Affinage

SCN2B

Sodium channel regulatory subunit beta-2 · UniProt O60939

Length
215 aa
Mass
24.3 kDa
Annotated
2026-06-10
73 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SCN2B encodes the voltage-gated sodium channel β2 subunit, an immunoglobulin-domain auxiliary protein that chaperones NaV α-subunits to the plasma membrane and directly modulates their gating (PMID:27932425, PMID:37544648). β2 covalently links to α-subunits through a single extracellular disulfide bond at Cys-26 within its Ig domain; loss of this linkage (C26A) disrupts β2 targeting to nodes of Ranvier and the axon initial segment and abolishes its association with the neuronal cytoskeleton (PMID:22992729). Correct surface delivery of β2 depends on its own biogenesis: the cytoplasmic tail, extracellular loop, and transmembrane domain are each required for folding and ER export, N-linked glycosylation at Asn-42/66/74 is needed for trafficking to the apical membrane, and S-acylation at Cys-182 promotes association with cholesterol-rich lipid rafts and polarized apical localization (PMID:31511323, PMID:33602743, PMID:39343005). β2 also homodimerizes, and its trafficking is independent of NaV1.5 even though β2 perturbations impair NaV1.5 surface localization (PMID:39343005). In an isogenic β-subunit-null background, β2 imparts distinct gating properties to NaV1.5 and, combined with β1, generates hybrid gating, while in neurons β2 normally promotes channel inactivation in opposition to β4 (PMID:37544648, PMID:19228957); in heart, β2 chaperones NaV1.5 to the surface and oppositely modulates late sodium current relative to β1 (PMID:27932425, PMID:21705762). Loss-of-function β2 mutations (R28Q/R28W, D211G) reduce sodium current density and NaV1.5 surface expression, linking SCN2B to atrial fibrillation and Brugada syndrome (PMID:19808477, PMID:23559163, PMID:28597987). Beyond channel biology, β2 acts as a laminin-binding cell adhesion molecule promoting prostate cancer cell migration and invasion (PMID:24892658), and it is a BACE1 substrate whose cleavage couples β2 levels to APP processing in Alzheimer's disease models (PMID:29245901). SCN2B expression is post-transcriptionally repressed by multiple microRNAs (miR-449a, miR-133b-3p, miR-143-3p, miR-6954-3p), with this regulation shaping neuronal outgrowth and neuropathic pain (PMID:32124967, PMID:30018017, PMID:38866121).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2008 Medium

    Establishing whether β2 has a pathophysiological role in CNS disease, the finding that Scn2b deletion is neuroprotective tied β2 to Na+ channel surface regulation along demyelinated axons.

    Evidence EAE induction in Scn2b−/− mice with histological and immune readouts

    PMID:19013247

    Open questions at the time
    • Did not resolve which axonal Na+ channels are affected
    • No direct molecular link between β2 loss and axonal protection
  2. 2009 Medium

    To test whether β2 loss-of-function contributes to human arrhythmia, R28Q/R28W mutants were shown to reduce SCN5A current and alter gating, implicating β2 in atrial fibrillation susceptibility.

    Evidence Heterologous coexpression in CHO cells with patch-clamp

    PMID:19808477

    Open questions at the time
    • Mechanism (trafficking vs gating) not separated
    • Heterologous system only; no patient tissue
  3. 2009 Medium

    Clarifying how β-subunits balance channel kinetics, β2 was shown to normally promote inactivation, antagonizing β4 and modulating β1 effects.

    Evidence Whole-cell patch-clamp in neurons from Scn1b and Scn1b/Scn2b null mice

    PMID:19228957

    Open questions at the time
    • Specific α-subunit partners not defined
    • Molecular basis of antagonism unresolved
  4. 2011 Medium

    Addressing whether β-subunits shape pathological late current, β2 silencing was found to increase INaL opposite to β1, defining divergent β1/β2 modulation in normal and failing hearts.

