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
- Nanocellulose has long been studied as a bioactive material for tissue engineering; however, the mechanisms underlying its surface chemistry-mediated immune reprogramming remain unclear. Herein, we report a comprehensive multi-omics study of pristine cellulose nanocrystals (CNCs) and amide-functionalized CNCs (a-CNCs) to elucidate their '' interaction and impact on tissue-resident macrophages . Using integrated scRNA-Seq, bulk RNA-Seq, pharmacological inhibition, and histological profiling, we reveal that a-CNCs exhibit outstanding biocompatibility, showing no pro-inflammatory activation of macrophages across major organs within 14-day subacute window. In particular, a-CNCs exposure correlates with enhanced voltage-gated ion channel ( and ) and signaling, while suppressing -driven pro-inflammatory signals. This suggest that ion channel activation is strongly associated with M2 macrophage polarization. Moreover, a 28-day splenocytes profiling revealed no observable increase in CD4/CD8 T cells, suggesting non-adaptive immune response after a-CNC exposure. Concurrently, pseudotime mapping further discloses that a-CNC exposure preserves natural macrophage developmental trajectories across organ niches, while pristine CNCs induce mild M1-skewing in the spleen. validation confirms that a-CNCs intrinsically drive a pro-healing phenotype in macrophages, underscoring that macro-scale immune behavior can be transcriptionally triggered through nano-level surface chemistry of CNCs. - Source: PubMed
Publication date: 2026/04/09
Dutta Sayan DebAn Jeong ManMondal JagannathBose SubhankarJana Santosh KumarSeol YoujinMaity Chandan KumanLee Yong-KyuLim Ki-Taek - Epilepsy is a chronic neurological disorder characterized by recurrent seizures, with variants in ion channel genes such as SCN1A, SCN1B, and CACNA2D2 implicated in neuronal excitability. This research aims to explore genetic polymorphisms in the SCN1A, SCN1B, and CACNA2D2 genes among Turkish epilepsy patients and assess their impact on responsiveness to antiseizure medications (ASMs). - Source: PubMed
Publication date: 2026/04/10
Todurga-Seven Zeynep GizemPekkoc-Uyanik Kubra CigdemAgay Erhan Rasit - Electrical communication between excitable cells depends on both direct gap junction (GJ) currents and field mediated ephaptic interactions, but their relative contributions have remained difficult to quantify experimentally, limiting mechanistic insight into arrhythmia and other disorders of bioelectric signaling in excitable tissues. Building on the concept of a nanoscale, sodium channel rich perinexus at the cardiac intercalated disc, we developed a Single on Paired (SoP) preparation in which whole cell sodium current is recorded from one adult ventricular myocyte that remains end to end coupled to an intact partner. This configuration revealed a composite two-cell sodium current characterized by a unique pre peak waveform which exhibits two slopes in the rising phase, and a pronounced activation jump in sodium current amplitude between closely spaced voltage steps. This feature was absent in isolated single myocytes and interpretable as an Intercalated Disc Signature of intercellular activation. By combining graded GJ inhibition, perinexal widening via a Scn1b derived competitive adhesion peptide, and controlled modulation of extracellular sodium, we show that low sodium conditions favor GJ dominated activation, whereas at higher, more physiological sodium levels, perinexus centered ephaptic mechanisms provide substantial support for intercellular activation. A complementary two-cell computational model, simulating our SoP model and incorporating lateral and junctional sodium channels, reproduces the two-cell Intercalated Disc Signature and predicts a shift from GJ dominated activation at low sodium to ephaptic dominated support at higher, more physiological sodium concentrations when GJ conductance is reduced. Together, these results provide direct experimental evidence for a specific structural and molecular substrate of ephaptic coupling in the heart and establish a framework for dissecting how nanoscale extracellular cleft geometry, channel organization, sodium level, and GJ conductance jointly tune electric field based mechanisms of activation in excitable tissues, with implications for paradoxical clinical responses to anti arrhythmic interventions. - Source: PubMed
Publication date: 2026/03/06
Wu XiaoboSwanger Sharon AMeier Linnea Elisabeth BornkastDennison Clare LWeinberg Seth HPoelzing StevenGourdie Robert G - - Source: PubMed
Publication date: 2025/12/24
Ojiro RyotaTakahashi YasunoriTang QianSakamaki YuriShobudani MomokaZou XinyuKobayashi MioEbizuka YuriKigata TetsuhitoShibutani Makoto - Migraine and epilepsy are distinct neurological disorders that co-occur as comorbid conditions as well. Despite their clinical differences, these disorders exhibit some overlapping symptoms and share underlying pathophysiological mechanisms driven by a common genetic contribution. - Source: PubMed
Publication date: 2025/12/12
Sahu PrachiKashyap SohitKumar AnilMunshi Anjana