mProX™ Human SCN9A Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Ion Channel Cell Lines
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Published Data
Fig.1 Biophysical properties of NaV1.7-1150R and NaV1.7-1150W currents.
Current responses in a whole-cell voltage clamp recording applied at 0.5 Hz for a HEK293 cell expressing Nav1.7-1150W to 50-ms voltage steps of 5-mV increments between −70 and +40 mV from a holding potential of −100 mV.
Ref: Reimann, Frank, et al. "Pain perception is altered by a nucleotide polymorphism in SCN9A." Proceedings of the National Academy of Sciences 107.11 (2010): 5148-5153.
Pubmed: 20212137
DOI: 10.1073/pnas.0913181107
Research Highlights
Mutations causing a gain of function in NaV1.7 result in painful circumstances, whereas mutations causing a loss of function result in total insensitivity to pain. A small number of NaV1.9 mutations have been linked to pain insensitivity, while the majority induce painful disorders. These channels are potential targets for novel analgesic medications due to their important functions in pain and low expression in the heart muscle and central nervous system.
Baker, Mark D., and Mohammed A. Nassar. "Painful and painless mutations of SCN9A and SCN11A voltage-gated sodium channels." Pflügers Archiv-European Journal of Physiology 472 (2020): 865-880.
Pubmed:
32601768
DOI:
10.1007/s00424-020-02419-9
Children with inherited erythromelalgia are more likely to experience severe morbidity and difficult-to-manage pain. The discovery of genotype-phenotype connections will be strengthened by standardized reporting of outcome and management in bigger series. Long-term therapy with higher efficacy are a major unmet therapeutic need.
Arthur, Luke, et al. "Pediatric erythromelalgia and SCN9A mutations: systematic review and single-center case series." The Journal of Pediatrics 206 (2019): 217-224.
Pubmed:
30416015
DOI:
10.1016/j.jpeds.2018.10.024
