the Rb/E2F pathway and mitotic gene repression in the regulation of senescence."
SCN9A affects activation
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SCN9A inhibits activation. 1 / 1
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sparser
"We further demonstrated that PNI significantly inhibited microglial autophagy activation, whereas miR-195 inhibitor treatment increased autophagy activation and suppressed neuroinflammation in vivo and in vitro."
SCN9A affects UL83
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"P-p65 could bind with SCN9A proximal promoter region for primer 2, primer 7, primer 8, primer 9."
SCN9A affects TIPN
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SCN9A binds TIPN. 1 / 1
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"Our aim was to determine the association between TIPN and SCN9A and SCN10A polymorphisms."
SCN9A affects STAT3
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SCN9A activates STAT3. 1 / 1
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sparser
"In addition, the involvement of STAT3 in spinal astrocytes has remained controversial because it has been reported that PNI activates STAT3 in astrocytes and microglia and that intrathecal administration of an inhibitor of JAK, which is an upstream activator of STAT3, suppresses the induction or established tactile allodynia after PNI in rats xref xref xref ."
SCN9A affects SOCS3
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sparser
"We observed that low expression of SOCS3 and pN1 in tumors was associated with a poor prognosis independent of other clinical covariates, and the pTNM stage I was associated with a better prognosis compared to pTNM stage IIB (Table  xref )."
SCN9A affects Rb/E2F
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SCN9A activates Rb/E2F. 1 / 1
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"Taken together, our work delineates a new pathway, which involves the NF-kappaB transcription factor, SCN9A expression, plasma membrane depolarization, increased calcium, the Rb/E2F pathway and mitotic gene repression in the regulation of senescence."
SCN9A affects RPS6
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SCN9A activates RPS6. 1 / 1
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"A similar deletion in DIIS6 of SCN9A was shown to disrupt radial tuning of the domain II S6 helix, with helical displacement of an activation gate residue that pathologically altered activation."
SCN9A affects POMC sh
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SCN9A inhibits POMC sh. 1 / 1
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"Scn9a knock-down in POMC neurons also greatly disrupted the input-output function (POMC sh (Scn9a) : 65.6 +/- 4.5 inputs/AP; Pomc topazFP : 3.2 +/- 0.5 inputs/AP; unpaired t test, p < 0.001; XREF_FIG G)."
SCN9A affects PEPD
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sparser
"In contrast to IE, the SCN9A mutations associated with PEPD alter Na v 1.7 by impairing inactivation of the channel leading to an enhanced persistent current. xref A key unanswered question is why the Na v 1.7 mutations associated with IE and PEPD cause such different phenotypic expression particularly in terms of the distal predominance of symptoms in the former and proximal in the latter."
SCN9A affects PE
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SCN9A activates PE. 1 / 1
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"PE is exclusively caused by mutations in SCN9A, the encoding gene of sodium channel subtype Nav1.7 and can be sub-classified into familial (inherited erythromelalgia) and sporadic forms."
SCN9A affects PAMR1
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SCN9A activates PAMR1. 1 / 1
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"Studies of other mutations in SCN9A (S241T, V400M, A863P, etc.) all showed aforementioned alterations in channel properties and increased ramp currents."
SCN9A affects NUP107-160 subcomplex members
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Modified SCN9A increases the amount of NUP107-160 subcomplex members. 1 / 1
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"Loss of L. japonicus NENA and NUP85 reduced the protein levels of other putative NUP107-160 subcomplex members."
SCN9A affects NGF
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SCN9A activates NGF. 1 / 1
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"SCN9A gene modification can promote the expression of Nav1.8 and Nav1.9 channels, in addition to NGF which may provide a novel therapeutic basis for treating of D-IBS."
SCN9A affects Kir2.2
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SCN9A inhibits Kir2.2. 1 / 1
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"Overexpression of myocardin in iPSC-MSC enhanced the expression of SCN9A and CACNA1C, but reduced that of KCa3.1 and Kir2.2 in iPSC-MSCs."
SCN9A affects IRF5
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SCN9A activates IRF5. 1 / 1
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sparser
"Increases in IRF8 expression after PNI activates IRF5 which binds specifically to the promotor of P2rx4, leading to an upregulation of P2X4 receptor (P2X4R) expression on microglia [ xref , xref ] (see Fig.  xref )."