    Evidence siRNA knockdown and patch-clamp in isolated ventricular cardiomyocytes

    PMID:21705762

    Open questions at the time
    • Direct vs indirect effect on INaL not distinguished
    • Structural basis of opposing modulation unknown
  5. 2012 High

    Defining the molecular basis of the α–β2 covalent linkage, Cys-26 was identified as the disulfide-bonding residue required for β2 targeting and cytoskeletal association.

    Evidence Site-directed mutagenesis, myelinating co-culture, neuron imaging, detergent extraction

    PMID:22992729

    Open questions at the time
    • Cytoskeletal binding partner not identified
    • Which α-subunit cysteine pairs with Cys-26 not defined
  6. 2014 Medium

    Extending β2 function beyond ion channels, β2 was shown to act as a laminin-binding adhesion molecule driving cancer cell migration and invasion.

    Evidence β2 overexpression in LNCaP cells, organotypic co-culture, AFM laminin binding

    PMID:24892658

    Open questions at the time
    • Adhesion signaling downstream of laminin binding unknown
    • In vivo relevance to prostate cancer not established
  7. 2017 Medium

    Resolving the mechanism of a Brugada mutation, D211G β2 was shown to reach the membrane normally but fail to promote NaV1.5 surface localization, separating β2 trafficking from chaperone function.

    Evidence Immunofluorescence and surface assays in MDCK and HL-1 cells

    PMID:28597987

    Open questions at the time
    • Structural cause of chaperone failure not defined
    • Cell-line models, not cardiac tissue
  8. 2017 Medium

    Linking β2 to amyloid pathology, β2 was confirmed as a BACE1 substrate whose knockdown restores Na+ current and shifts APP processing toward non-amyloidogenic pathways.

    Evidence Nav β2 knockdown in APP/PS1 mice with electrophysiology, behavior, biochemistry

    PMID:29245901

    Open questions at the time
    • Causal direction between β2 cleavage and APP processing unresolved
    • Cleavage fragment function not characterized
  9. 2016 High

    Establishing that β2 is the cardiac NaV1.5 chaperone, Scn2b null mice showed reduced ventricular current with unchanged NaV1.5 protein plus AF susceptibility, fibrosis and repolarization dispersion.

    Evidence Scn2b knockout mouse with patch-clamp, Western blot, in vivo electrophysiology

    PMID:27932425

    Open questions at the time
    • Trafficking step controlled by β2 not pinpointed
    • Cause of K+ current reduction unexplained
  10. 2019 High

    Defining the trafficking requirement for chaperone function, N-glycosylation of β2 was shown to be required for apical surface delivery and promotion of NaV1.5 surface localization.

    Evidence Glycosylation site mutagenesis in polarized MDCK cells with biotinylation and FRAP

    PMID:31511323

    Open questions at the time
    • Glycan recognition machinery for ER export unknown
    • Why a single site suffices not explained mechanistically
  11. 2021 High

    Identifying a lipid-based localization signal, β2 was shown to be palmitoylated at Cys-182, driving lipid raft association and apical polarity independent of its chaperone activity.

    Evidence Acyl-biotin exchange, C182S mutagenesis, cholesterol depletion, DRM fractionation, FRAP in MDCK cells

    PMID:33602743

    Open questions at the time
    • Palmitoyl transferase not identified
    • Functional consequence of raft localization for channel signaling unknown
  12. 2023 High

    Demonstrating direct gating modulation, an isogenic β-subunit-null human cell line showed β2 confers unique NaV1.5 gating and hybrid properties with β1.

    Evidence CRISPR β-null (BeHAPe) cells with ectopic β-subunit expression and patch-clamp

    PMID:37544648

    Open questions at the time
    • Structural interface mediating gating change not mapped
    • Endogenous stoichiometry not addressed
  13. 2024 High

    Mapping the determinants of β2 biogenesis, systematic domain perturbation showed all three β2 domains are required for folding and ER export, that β2 homodimerizes, and that β2 traffics independently of NaV1.5.

