hSCN9A Mouse
製品名
hSCN9A Mouse
製品ID
C002105
系統名
C57BL/6NCya-Scn9atm2(hSCN9A)/Cya
背景情報
C57BL/6NCya
状況
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製品タイプ
年齢
遺伝子型
性別
数量
遺伝子名
遺伝子別名
PN1, ETHA, NENA, SFNP, FEB3B, NE-NA, GEFSP7, HSAN2D, Nav1.7
NCBI ID
染色体
Chr 2
MGI ID
さらに
系統詳細
The SCN9A gene encodes the sodium channel protein Nav1.7 and is closely associated with peripheral neuropathic pain and several related rare genetic disorders. The Nav1.7 sodium channel mediates the flow of sodium ions across the cell membrane and plays an important role in the generation and transmission of electrical signals in neurons. Studies have shown that genetic variants in SCN9A are closely associated with several inherited pain disorders, including inherited erythromelalgia (IEM), small fiber neuropathy (SFN), and congenital insensitivity to pain (CIP) [1-2]. As a voltage-gated sodium channel, Nav1.7 is mainly expressed in sensory and sympathetic neurons of the peripheral nervous system and is highly expressed in the dorsal root ganglia (DRG), where it plays a critical role in the generation and transmission of pain signals [3]. Studies have suggested that downregulation of SCN9A expression or selective inhibition of Nav1.7 may represent a potential analgesic strategy for investigating acute, inflammatory, and neuropathic pain [4].
The hSCN9A Mouse is a humanized Scn9a model. The coding sequences of exon 2 plus partial intron 2 of mouse Scn9a were replaced with the Kozak-Human SCN9A CDS-3'UTR of Human SCN9A-WPRE-BGH pA cassette. Its applications mainly include mechanistic studies of inherited erythromelalgia (IEM), small fiber neuropathy (SFN), and congenital insensitivity to pain (CIP), as well as the exploration of therapeutic strategies targeting human Nav1.7. This model may be used to evaluate the potential effects of Nav1.7 inhibitors, antisense nucleic acid-based approaches, and gene therapies and to support drug screening and pharmacological evaluation for SCN9A-related disorders.
参考文献
Ghanty I, Perez-Palma E, Villaman C, et al. SCN9A should not be considered an epilepsy gene; Refuting a gene-disease association. Epilepsia. 2025;66(9):3516-3527.
Gomez K, Stratton HJ, Duran P, et al. Identification and targeting of a unique NaV1.7 domain driving chronic pain. Proc Natl Acad Sci U S A. 2023;120(32):e2217800120.
Waxman SG. NaV1.7: A central role in pain. Neuron. 2023;111(17):2615-2617.
Sutemieva JA, Sobenin DV. Voltage-gated sodium channels in pain: Which channels, which blockers, and where NaV1.7 fits. Prog Biophys Mol Biol. 2026;200:138-162.
系統作製戦略
The coding sequences of exon 2 plus partial intron 2 of mouse Scn9a were replaced with the Kozak-Human SCN9A CDS-3'UTR of Human SCN9A-WPRE-BGH pA cassette.
Figure 1. Gene editing strategy of hSCN9A mice.
適用分野
Analgesic Drug Screening: Used to evaluate the potential analgesic effects and safety of therapeutic strategies targeting human Nav1.7, including small-molecule inhibitors, antisense oligonucleotides/PNA approaches, and gene therapies;
Mechanistic Studies of Inherited Erythromelalgia (IEM): Used to investigate the mechanisms associated with gain-of-function variants of human Nav1.7 in inherited erythromelalgia (IEM) and to explore potential therapeutic strategies;
Congenital Insensitivity to Pain (CIP) Studies: Used to investigate the mechanisms associated with loss-of-function variants of human Nav1.7 in congenital insensitivity to pain (CIP), as well as the molecular mechanisms underlying impaired pain signal transmission;
Small Fiber Neuropathy (SFN) Studies: Used to investigate the pathological mechanisms of SCN9A variant-associated small fiber neuropathy (SFN) and to explore potential therapeutic targets.
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