SCN9A affects HLA-B
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sparser
"Here we utilize multi-attribute positional scan (MAPS) analoging, combining high-throughput synthesis and electrophysiology, to interrogate the interaction of GpTx-1 with NaV1.7 and related NaV subtypes."
SCN9A affects Glu-Met
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Mutated SCN9A activates Glu-Met. 1 / 1
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"We report a 49-year-old male with primary EM caused by SCN9A mutation (p.F216S), in whom an autonomic reflex screening test revealed a mild sudomotor dysfunction."
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sparser
"FMS has also been recently associated with a specific SCN9A polymorphism [ xref ], providing potential additional evidence of convergence between FMS and SFPN."
SCN9A affects FGF14
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signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
SCN9A affects FGF13
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signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
SCN9A affects FGF12
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signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
SCN9A affects FGF11
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signor
"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."
SCN9A affects FAAH
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sparser
"Variants within in the SCN9A and FAAH genes were associated with the risk of pain in PD patients."
SCN9A affects EPSPs
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SCN9A binds EPSPs. 1 / 1
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"Therefore, Scn9a expression is associated with sustained EPSPs and near-perfect synaptic integration properties in several hypothalamic cell types tested here, including AGRP, POMC, and PVH neurons, which are critical regulators of energy homeostasis."
SCN9A affects COIL
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SCN9A activates COIL. 1 / 1
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"After coregistration, NeNa visualizes in real time where the device is located with respect to the head, brain structures, and activated areas, enabling precise placement of the TMS coil over a predefined target region."
SCN9A affects Analgesia
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eidos
"From our understanding , inhibition of Nav1.7 may produce analgesia rather than pain ."
SCN9A affects Action potential
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SCN9A activates Action potential. 1 / 1
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signor
"The expression of voltage-gated sodium channels (NaVs) is a key feature for initiation and conduction of action potentials in excitable tissues and cells such as cardiac and skeletal muscle and neurons."
SCN9A affects ATXN3
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sparser
"Further supporting the notion of C1719 being pathogenic, this conserved cysteine was found mutated (C1756G) in SCN1A in a patient with severe myoclonic epilepsy in infancy ( xref ), an autosomal dominant condition (OMIM 607208) that has also been associated with mutations in SCN9A ( xref )."
POU4F1 affects SCN9A
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Transcriptionally active POU4F1 increases the amount of SCN9A. 1 / 1
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signor
"In neuroblastoma ND7 cells, a nuclear interaction between the developmentally regulated transcription factor Brn-3a and AR resulted in a complex which bound to multiple elements within the promoter region of SCN9A (Nav1.7) and upregulated channel expression."
PLA1A affects SCN9A
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PLA1A inhibits SCN9A. 1 / 1
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"When we plotted normalized fold changes on a log 2 scale, the results demonstrated that Dlg3, Rasgrf1 and Slc4a3 were degraded by NMD in DKO relative to WT mice, while Stx2 and Scn9a degradation by NMD in WT mice was alleviated in NOVA DKO animals (XREF_FIG; XREF_FIG)."
PKC affects SCN9A
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PKC inhibits SCN9A. 1 / 1
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"In contrast, inhibition of PKC with the specific inhibitor Go6976 led to a modest but significant reduction in the percentage of NKX6-1 + cells, suggesting that PKC signaling plays some role in the development of NKX6-1 + progenitors, and that the pathway was already active in our NENA induced population."
PEPD affects SCN9A
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sparser
"In contrast to IE, the SCN9A mutations associated with PEPD alter Na v 1.7 by impairing inactivation of the channel leading to an enhanced persistent current. xref A key unanswered question is why the Na v 1.7 mutations associated with IE and PEPD cause such different phenotypic expression particularly in terms of the distal predominance of symptoms in the former and proximal in the latter."
PA affects SCN9A
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PA inhibits SCN9A. 1 / 1
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eidos
"In the present study , we investigated whether GJG , PA , and neoline could inhibit Nav1.7 voltage-gated sodium channel ( VGSC ) current and whether neoline could ameliorate mechanical hyperalgesia in diabetic mice ."