    Evidence Domain deletion constructs in MDCK cells with biotinylation, glycosylation, co-IP

    PMID:39343005

    Open questions at the time
    • Functional role of β2 homodimers unknown
    • How β2 grabs NaV1.5 during co-trafficking unresolved
  14. 2024 Medium

    Consolidating microRNA control of β2, multiple miRNAs (miR-449a, miR-133b-3p/143-3p, miR-6954-3p) were shown to bind the SCN2B 3'-UTR and regulate neuronal outgrowth and neuropathic pain in vivo.

    Evidence Luciferase 3'-UTR reporters, Ago-RIP, lentiviral/agomir delivery, behavioral pain assays

    PMID:30018017 PMID:32124967 PMID:38866121

    Open questions at the time
    • Combinatorial vs individual miRNA contributions unresolved
    • Upstream control of these miRNAs not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How β2 physically engages the NaV α-subunit pore during co-trafficking and gating modulation, and the identity of its cytoskeletal and trafficking partners, remains unresolved.
  • No structure of the β2–α complex defining the interaction interface
  • Cytoskeletal binding partner downstream of Cys-26 linkage unidentified
  • ER export receptor recognizing β2 glycans unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0005198 structural molecule activity 2 GO:0098631 cell adhesion mediator activity 1
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 2
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-1643685 Disease 3 R-HSA-397014 Muscle contraction 2
Partners
BACE1LAMININSCN1BSCN5A
Complex memberships
voltage-gated sodium channel complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 SCN2B mutations R28Q and R28W reduce SCN5A-mediated sodium current and alter channel gating when coexpressed in CHO cells, establishing loss-of-function of the β2 subunit as a mechanism contributing to atrial fibrillation susceptibility. Heterologous expression in CHO cells with patch-clamp electrophysiology Circulation. Arrhythmia and electrophysiology Medium 19808477
2009 In neurons from Scn2b null mice, β4-expressing cells showed slowed entry into inactivated states, demonstrating that β2 subunits normally promote Na+ channel inactivation; β1 and β4 have antagonistic roles on inactivation that are modulated by β2. Whole-cell patch-clamp in cultured hippocampal neurons from Scn1b and Scn1b/Scn2b null mice The Journal of neuroscience Medium 19228957
2012 A single extracellular cysteine residue, Cys-26 within the immunoglobulin domain of β2, is responsible for the disulfide linkage between the Na+ channel α and β2 subunits; loss of this covalent linkage (C26A mutation) disrupts β2 targeting to nodes of Ranvier and the axon initial segment and prevents β2 association with the neuronal cytoskeleton. Mutagenesis of β2 cDNA constructs, myelinating co-culture system, primary hippocampal neuron imaging, Triton X-100 detergent extraction The Journal of biological chemistry High 22992729
2013 The Brugada syndrome-associated β2 missense mutation D211G reduces Nav1.5 sodium current density by ~39% without affecting unitary channel conductance; membrane protein detection experiments indicate the mutant decreases Nav1.5 cell surface expression. Patch-clamp electrophysiology (whole-cell and single-channel), cell surface biotinylation in heterologous expression system Human mutation Medium 23559163
2016 Scn2b null mice exhibit reduced sodium and potassium current densities in ventricular myocytes and conduction slowing in the right ventricular outflow tract, with Nav1.5 protein levels unchanged, indicating that the primary function of β2 in the ventricle is to chaperone voltage-gated Na+ channel α-subunits to the plasma membrane. Scn2b deletion also causes atrial fibrillation susceptibility with increased fibrosis and higher repolarization dispersion. Whole-animal Scn2b knockout mouse model; patch-clamp electrophysiology, Western blot, in vivo electrophysiology studies Circulation. Arrhythmia and electrophysiology High 27932425
