"We further showed that VPA downregulated the expression of methyl-CpG-binding domain protein 2 (MBD2) at the posttranscriptional level and knockdown of MBD2 increased Scn3a expression."
"We further showed that VPA downregulated the expression of methyl-CpG-binding domain protein 2 (MBD2) at the posttranscriptional level and knockdown of MBD2 increased Scn3a expression."
"Knockdown of MBD2 in mouse N1E-115 cells led to the -39 C methylation and the downregulation of Scn3a transcription by decreasing the Scn3a promoter activity."
"We found that miR-30b directly targeted SCN3A 3 ' UTR both in vitro and in vivo, and that miR-30b alleviated neuropathic pain by suppressing the expression of Nav1.3 in DRG neurons and spinal cord following SNL."
"However, it did address the fact that miR-30b directly regulated SCN3A and further demonstrated that miR-30b had a potential use for the therapy invention for the treatment of neuropathic pain."
"However, miR-30b overexpression, by transfecting miR-30b agomir, reversed the up-regulation of SCN3A and Nav1.3 and attenuated the down-regulation of miR-30b."
"Furthermore, VPA, instead of other two anticonvulsant drugs, induced the expressions of Scn3a and Mbd2 and reduced Fto expression in the hippocampus of VPA treated seizure mice."
"Whereas TTX inhibited glucagon secretion at 1 mm glucose in Scn3a +/- islets, it was without inhibitory effect in Scn3a - / - islets : if anything, it tended to stimulate glucagon secretion, possibly reflecting relief from paracrine inhibition."
"It is known that SCN1A (Smith et al., 1998), SCN2A (Noda et al., 1986; Suzuki et al., 1988; Smith et al., 1998), SCN3A (Suzuki et al., 1988), and SCN8A (Smith et al., 1998) alpha subunits bind tetrodotoxin and STX with comparable affinities."
"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-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."
"Lower levels of SCN1A, SCN2A, SCN3A, SCN4A and SCN8A expression have also been reported in heart and shown to contribute approximately 23% of the total functional sodium channels in mouse ventricular myocytes and 27% in human atrial myocytes, based on TTX sensitivity."
"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."
"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)."
"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)."
"These findings indicate that SCN3A might be repressed by the LSD1 corepressor complex through a mechanism similar to that reported in HeLa cells 14,26 and that PHF21A might be similarly required for LSD1 promoter occupancy in lymphoblasts."
"In support of this hypothesis, ChIP results showed a significant reduction of LSD1 binding to the SCN3A promoter in DGAP012 and MCN1762 cells compared to normal control cells ( Figure 6 C)."
"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."
"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."
"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."
"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."
"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."
"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."
"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."
"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."
"Scn1b null ventricular CMs exhibit prolonged AP repolarization, increased Scn5a/Na v 1.5 gene and protein expression, increased Scn3a expression, increased transient and persistent I Na density, and prolonged QT and RR intervals."
"It is known that SCN1A (Smith et al., 1998), SCN2A (Noda et al., 1986; Suzuki et al., 1988; Smith et al., 1998), SCN3A (Suzuki et al., 1988), and SCN8A (Smith et al., 1998) alpha subunits bind tetrodotoxin and STX with comparable affinities."
"It is known that SCN1A (Smith et al., 1998), SCN2A (Noda et al., 1986; Suzuki et al., 1988; Smith et al., 1998), SCN3A (Suzuki et al., 1988), and SCN8A (Smith et al., 1998) alpha subunits bind tetrodotoxin and STX with comparable affinities."
"Using Target Scan software, we discovered that SCN3A is the major target of miR-30b, and we then determined whether miR-30b regulated the expression of Nav1.3 by transfecting miR-30b agomir through the stimulation of TNF-alpha or by transfecting miR-30b antagomir in primary dorsal root ganglion (DRG) neurons."
"Even though the relative expression of Na V 1.3 and Na V 1.7 differs in insulin secreting beta cells, with Na V 1.7 being the dominant subtype, it has been shown that knocking out the sodium voltage gated channel alpha subunit 3 Scn3A (part of Na V 1.3 channel) reduces glucose stimulated insulin secretion in mice [XREF_BIBR]."
"It is known that SCN1A (Smith et al., 1998), SCN2A (Noda et al., 1986; Suzuki et al., 1988; Smith et al., 1998), SCN3A (Suzuki et al., 1988), and SCN8A (Smith et al., 1998) alpha subunits bind tetrodotoxin and STX with comparable affinities."
"In support of this hypothesis, ChIP results showed a significant reduction of LSD1 binding to the SCN3A promoter in DGAP012 and MCN1762 cells compared to normal control cells ( Figure 6 C)."
"XREF_BIBR Scn3a is obviously important in insulin secretion, since genetic ablation of Scn3a reduces insulin secretion, while genetic ablation of Scn9a does not affect insulin secretion."
"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."
"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."
"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."
"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."
"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."
"The molecular mechanisms of this modulation require further investigation to know if Nav1.3 is directly phosphorylated by PKC such as the Nav1.8 subunit [47]."
"MeJA treatment resulted in the higher transcript level of PhCAD3, PhCAD4, and NAC3 after actinomycin D treatment which indicated that MeJA increased the mRNA stability of PhCAD3, PhCAD4, and NAC3 up to 1.61-, 1.9-, and 2.46-fold, respectively, after 2 h."
"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."
"We found that de-conjugation of SUMO-2/3 led to de-repression, loss of promoter occupancy by CoREST1 and LSD1, increased H3K4 methylation, and increased H3 acetylation of the SCN1A and SCN3A genes, but did not affect another CoREST1 and LSD1 target gene, SCN2A2."
"In GRNII, the master regulators of ABA signaling GBF2, GBF3, ABF3 and ABF4, and the senescence inducing NAC factors NAP, NAC6 and ORE1 and ATAF1 as well as NAC047 and NAC3 could bind these motifs."
"In GRNII, the master regulators of ABA signaling GBF2, GBF3, ABF3 and ABF4, and the senescence inducing NAC factors NAP, NAC6 and ORE1 and ATAF1 as well as NAC047 and NAC3 could bind these motifs."
"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 ."
"In GRNII, the master regulators of ABA signaling GBF2, GBF3, ABF3 and ABF4, and the senescence-inducing NAC factors NAP, NAC6/ORE1 and ATAF1 as well as NAC047 and NAC3 could bind these motifs (Supplementary Figure xref and Dataset xref ; xref ; xref ; xref ; xref ; xref )."
"We discuss the association of SCN2A, SCN3A, GRB14, COBLL1 and SCL38A11 deletions with ASD and Tourette syndrome and possible implications for treatment."
"In GRNII, the master regulators of ABA signaling GBF2, GBF3, ABF3 and ABF4, and the senescence inducing NAC factors NAP, NAC6 and ORE1 and ATAF1 as well as NAC047 and NAC3 could bind these motifs."
"In GRNII, the master regulators of ABA signaling GBF2, GBF3, ABF3 and ABF4, and the senescence inducing NAC factors NAP, NAC6 and ORE1 and ATAF1 as well as NAC047 and NAC3 could bind these motifs."
"Furthermore, administration of KD generates beta-hydroxybutyric acid which rescues the abnormal expressions of Scn1a and Scn3a by weakening the GAPDH 's binding to the element."