anti-Sodium Channel, Voltage-Gated, Type II, alpha Subunit (SCN2A) Anticorps

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains and one or more regulatory beta subunits. De plus, nous expédions SCN2A Protéines (6) et beaucoup plus de produits pour cette protéine.

afficher tous les anticorps Gène GeneID UniProt
SCN2A 110876  
SCN2A 24766 P04775
SCN2A 6326 Q99250
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Top anti-SCN2A Anticorps sur anticorps-enligne.fr

Showing 10 out of 48 products:

Catalogue No. Reactivité Hôte Conjugué Application Images Quantité Livraison Prix Détails
Mammifères Souris Inconjugué ISt, IHC, WB   5 mL 2 to 6 Days
$403.33
Détails
Humain Lapin Inconjugué WB Western blot analysis of extracts of U-87MG and K562 cells, using SCN2A antibody. Western blot analysis of extracts of various cell lines, using SCN2A antibody (ABIN4905095) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit. Exposure time: 5s. 100 μL 11 to 13 Days
$363.06
Détails
Rat Souris Inconjugué FM, IHC, IP, WB Nav1.2 Western Blot. Western Blot of mouse anti-Nav1.2 antibody. Lane 1: Rat Brian Membrane tissue. Primary antibody: Nav1.2 antibody at 1:1000 for overnight at 4°C. Secondary antibody: Goat anti-mouse IgG HRP secondary antibody at 1:10,000 for 45 min at RT. Block: 5% Blotto overnight 4°C. Predicted/Observed size: 227.8kDa/250kD. Other band(s): none. Nav1.2 Immunohistochemistry. Immunohistochemistry of mouse anti-Nav1.2 antibody. Tissue: Frozen sections of mouse brain extract. Primary Antibody: Nav1.2 antibody at 1 μg/mL for 1h at RT. Secondary antibody: Peroxidase mouse secondary at 1:10,000 for 45 min at RT. Localization: Membrane. Staining: Nav1.2 as brown signal. 100 μg 1 to 2 Days
$405.90
Détails
Humain Lapin Inconjugué IHC (p) Immunohistochemistry analysis of SCN2A Antibody in paraffin-embedded human brain tissue. 0.1 mg 6 to 8 Days
$434.50
Détails
Rat Souris Biotin IHC (p), WB Immunohistochemical staining (Formalin-fixed paraffin-embedded sections) of mouse brain with Scn2a1 monoclonal antibody, clone CJ6 (Biotin) . 100 μg 11 to 12 Days
$577.33
Détails
Rat Souris Inconjugué IHC (p), WB Immunohistochemical staining (Formalin-fixed paraffin-embedded sections) of mouse brain with Scn2a1 monoclonal antibody, clone CJ6 . 100 μg 11 to 12 Days
$460.00
Détails
Humain Souris Inconjugué ELISA, WB Western Blot detection against Immunogen (36.01 KDa) . 50 μL 11 to 12 Days
$305.71
Détails
Humain Lapin Inconjugué IHC, IHC (p)   100 μL 11 to 14 Days
$522.50
Détails
Humain Lapin Inconjugué ELISA, IHC, IHC (p)   100 μL 11 to 14 Days
$757.17
Détails
Rat Lapin Inconjugué IHC, WB   50 μL 11 to 16 Days
$700.86
Détails

anti-SCN2A Anticorps mieux référencés

  1. Mammalian Monoclonal SCN2A Primary Antibody pour ISt, IHC - ABIN1304839 : Gazina, Leaw, Richards, Wimmer, Kim, Aumann, Featherby, Churilov, Hammond, Reid, Petrou: 'Neonatal' Nav1.2 reduces neuronal excitability and affects seizure susceptibility and behaviour. dans Human molecular genetics 2015 (PubMed)
    Show all 39 Pubmed References

Plus d’anticorps contre SCN2A partenaires d’interaction

Mouse (Murine) Sodium Channel, Voltage-Gated, Type II, alpha Subunit (SCN2A) interaction partners

  1. NaV1.2 is unexpectedly critical for dendritic excitability and synaptic function in mature pyramidal neurons in addition to regulating early developmental axonal excitability. NaV1.2 loss reduced action potential backpropagation into dendrites, impairing synaptic plasticity and synaptic strength, even when NaV1.2 expression was disrupted in a cell-autonomous fashion late in development.

  2. Scn2aKO/+ mice exhibit a spectrum of phenotypes commonly observed in models of schizophrenia and autism spectrum disorder.

  3. We report that mice heterozygous for the gene Scn2a, a site of frequent de novo mutations in humans with intellectual disability, displayed impaired spatial memory.