2008 Loss of Na+ channel β2 subunits (Scn2b null mice) is neuroprotective in experimental allergic encephalomyelitis (EAE), reducing symptom severity, axonal degeneration, and axonal loss without compromising peripheral immune function, consistent with β2's role in regulating Na+ channel cell surface expression along demyelinated axons. EAE induction in Scn2b−/− and wild-type mice; histological assessment of axonal degeneration, immune cell infiltration assays, T cell proliferation and cytokine assays Molecular and cellular neurosciences Medium 19013247
2011 Post-transcriptional silencing of SCN2B (Navβ2) in ventricular cardiomyocytes increases late sodium current (INaL) density and slows its decay, an effect opposite to SCN1B silencing, demonstrating that β1 and β2 subunits exert oppositely directed modulation of INaL in both normal and failing dog hearts. siRNA knockdown via viral delivery, whole-cell and perforated patch-clamp in freshly isolated ventricular cardiomyocytes, RT-PCR and Western blot American journal of physiology. Heart and circulatory physiology Medium 21705762
2010 Scn2b null mice show that β2 subunits modify the pharmacological properties of Na+ channels: loss of β2 does not alter classical carbamazepine effects on transient Na+ current (INaT) use-dependent block or inactivation voltage dependence, but absence of β2 (along with β1) reveals a paradoxical CBZ-induced shift of INaP activation to hyperpolarized potentials, indicating β subunits shape antiepileptic drug sensitivity. Whole-cell patch-clamp in hippocampal neurons from Scn2b null and wild-type mice; current-clamp and computational modeling The Journal of neuroscience Medium 20573896
2019 N-linked glycosylation of the β2 subunit at residues Asn-42, Asn-66, and Asn-74 (sialylated only at Asn-42) is required for efficient β2 trafficking to the apical plasma membrane; fully nonglycosylated β2 is retained in the ER and is defective in promoting NaV1.5 cell surface localization, while a single intact glycosylation site restores this function. Heterologous expression in polarized MDCK cells; mutagenesis, glycosylation assays in vitro and in vivo, immunofluorescence, surface biotinylation, FRAP The Journal of biological chemistry High 31511323
2017 The BrS-associated β2 mutation D211G reaches the plasma membrane normally but is defective in promoting Nav1.5 localization to the cell surface, demonstrating that β2 promotes Nav1.5 trafficking to the surface and that this function is disrupted by the D211G mutation. Immunofluorescence localization and cell surface assays in polarized MDCK cells and HL-1 cardiomyocyte-like cells Biology of the cell Medium 28597987
2021 The β2 subunit is S-acylated (palmitoylated) at Cys-182, and this modification promotes β2 association with cholesterol-rich lipid rafts and contributes to its polarized apical localization; depletion of plasma membrane cholesterol mislocalizes β2 to the basolateral domain. β2 palmitoylation is not required for promoting α subunit surface expression. Acyl-biotin exchange assay, mutagenesis (C182S), cholesterol depletion, detergent-resistant membrane fractionation, FRAP, immunofluorescence in polarized MDCK cells Journal of cell science High 33602743
2014 The β2 subunit (SCN2B) functions as a cell adhesion molecule in prostate cancer cells: overexpression of β2 in weakly aggressive LNCaP cells enhances association with nerve axons, increases migration and invasion on laminin, and recombinant β2 ectodomain binds laminin directly in atomic force microscopy assays. β2 overexpression in LNCaP cells, ex vivo organotypic spinal cord co-culture, functional migration/invasion assays, atomic force microscopy binding assays PloS one Medium 24892658