NUP85 affects SCN9A
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"Additionally, positive interaction of L. japonicus NUP85 and NENA (SEH1) in yeast-two-hybrid analysis is consistent with the arrangement of the homologous proteins in the S. cerevisiae NUP84 complex."
NTRK1 affects SCN9A, and SLC2A2
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"Further to this, WES analysis in probands lacking mutations in OI genes revealed deleterious variants in SCN9A , NTRK1 , and SLC2A2 , which are associated with congenital indifference to pain (CIP) and Fanconi-Bickel syndrome (FBS)."
NT5C3A affects SCN9A, SERPINE2, and TTR
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sparser
"First, our study for the first time indicated that preoperative neutrophil count and nutritional status as prealbumin level and PNI are significantly associated with ≥ grade 3 neutropenia event in cycle 1 of gastric cancer patients receiving CAPEOX/XELOX adjuvant chemotherapy."
NOVA affects SCN9A
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NOVA decreases the amount of SCN9A. 1 / 1
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"Western blot analysis revealed a marked reduction (~ 12-fold) of SCN9a protein in NOVA DKO brain (XREF_FIG), indicating that NOVA normally acts to suppress SCN9a expression at both the RNA and protein levels in the brain."
NOG affects SCN9A
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Transcriptionally active NOG increases the amount of SCN9A. 1 / 1
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biopax:ctd
No evidence text available
NGF affects SCN9A
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Transcriptionally active NGF increases the amount of SCN9A. 1 / 1
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signor
"Long-term (more than 24 h) treatment with nerve growth factor (NGF) upregulated Nav1.7 functional expression in the strongly metastatic MAT-LyLu rat PCa cell line; acute application had no effect"
MiR-30b affects SCN9A
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Modified MiR-30b decreases the amount of SCN9A. 1 / 1
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"MiR-30b over-expression in spared nerve injury rats inhibited SCN9A transcription, resulting in pain relief."
MYOCD affects SCN9A
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Modified MYOCD increases the amount of SCN9A. 1 / 1
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"Overexpression of myocardin in iPSC-MSC enhanced the expression of SCN9A and CACNA1C, but reduced that of KCa3.1 and Kir2.2 in iPSC-MSCs."
MAPK14 affects OPRM1, P2RX3, PTGS2, SCN9A, and TRPV3
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"Expression of TRPV3, OPRM1, P2X3, SCN9A, PTGS2, and MAPK14 were associated with PBI score."
IL10 affects SCN9A
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Transcriptionally active IL10 decreases the amount of SCN9A. 1 / 1
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signor
"Interleukin-10 down-regulates voltage gated sodium channels in rat dorsal root ganglion neurons. Consistent with the electrophysiological results, real-time PCR and western blot revealed that IL-10 (200 pg/ml) down-regulated VGSCs in both mRNA and protein levels and reversed the up-regulation of VGSCs by TNF-α."
HpTx1.HpTx1 affects SCN9A
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HpTx1.HpTx1 inhibits SCN9A. 1 / 1
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eidos
"These data suggested that the observed effect on TTX-S Navcurrents mainly arise from Nav1.7 inhibition by HpTx1.HpTx1 inhibits Nav1.7 currents and enhances Nav1.9 activity.aThe dose-dependent inhibition of hNav1.7 currents by HpTx1 ( n = 7 ) ."
HpTx1 treatment affects SCN9A
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HpTx1 treatment inhibits SCN9A. 1 / 1
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eidos
"Our data suggest that the inhibition of Nav1.7 by HpTx1 treatment may be considered analogous to KO of Nav1.7 to some extent ."
HpTx1 affects SCN9A
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HpTx1 inhibits SCN9A. 1 / 1
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eidos
"HpTx1 inhibits Nav1.7 and activates Nav1.9 but does not affect Nav1.8 ."
HLA-B affects SCN9A
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sparser
"Here we utilize multi-attribute positional scan (MAPS) analoging, combining high-throughput synthesis and electrophysiology, to interrogate the interaction of GpTx-1 with NaV1.7 and related NaV subtypes."
