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hSCN9A Mouse
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hSCN9A Mouse
제품명
hSCN9A Mouse
제품 ID
C002105
품종 계통
C57BL/6NCya-Scn9atm2(hSCN9A)/Cya
Backgroud
C57BL/6NCya
상태
이 마우스 계통을 논문에서 사용할 경우, “hSCN9A Mouse (카탈로그 번호 C002105)은 Cyagen에서 구입하였습니다.”라고 명시해 주시기 바랍니다.
구매 가능한 제품 종류
연령
Genotype
성별
수량
표준 제공 조건은 최소 3마리의 이형접합(heterozygous) 보균자를 보장합니다. 동형접합(homozygous) 보균자 및/또는 특정 성별에 대한 브리딩 서비스도 제공됩니다.
가격 문의
기본 정보
관련 자료
기본 정보
유전자명
유전자 별칭
PN1, ETHA, NENA, SFNP, FEB3B, NE-NA, GEFSP7, HSAN2D, Nav1.7
NCBI ID
염색체
Chr 2
MGI ID
Datasheet
품종 계통 설명
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), congenital insensitivity to pain (CIP), and SCN9A-associated epileptic encephalopathies, 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.
Reference
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.
변형 전략
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.
응용 분야
Analgesic Drug Screening: Used to evaluate the potential analgesic effects and safety of therapeutic strategies targeting human Nav1.7, including small-molecule inhibitors, antisense PNA approaches such as OLP-1002, 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;
SCN9A-Associated Epilepsy and Epileptic Encephalopathy Studies: Used to investigate the mechanisms associated with SCN9A variants in epilepsy and epileptic encephalopathies and to explore the potential role of Nav1.7 in related neurological disorders.
관련 자료
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