2017 Navβ2 (SCN2B) knockdown in APP/PS1 Alzheimer's disease mice partially reverses abnormal Navβ2 cleavage by BACE1, restores sodium current density in hippocampal neurons, and shifts APP processing towards non-amyloidogenic pathways, indicating that β2 is a substrate of BACE1 and that β2 levels modulate both Na+ channel surface expression and APP metabolism. Transgenic Navβ2 knockdown in APP/PS1 mice; EEG, patch-clamp, Morris water maze, Western blot, biochemical APP processing assays Oncotarget Medium 29245901
2019 miR-449a regulates SCN2B expression by binding to the 3'-UTR seed region of SCN2B mRNA, as confirmed by dual-luciferase reporter assay and anti-Ago co-immunoprecipitation; overexpression of miR-449a or inhibition of SCN2B promotes hippocampal neuron extension in vitro. Dual-luciferase reporter assay, anti-Ago co-immunoprecipitation with Affymetrix microarray, miRNA microarray, neuronal morphology assay International journal of molecular medicine Medium 32124967
2019 miR-34a targets the 3'-UTR of SCN2B mRNA in dorsal root ganglion neurons, confirmed by luciferase assay; miR-34a is downregulated in a rat model of chronic neuropathic pain, suggesting it is an upstream negative regulator of SCN2B expression in the peripheral nervous system. Luciferase 3'-UTR reporter assay, miRNA microarray, qPCR, ELISA Neuroscience letters Low 31278961
2018 miR-133b-3p and miR-143-3p reduce expression from a reporter construct containing the 3'-UTR of Scn2b, and lentiviral delivery of these miRNAs reduces Scn2b mRNA in dorsal root ganglia; intrathecal injection prevents development of persistent mechanical and cold allodynia following peripheral nerve injury. 3'-UTR luciferase reporter assay, lentiviral miRNA delivery, qPCR, behavioral pain assays in rats Neuroscience Medium 30018017
2020 SCN2B R137H mutation does not produce apparent functional effects on NaV1.5 gating by electrophysiology, but X-ray crystallography reveals structural changes in the β2 subunit. Structural mapping onto neuronal NaV channel structures suggests altered interaction patterns with non-cardiac NaV subtypes as a possible alternative mechanism. X-ray crystallography, whole-cell patch-clamp electrophysiology with NaV1.5 Bioelectricity Medium 34476357
2023 In a cell line devoid of all endogenous NaV β-subunits (BeHAPe cells), each β-subunit including β2 imparts unique gating properties to NaV1.5; combining β1 and β2 with NaV1.5 generates hybrid gating properties distinct from either subunit alone, demonstrating direct modulation of NaV1.5 gating by β2. CRISPR-engineered β-subunit-null human cell line, ectopic expression, whole-cell patch-clamp electrophysiology The Journal of biological chemistry High 37544648
2024 The cytoplasmic tail, extracellular loop, and transmembrane domain of β2 are each required for proper β2 folding and export to the cell surface; loss or substantial alteration of any of these domains leads to ER accumulation and impaired complex N-glycosylation. β2 also forms homodimers. NaV1.5 does not influence β2 trafficking, surface localization, or homodimer formation, but β2 domain perturbations affect NaV1.5 surface localization. Domain deletion/mutation constructs expressed in polarized MDCK cells; immunofluorescence, surface biotinylation, glycosylation analysis, co-immunoprecipitation The Journal of biological chemistry High 39343005
2024 SCN2B expression increases in trigeminal ganglion neurons after chronic constriction injury of the infraorbital nerve; silencing SCN2B reduces pain hypersensitivity; miR-6954-3p is downregulated and directly targets the 3'-UTR of Scn2b mRNA (confirmed by luciferase assay), and intraganglionic delivery of miR-6954-3p agomir reduces SCN2B protein and increases pain threshold in CCI-ION mice. CCI-ION mouse model, siRNA knockdown, luciferase 3'-UTR assay, FISH, immunofluorescence, von Frey behavioral testing, Western blot, qRT-PCR The journal of pain Medium 38866121

