Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A) ELISA Kits

Cow (Bovine) Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A) Interaktionspartner

1. TNF-alpha (zeige TNF ELISA Kits) up-regulates NaV1.7 mRNA in both adrenal chromaffin cells and dorsal root ganglia (DRG) neurons, highlighting the peripheral nociceptive mechanism of TNF-alpha (zeige TNF ELISA Kits)

2. Findings suggest that the endothelin-1 (zeige EDN1 ELISA Kits)-induced down-regulation of NaV1.7 (SCN9A) diminishes NaV1.7-related catecholamine secretion and dephosphorylation of tau.

3. Nav1.7-Ca2 (zeige CA2 ELISA Kits)+ influx-induced increased phosphorylations of extracellular signal-regulated kinase (ERK (zeige MAPK1 ELISA Kits)) and p38 (zeige MAPK14 ELISA Kits) attenuate tau phosphorylation via glycogen synthase kinase-3beta: priming of Nav1.7 gating by ERK (zeige MAPK1 ELISA Kits) and p38 (zeige MAPK14 ELISA Kits)

4. constitutively phosphorylated/activated ERK (zeige MAPK1 ELISA Kits) destabilizes Na(+) channel alpha-subunit (zeige POLG ELISA Kits) mRNA via translational event, which negatively regulates steady-state level of alpha-subunit (zeige POLG ELISA Kits) mRNA and cell surface expression of functional Na(+) channels.

5. Na influx via scn9a converged on inhibitory phosphorylation of glycogen synthase kinase-3beta, decreasing tau phosphorylation

Mouse (Murine) Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A) Interaktionspartner

1. Nav1.7, known to regulate opioid receptor efficacy, interacts with the G protein-regulated inducer of neurite outgrowth (Gprin1), an opioid receptor-binding protein, demonstrating a physical and functional link between Nav1.7 and opioid signalling.

2. the NaV1.7 channel is an important mechanism underlying hyperalgesia

3. Voltage-gated sodium channel Nav1.7 controls the efficacy and balance of heterotrimeric guanine nucleotide-binding protein-coupled receptor (GPCR)-mediated pro- and antinociceptive intracellular signaling.

4. the FGF13 (zeige FGF13 ELISA Kits)/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals

5. this paper shows that Nav1.7, by coupling with CRMP1 (zeige CRMP1 ELISA Kits), mediates the axonal retrograde signaling of Sema3A (zeige SEMA3A ELISA Kits) in axonal guidance

6. Experiments show that integration of synaptic inputs over time by Nav1.7 is critical for body weight regulation and reveal a mechanism for synaptic control of circuits regulating long term homeostatic functions.

7. Nav1.7 deletion has profound effects on gene expression, leading to an upregulation of enkephalin precursor Penk (zeige PENK ELISA Kits) mRNA and met-enkephalin protein in sensory neurons.

8. Global Nav1.7 knockouts showed no defects in mechanical sensitivity or overall movement yet were completely insensitive to painful tactile, thermal, and chemical stimuli and were anosmic.

9. Sodium channel Nav1.7, encoded by SCN9A, is expressed in DRG neurons and regulates their excitability.

10. a novel regulatory mechanism that utilizes CRMP2 (zeige DPYSL2 ELISA Kits) SUMOylation to choreograph NaV1.7 trafficking.

Human Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A) Interaktionspartner

1. Nav1.7 is a substrate for Fyn (zeige FYN ELISA Kits) kinase.

2. This study demonstrated that the higher expression Nav1.7 in human Dorsal Root Ganglion Neurons.

3. cross-talk between distinct CRMP2 (zeige DPYSL2 ELISA Kits) posttranslational modifications is a key factor in determining NaV1.7 trafficking and localization

4. Authors introduced mutations into Nav1.7 and Nav1.6 (zeige SCN8A ELISA Kits) that either enhance or impair slow inactivation (SI) in order to investigate their effects on resurgent currents. The results show that enhanced SI is accompanied by impaired resurgent currents, which suggests that SI may interfere with open-channel block.

5. 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.

6. We exploited existing technologies in a novel manner to identify selective antagonists of NaV1.7. A full-deck high-throughput screen was developed for both NaV1.7 and cardiac NaV1.5 channels using a cell-based membrane potential dye FLIPR assay

7. Genetic polymorphisms of SCN9A are associated with protection for severe neuropathy induced by oxaliplatin in digestive cancer.

8. the results of this study provide mechanistic evidence for a time-dependent increase in intracellular [Ca2 (zeige CA2 ELISA Kits)+]i and energetic compromise in the neurites of dorsal root ganglia neurons expressing G856D mutant Nav1.7 channels.

9. the FGF13 (zeige FGF13 ELISA Kits)/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals

10. 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.