GJG affects SCN9A
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GJG inhibits SCN9A. 1 / 1
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eidos
"In the present study , we investigated whether GJG , PA , and neoline could inhibit Nav1.7 voltage-gated sodium channel ( VGSC ) current and whether neoline could ameliorate mechanical hyperalgesia in diabetic mice ."
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"FMS has also been recently associated with a specific SCN9A polymorphism [ xref ], providing potential additional evidence of convergence between FMS and SFPN."
FYN affects SCN9A
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FYN phosphorylates SCN9A on tyrosine. 1 / 1
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rlimsp
"Nav1.7 is phosphorylated by Fyn tyrosine kinase which modulates channel expression and gating in a cell type-dependent manner."
FAAH affects SCN9A
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sparser
"Variants within in the SCN9A and FAAH genes were associated with the risk of pain in PD patients."
F2R affects SCN9A
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F2R inhibits SCN9A. 1 / 1
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"MMP1 silencing with shRNA or treatment with either a PAR1 or an NK1R antagonist inhibited PNI."
EthR affects SCN9A
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EthR inhibits SCN9A. 1 / 1
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eidos
"Because EthA is natively repressed by EthR , resistance to ethionamide treatment is common ."
ESR2 affects SCN9A
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Transcriptionally active ESR2 decreases the amount of SCN9A. 1 / 1
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signor
"17β-Estradiol regulates the gene expression of voltage-gated sodium channels. . In this study, we investigate the mRNA expressions of Nav channel subtypes mediated differentially by the ERs in the DRGs of wild-type (WT) and estrogen receptor knockout (αERKO and βERKO) mice. In the present study, by means of quantitative real-time PCR, we found that the expressions of Nav1.1, Nav1.7, Nav1.8, and Nav1.9 subtypes were elevated in αERKO and βERKO mice"
ESR1 affects SCN9A
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Transcriptionally active ESR1 decreases the amount of SCN9A. 1 / 1
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signor
"17β-Estradiol regulates the gene expression of voltage-gated sodium channels. . In this study, we investigate the mRNA expressions of Nav channel subtypes mediated differentially by the ERs in the DRGs of wild-type (WT) and estrogen receptor knockout (αERKO and βERKO) mice. In the present study, by means of quantitative real-time PCR, we found that the expressions of Nav1.1, Nav1.7, Nav1.8, and Nav1.9 subtypes were elevated in αERKO and βERKO mice"
EPSPs affects SCN9A
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SCN9A binds EPSPs. 1 / 1
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sparser
"Therefore, Scn9a expression is associated with sustained EPSPs and near-perfect synaptic integration properties in several hypothalamic cell types tested here, including AGRP, POMC, and PVH neurons, which are critical regulators of energy homeostasis."
DPYSL2 affects SCN9A, and UBE2I
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sparser
"Using a rational design strategy, we identified a heptamer peptide harboring CRMP2's SUMO motif that disrupted the CRMP2-Ubc9 interaction, inhibited CRMP2 SUMOylation, inhibited NaV1.7 membrane trafficking, and specifically inhibited NaV1.7 sodium influx in sensory neurons."
DHPS affects SCN2A, SCN3A, and SCN9A
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"Mutations in SCN1A— and to a lesser extent SCN2A , SCN3A , and SCN9A— are associated with a variety of monogenic childhood epilepsies such as DS in humans xref – xref ."
Cxcr5 affects NT5C3A, SCN9A, SERPINE2, and nlr
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sparser
"PNI and NLR were associated with the onset of irAEs."
ATXN3 affects SCN9A
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sparser
"Further supporting the notion of C1719 being pathogenic, this conserved cysteine was found mutated (C1756G) in SCN1A in a patient with severe myoclonic epilepsy in infancy ( xref ), an autosomal dominant condition (OMIM 607208) that has also been associated with mutations in SCN9A ( xref )."
AR affects SCN9A
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Transcriptionally active AR increases the amount of SCN9A. 1 / 1
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signor
"In neuroblastoma ND7 cells, a nuclear interaction between the developmentally regulated transcription factor Brn-3a and AR resulted in a complex which bound to multiple elements within the promoter region of SCN9A (Nav1.7) and upregulated channel expression."