Source papers

Stage 0 corpus · 73 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Mutations in sodium channel β1- and β2-subunits associated with atrial fibrillation. Circulation. Arrhythmia and electrophysiology 187 19808477
2004 Mutations of neuronal voltage-gated Na+ channel alpha 1 subunit gene SCN1A in core severe myoclonic epilepsy in infancy (SMEI) and in borderline SMEI (SMEB). Epilepsia 157 14738421
2009 Regulation of persistent Na current by interactions between beta subunits of voltage-gated Na channels. The Journal of neuroscience : the official journal of the Society for Neuroscience 144 19228957
2002 Generalized epilepsy with febrile seizures plus: mutation of the sodium channel subunit SCN1B. Neurology 119 12011299
2008 A novel adhesion molecule in human breast cancer cells: voltage-gated Na+ channel beta1 subunit. The international journal of biochemistry & cell biology 94 19041953
2013 A missense mutation in the sodium channel β2 subunit reveals SCN2B as a new candidate gene for Brugada syndrome. Human mutation 83 23559163
2020 Genetic regulatory subnetworks and key regulating genes in rat hippocampus perturbed by prenatal malnutrition: implications for major brain disorders. Aging 68 32392183
2010 Functional dominant-negative mutation of sodium channel subunit gene SCN3B associated with atrial fibrillation in a Chinese GeneID population. Biochemical and biophysical research communications 65 20558140
2012 Identification of the cysteine residue responsible for disulfide linkage of Na+ channel α and β2 subunits. The Journal of biological chemistry 64 22992729
2013 Mutations of the SCN4B-encoded sodium channel β4 subunit in familial atrial fibrillation. International journal of molecular medicine 58 23604097
2010 Efficacy loss of the anticonvulsant carbamazepine in mice lacking sodium channel beta subunits via paradoxical effects on persistent sodium currents. The Journal of neuroscience : the official journal of the Society for Neuroscience 58 20573896
2021 Extracellular matrix remodeling precedes atrial fibrillation: Results of the PREDICT-AF trial. Heart rhythm 48 34332113
2016 Regulation of SCN3B/scn3b by Interleukin 2 (IL-2): IL-2 modulates SCN3B/scn3b transcript expression and increases sodium current in myocardial cells. BMC cardiovascular disorders 45 26728597
2008 Loss of Na+ channel beta2 subunits is neuroprotective in a mouse model of multiple sclerosis. Molecular and cellular neurosciences 45 19013247
2016 Scn2b Deletion in Mice Results in Ventricular and Atrial Arrhythmias. Circulation. Arrhythmia and electrophysiology 42 27932425
2011 Na+ channel Scn1b gene regulates dorsal root ganglion nociceptor excitability in vivo. The Journal of biological chemistry 41 21555511
2007 Exclusion of multiple candidate genes and large genomic rearrangements in SCN5A in a Dutch Brugada syndrome cohort. Heart rhythm 40 17556197
2019 Genetic interpretation and clinical translation of minor genes related to Brugada syndrome. Human mutation 36 30821013
2012 Prevalence of SCN1A mutations in children with suspected Dravet syndrome and intractable childhood epilepsy. Epilepsy research 34 23195492
2014 Is sudden unexplained nocturnal death syndrome in Southern China a cardiac sodium channel dysfunction disorder? Forensic science international 33 24529773
2020 Genetic variants of uncertain significance: How to match scientific rigour and standard of proof in sudden cardiac death? Legal medicine (Tokyo, Japan) 32 32361481
2014 A missense mutation in the sodium channel β1b subunit reveals SCN1B as a susceptibility gene underlying long QT syndrome. Heart rhythm 32 24662403
2013 Case-control association study of polymorphisms in the voltage-gated sodium channel genes SCN1A, SCN2A, SCN3A, SCN1B, and SCN2B and epilepsy. Human genetics 31 24337656
2016 Transcriptomic investigation of meat tenderness in two Italian cattle breeds. Animal genetics 30 26857751
