Ask about this productRelated genes to: SCN1B antibody
- Gene:
- SCN1B NIH gene
- Name:
- sodium voltage-gated channel beta subunit 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-14
- Date modifiied:
- 2019-04-23
Related products to: SCN1B antibody
Related articles to: SCN1B antibody
- Macrophage-based cell therapy represents a promising approach to the acute respiratory distress syndrome (ARDS) therapy. This study investigates the potential use of adoptive transfer of siRNA-modified macrophages to influence the progression of ARDS. - Source: PubMed
Publication date: 2026/08/26
Kiseleva ViktoriiaVishnyakova PolinaKosyreva AnnaKarpulevich EvgenyTsvetkov IvanMashkova OlgaKuznetsova MariaBagdasarian AidaKaryagina VictoriaKiselev IvanLokhonina AnastasiaBogoyavlenskaya AnastasiyaKudryavtsev DenisArutyunyan IrinaSoboleva AnnaRyabova AnastasiaElchaninov AndreySukhikh GennadyFatkhudinov Timur - Voltage-gated sodium (Nav) channels are key determinants of neuronal excitability, shaping action potential waveforms, repetitive firing patterns and responses to synaptic inputs, as well as controlling the output of neural circuits and influencing short- and long-term plasticity and homoeostasis. The firing and response properties of mammalian central neurons are highly variable, reflecting differences in the Nav (and other) channels expressed and the synaptic connectivity of the circuits in which the cells participate. Transient (I), persistent (I) and resurgent (I) Nav current components have been distinguished, and considerable progress has been made in defining their roles in regulating the firing properties of central neurons and the mechanisms underlying their generation. In addition, it is well established that native neuronal Nav channels function in macromolecular complexes, comprising a pore-forming α subunit assembled with multiple accessory/auxiliary proteins that influence channel expression, localization and biophysical properties. In mature central neurons, the Nav1.1, Nav1.2 and Nav1.6 α subunits are differentially expressed, together with one or more of the Nav beta (Navβ1-4), intracellular fibroblast growth factor (iFGF11-14), ankyrin (Ankyrin-B, -G, -R) and other auxiliary proteins, generating Nav channels with diverse cell-type- and circuit-specific expression patterns, subcellular distributions, gating properties, and physiological roles. Variants in the genes encoding these Nav α subunits (SCN1A, SCN2A, SCN8A), as well as Navβ1 (SCN1B), iFGFs (FGF12, FGF13, FGF14), ankyrins (ANK1, ANK2, ANK3), and other Nav channel auxiliary and interacting proteins, have been linked to several congenital neurological disorders, including epilepsy and ataxia, as well as to neurodevelopmental, neurodegenerative and psychiatric diseases. - Source: PubMed
Publication date: 2026/08/05
Ransdell Joseph LNerbonne Jeanne M - encodes the β-subunits of the main cardiac voltage-gated sodium channel, Na1.5. Variants are linked to cardiac conduction disease, often with concealed phenotypes. Whether β1-subunits regulate conduction through nanoscale intercalated disc (ID) structures, e.g. perinexi, and ephaptic coupling remains unresolved. - Source: PubMed
Publication date: 2026/06/19
Maisonneuve RowanBain ChandraDennison ClareWarren MarkHoeker Gregory SGourdie Robert GPoelzing Steven - Complex febrile seizures (CFS) confer an elevated risk of epilepsy progression; however, the underlying genetic architecture remains insufficiently characterized in Chinese pediatric populations. This study aimed to delineate the mutational landscape and genotype-phenotype associations in a clinically stratified high-risk febrile seizure cohort. - Source: PubMed
Publication date: 2026/06/05
Deng XiaolongXu YanChen XuePan JuanHuang ShengSun Dan - Fenfluramine is approved for Dravet syndrome and Lennox-Gastaut syndrome (LGS) in children under two years of age and is increasingly used off-label for developmental and epileptic encephalopathies (DEEs). Due to the risk of pulmonary arterial hypertension (PAH) and valvular disease, serial echocardiographic monitoring is required. While fenfluramine-associated cardiac toxicity is well described in adults, data in pediatric patients, especially those under two years of age, remain limited. We report a child under two years of age with SCN1B-related DEE who developed asymptomatic fenfluramine-associated PAH after one year of treatment. Fenfluramine resulted in marked seizure reduction but was discontinued after the detection of PAH. Subsequent echocardiography demonstrated resolution of PAH, accompanied by worsening seizure burden. This case emphasizes the rare occurrence of fenfluramine-associated PAH in children under two years of age and underscores the importance of vigilant cardiac surveillance in this population. - Source: PubMed
Publication date: 2026/05/06
Ndukwe UzomaParkey AdrianneSamanta DebopamMasri AbdelrahmanWillis Erin