| + |
POU4F1 | up-regulates quantity by expression 
transcriptional regulation
|
SCN9A |
0.303 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253465 |
|
|
Mus musculus |
Neuroblastoma Cell |
| pmid |
sentence |
| 24493753 |
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. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
FGF11 | down-regulates activity 
binding
|
SCN9A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253426 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 20679355 |
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. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FGF12 | down-regulates activity
binding
|
SCN9A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253424 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 20679355 |
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. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FGF13 | down-regulates activity
binding
|
SCN9A |
0.366 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253423 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 20679355 |
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. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ESR1 | down-regulates quantity by repression 
transcriptional regulation
|
SCN9A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253469 |
|
|
Mus musculus |
Neuron |
| pmid |
sentence |
| 22169964 |
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 |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Tissue: |
Spinal Ganglion |
| + |
SCN9A | up-regulates
|
Action_potential |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253449 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26043074 |
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. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NEDD4L | down-regulates quantity by destabilization
ubiquitination
|
SCN9A |
0.341 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253458 |
|
|
Mus musculus |
Neuron |
| pmid |
sentence |
| 23778145 |
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). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
AR | up-regulates quantity by expression 
transcriptional regulation
|
SCN9A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253466 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 24493753 |
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. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ESR2 | down-regulates quantity by repression
transcriptional regulation
|
SCN9A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253473 |
|
|
Mus musculus |
Neuron |
| pmid |
sentence |
| 22169964 |
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 |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Tissue: |
Spinal Ganglion |
| + |
TNF | up-regulates activity
|
SCN9A |
0.254 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253488 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
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. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
NGF | up-regulates quantity by expression
transcriptional regulation
|
SCN9A |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253495 |
|
|
Rattus norvegicus |
Mat-Ly-Lu Cell |
| pmid |
sentence |
| 24493753 |
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 |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN9A |
0.254 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253479 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
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. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
IL10 | down-regulates quantity by repression
transcriptional regulation
|
SCN9A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253498 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 23357618 |
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. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
SCN9A | up-regulates quantity
relocalization
|
sodium(1+) |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253403 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27262167 |
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. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
FGF14 | down-regulates activity
binding
|
SCN9A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253425 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 20679355 |
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. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
SCN9A
- 
- 