2011 Post-transcriptional silencing of SCN1B and SCN2B genes modulates late sodium current in cardiac myocytes from normal dogs and dogs with chronic heart failure. American journal of physiology. Heart and circulatory physiology 26 21705762
2022 Modulating effects of FGF12 variants on NaV1.2 and NaV1.6 being associated with developmental and epileptic encephalopathy and Autism spectrum disorder: A case series. EBioMedicine 24 36029553
2019 Significant association of rare variant p.Gly8Ser in cardiac sodium channel β4-subunit SCN4B with atrial fibrillation. Annals of human genetics 23 30821358
2015 The role of the sodium current complex in a nonreferred nationwide cohort of sudden infant death syndrome. Heart rhythm 22 25757662
2017 Navβ2 knockdown improves cognition in APP/PS1 mice by partially inhibiting seizures and APP amyloid processing. Oncotarget 21 29245901
2015 Sodium Channel Voltage-Gated Beta 2 Plays a Vital Role in Brain Aging Associated with Synaptic Plasticity and Expression of COX5A and FGF-2. Molecular neurobiology 21 25575679
2019 MiR-34a is differentially expressed in dorsal root ganglia in a rat model of chronic neuropathic pain. Neuroscience letters 20 31278961
2014 Identification of beta-2 as a key cell adhesion molecule in PCa cell neurotropic behavior: a novel ex vivo and biophysical approach. PloS one 20 24892658
2011 Increased expression of the beta3 subunit of voltage-gated Na+ channels in the spinal cord of the SOD1G93A mouse. Molecular and cellular neurosciences 20 21458573
2020 MicroRNA‑449a regulates the progression of brain aging by targeting SCN2B in SAMP8 mice. International journal of molecular medicine 19 32124967
2019 N-Glycosylation of the voltage-gated sodium channel β2 subunit is required for efficient trafficking of NaV1.5/β2 to the plasma membrane. The Journal of biological chemistry 19 31511323
2013 The effects of eslicarbazepine on persistent Na⁺ current and the role of the Na⁺ channel β subunits. Epilepsy research 19 24368131
2017 Trafficking and localisation to the plasma membrane of Nav 1.5 promoted by the β2 subunit is defective due to a β2 mutation associated with Brugada syndrome. Biology of the cell 18 28597987
2019 Identification of relevant hub genes for early intervention at gene coexpression modules with altered predicted expression in schizophrenia. Progress in neuro-psychopharmacology & biological psychiatry 17 31715283
2006 Phenotypes and genotypes in epilepsy with febrile seizures plus. Epilepsy research 17 16884893
2022 Comprehensive Analysis of circRNA-miRNA-mRNA Regulatory Network and Novel Potential Biomarkers in Acute Myocardial Infarction. Frontiers in cardiovascular medicine 16 35872921
2000 The voltage-gated sodium channel beta2-subunit gene and idiopathic generalized epilepsy. Neuroreport 15 10976944
2023 Biophysical properties of NaV1.5 channels from atrial-like and ventricular-like cardiomyocytes derived from human induced pluripotent stem cells. Scientific reports 14 38001331
2019 Trafficking and Function of the Voltage-Gated Sodium Channel β2 Subunit. Biomolecules 14 31614896
2019 SCN1B and SCN2B gene variants analysis in dravet syndrome patients: Analysis of 22 cases. Medicine 13 30921204
2018 Intrathecal Injection of miR-133b-3p or miR-143-3p Prevents the Development of Persistent Cold and Mechanical Allodynia Following a Peripheral Nerve Injury in Rats. Neuroscience 12 30018017
2024 Structural variants involving MLLT10 fusion are associated with adverse outcomes in pediatric acute myeloid leukemia. Blood advances 11 38306602
2016 SCN2B in the Rat Trigeminal Ganglion and Trigeminal Sensory Nuclei. Cellular and molecular neurobiology 9 26852328
2021 The voltage-gated sodium channel β2 subunit associates with lipid rafts by S-palmitoylation. Journal of cell science 8 33602743
2021 RNA-sequence reveals differentially expressed genes affecting the crested trait of Wumeng crested chicken. Poultry science 7 34329989
