OriGene Logo
Left ProductsProducts divider ServicesServices divider technologyTechnology divider researchResearch divider TechsupportTechSupport divider AboutAbout Right

Video overview of cDNA clone offering
Video brochure for cDNA clone
Related Products

Over 1000 citations of OriGene cDNA clones
Epilepsy-associated GRIN2A mutations reduce NMDA receptor trafficking and agonist potency - molecular profiling and functional rescue Sci Rep 2017 [GRIN2A]

Engineering brown fat into skeletal muscle using ultrasound-targeted microbubble destruction gene delivery in obese Zucker rats: Proof of concept design IUBMB Life 2017 [BMP7]

Traditional Chinese medicine, Fuzheng Kang‑Ai decoction, inhibits metastasis of lung cancer cells through the STAT3/MMP9 pathway Mol Med Rep 2017 [PIAS3]

A Novel Egr-1-Agrin Pathway and Potential Implications for Regulation of Synaptic Physiology and Homeostasis at the Neuromuscular Junction Front Aging Neurosci 2017 [EGR1]

View All Citations >>


Human Nav1.7 Stable Cell Line

Human Nav1.7 Stable Cell Line


Human Nav1.7 (SCN9A) is a voltage-gated Na+ channel preferentially expressed in sensory neurones, which plays a key role in the depolarisation phase (upstroke) of the action potential. Mutations in this gene have been associated with primary erythermalgia, channelopathy-associated insensitivity to pain, and paroxysmal extreme pain disorder. Nav1.7 is of interest as a target for novel analgesics.

Essen Bioscience and OriGene have co-developed a stable human Nav1.7 alpha-subunit cell line in human embryonic kidney (HEK293) cells for various functional screening assays.

Submit a request for price and more technical information on cell culture protocol and cell line validation
Catalog #:SCL10001
Description:Human Nav1.7 Stable Cell Line – HEK293
Ref seq. NM_002977.1.
Other names: ETHA; FEB3B; Nav1.7; NE-NA; NENA; PN1
cDNA Clone:OriGene TrueClone SC309017 in pCMV-6-Neo
Format: 2 x 1 mL frozen cell vials each containing 1 x 106 cells
Mycoplasma:Negative by DNA staining and direct culture methods (ATTC – detailed information available upon request)
Cell Line Validation:
  1. Gene expression: qPCR experiments determined specific over-expression of SCN9A.
    Figure 1.
  2. Functional validation
    1. Current-Voltage relationship: activation
      The basic biophysical properties, expression levels, and pharmacology of Nav1.7-HEK293 cells were assessed using the IonWorks planar array electro-physiology platform. Figure 2, Figure 3
    2. Expression stability
      Stable expression of hNav1.7 over multiple cell passages is confirmed. Figure 4, Figure 5
    3. Pharmacology
      Inhibition of hNav1.7 Na+ currents by known Na+ channel blockers such as tetrodotoxin, ProTX-II, tetracaine and lidocaine. Figure 6
Growth Properties:Growth rates and percentage confluency were determined using an IncuCyte (Essen Bioscience) from images taken every 3 h over a 72 h period. The doubling time for the cell line was approximately 20 h for the linear section of the growth curve. Figure 7
Figure 1. qPCR data on specific over-expression of SCN9A
Fig 1
In a SYBR green qPCR experiment, specific over-expression of SCN9A was determined using gene specific primers. Data are shown as fold of over-expression after normalization against GAPDH.
Figure 2. Current-Voltage Relationship: Activation
Fig 2
A) Representative currents obtained by a family of depolarising pulses between -50 and +60 mV from a holding potential of -90 mV
B) Peak I-V relationship (mean ± SEM, n= 67)
C) Normalised G (conductance) -V plot. To ensure appropriate voltage-clamp only cells with peak current amplitudes ranging from 0.4 to 1.2 nA were included. The threshold for activation was -30 mV and peak currents were obtained between 0 and +10 mV). The reversal potential was +60mV, close to the theoretical value of +66mV, calculated using the Nernst equation. From the G-V plot the Boltzmann parameters for activation were: V½ -7.5 mV, slope of 5.4 (mV/e-fold)
Figure 3. Current-Voltage Relationship: Inactivation
Fig 3
The voltage-dependence of inactivation was measured by applying long (1 s) conditioning pulses to varying potentials (-110 to -30 mV) followed by a test pulse to 0 mV. The Boltzmann parameters for inactivation were: V½ -60mV and slope 5.4(mV/e-fold). Currents are normalised to the current evoked by the test pulse following a conditioning potential of -110 mV. Data is presented as mean of 50 cells. SEM are too small to be clearly visible.
Figure 4. Expression Profile
Fig 4
At a step potential of 0mV, peak inward currents of >0.4 nA were observed in 324 of 370 cells (87%), with a mean amplitude of 2.02 ± 1.00 nA (n=324; mean ± S.D.). The maximum current evoked from a depolarising pulse to 0 mV was divided into 0.2 nA bins.
Figure 5. Expression Stability
Fig 5
Stable expression of hNav1.7 over multiple cell passages. The ordinate shows the mean (±SD) Na+ current amplitudes obtained from population patch clamp recordings from a Vh of -80mV. Note the stable expression for >35 passages.
Figure 6. Pharmacology
Fig 6
Inhibition of hNav1.7 Na+ currents by known Na+ channel blockers. The IC50 values are close to those previously described: tetrodotoxin (15nM), ProTX-II (4.1nM), tetracaine (6.5M) and lidocaine (262M). Currents were evoked by a 20 ms test pulse to 0mV from a holding potential of -90mV in the absence (control) and presence of inhibitor.
Figure 7. Cell Growth Properties
Fig 7
Images of cells at 60% confluency at low and high (inset) magnification. Growth curve (confluency) for HEK hNav1.7 cells seeded at 10% confluency at 37C measured every 3 h for a total of 72 h.
Inc 5000 Healthcare Company