2024 Transcriptome-wide 1-methyladenosine functional profiling of messenger RNA and long non-coding RNA in bladder cancer. Frontiers in genetics 6 38482382
2022 Two Novel Functional Mutations in Promoter Region of SCN3B Gene Associated with Atrial Fibrillation. Life (Basel, Switzerland) 6 36362949
2022 Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42. Neural plasticity 6 36406589
2023 Comprehensive analyses identify potential biomarkers for encephalitis in HIV infection. Scientific reports 5 37891420
2017 Nine differentially expressed genes from a post mortem study and their association with suicidal status in a sample of suicide completers, attempters and controls. Journal of psychiatric research 5 28327445
2015 Functions of miR-9 and miR-9* during Aging in SAMP8 Mice and Their Possible Mechanisms. Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae 5 26149132
2023 Decreased FAM13B Expression Increases Atrial Fibrillation Susceptibility by Regulating Sodium Current and Calcium Handling. JACC. Basic to translational science 4 38094680
2023 A Contemporary Review of the Genomic Associations of Coronary Artery Myocardial Bridging. Genes 4 38136997
2010 A novel microsatellite polymorphism of sodium channel beta1-subunit gene (SCN1B) may underlie abnormal cardiac excitation manifested by coved-type ST-elevation compatible with Brugada syndrome in Japanese. International journal of clinical pharmacology and therapeutics 4 20137763
2024 Comparative Gene Signature of Nociceptors Innervating Mouse Molar Teeth, Cranial Meninges, and Cornea. Anesthesia and analgesia 3 38236765
2023 Multi-animal-model study reveals mutations in neural plasticity and nociception genes linked to excessive alcohol drinking. Alcohol, clinical & experimental research 3 37336636
2023 Beta-subunit-eliminated eHAP expression (BeHAPe) cells reveal subunit regulation of the cardiac voltage-gated sodium channel. The Journal of biological chemistry 3 37544648
2022 Identification of potential lncRNA-miRNA-mRNA regulatory network contributing to aldosterone-producing adenoma. Journal of cellular and molecular medicine 3 36305047
2010 Mutational analysis of SCN2B, SCN3B and SCN4B in a large Chinese Han family with generalized tonic-clonic seizure. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 3 20730464
1998 Exclusion of the SCN2B gene as candidate for CMT4B. European journal of human genetics : EJHG 3 9887383
2012 Mutation analysis of the candidate genes SCN1B-4B, FHL1, and LMNA in patients with arrhythmogenic right ventricular cardiomyopathy. Applied & translational genomics 2 27896052
2024 MicroRNA-6954-3p Downregulation Contributes to Orofacial Neuropathic Pain in Mice Via Targeting Voltage-Gated Sodium Channel β2 Subunit Protein. The journal of pain 1 38866121
2024 Role of protein domains in trafficking and localization of the voltage-gated sodium channel β2 subunit. The Journal of biological chemistry 1 39343005
2021 Computational study of zebrafish immune-targeted microarray data for prediction of preventive drug candidates. Veterinary research forum : an international quarterly journal 1 33953878
2020 Biophysical Investigation of Sodium Channel Interaction with β-Subunit Variants Associated with Arrhythmias. Bioelectricity 1 34476357
2018 Effects of 4,9-anhydrotetrodotoxin on voltage-gated Na+ channels of mouse vas deferens myocytes and recombinant NaV1.6 channels. Naunyn-Schmiedeberg's archives of pharmacology 1 29453527
2025 Relationship between the expression of striated preferentially expressed gene (SPEG) and the development of atrial fibrillation. Journal of thoracic disease 0 40223983
2025 From genes to lifestyle: A multi-dimensional framework for Alzheimer's disease prevention and therapy. Ageing research reviews 0 41271115
2025 PIK3R1 as the Hidden Hand in Arrhythmogenic Right Ventricular Cardiomyopathy Inflammation: Weaving Transcriptomic Signatures with Structural Therapeutic Insights. Pharmaceuticals (Basel, Switzerland) 0 41471362

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