  4. NaV1.2 in granule cells of the olfactory bulb is crucial for physiological dendritic GABA release and rapid discrimination of similar odorants with high accuracy.

  5. The findings suggest that impaired cortico-striatal excitatory transmission is a plausible mechanism that triggers epilepsy in Stxbp1 and Scn2a haplodeficient mice.

  6. in the absence of Nav1.6 expression, the AIS is occupied by Nav1.2 channels. However, APs are generated in the AIS, and differences in AP propagation to soma and dendrites are minimal.

  7. This study demonstrated that brain-specific Nav subunits revealed the expression of Nav 1.2 by most substantia nigra dopaminergic neurons.

  8. results therefore indicate that, while Nav1.1 is expressed in MEG-derived inhibitory neurons, Nav1.2 is expressed in caudal ganglionic eminence-derived disinhibitory interneurons in addition to excitatory neurons

  9. Inhibitory postsynaptic currents in NaV1.2 adult neurons were larger and the expression level of Scn2a mRNA was lower compared with the wild-type.

  10. Reducing of NaV1.2-mediated currents in interneurons promoted recurrent network activity.

  11. interaction with Sin3B influences Na(v)-channel trafficking or stability in the membrane.

  12. Nav1.2 expression levels are elevated in the brain of sodium channel blocker-treated animamls with experimental autoimmune encephalomyelitis.

  13. The present findings show a polarised distribution of Na(v)1.2 along the neuronal surface of granule cells and suggest its primary involvement in the transmission of information from granule cells to Purkinje cells.

  14. Immunohistochemical stainings of mouse cerebellum with a NaV1.2-specific antibody revealed a prominent increase in staining of the molecular layer during postnatal development.

  15. However, Na(v)1.2 channels show a greater accumulation of inactivation at higher frequencies of stimulation (20-100 Hz) than Na(v)1.6 and thus are likely to generate lower frequencies of firing.

  16. Nav channels generate and regenerate action potentials at multiple sites along the cochlear ganglion cells and nerve fibers, including the afferent endings, ganglionic initial segments, and nodes of Ranvier

  17. Genetic modifiers affect the severity of epilepsy caused by mutation of sodium channel Scn2a.

  18. an electrically induced signal can propagate along the vessel axis via the endothelium and can induce sequential activation of Na(v) and Ca(v)3.2 channels.

  19. The data support the hypothesis that modified Scn2a channels in Q54 mice result in network hyperexcitability of the hippocampus necessary for the development and maintenance of temporal lobe seizures.

  20. The results are consistent with a model in which Na(v)1.6 and Na(v)1.2 compete for binding partners at sites of high channel density

Human Sodium Channel, Voltage-Gated, Type II, alpha Subunit (SCN2A) interaction partners

  1. Results studied three newly identified variants causing distinct phenotypes observed in patients with epilepsy syndromes. Electrophysiological data showed an increased current density and an increased subthreshold sodium inward current upon an action potential stimulus (p.(Lys908Glu)), a hyperpolarizing shift of the activation curve (p.(Val208Glu) and p.(Thr773Ile)), and an increased persistent current (p.(Thr773Ile)).

  2. Genotype distributions of all selected SNPs were consistent with the Hardy-Weinberg equilibrium in epilepsy patients. SCN1A rs3812718 and SCN2A rs2304016 were found to be significantly associated with VPA response, both in monotherapy and in VPA-based polytherapy.

  3. This study reports the cryo-electron microscopy structure of human Nav1.2 bound to a peptidic pore blocker, the mu-conotoxin KIIIA, in the presence of an auxiliary subunit, beta2, to an overall resolution of 3.0 angstroms.

  4. Our study describes the heterogeneous clinical spectrum of SCN2A-associated episodic ataxia

  5. This study aimed to explore the connection between the 10-hydroxycarbazepine concentration and genes such as ATP-binding cassette B1 (ABCB1), ATP-binding cassette C2 (ABCC2), UDP-glucuronosyltransferase-2B7 and sodium voltage-gated channel alpha subunit 2 (SCN2A), which participate in the antiepileptic function of oxcarbazepine

  6. The clinical features of patients with SCN2A mutations include that main seizure onset is the neonate and early infancy, and the main seizure type is the focal seizure, manifested in clusters; de novo mutations often lead to severe phenotype with development delay.

  7. Chinese family with Juvenile-onset Myoclonus and a novel SCN2A point mutation, c.T4820C, which contains a highly conserved amino acid substitution within segment S5 (p.V1607A) was reported.

  8. Study represents the first evidence of the abnormal changes in voltage-gated sodium channels subtypes (including Nav1.2) and CaM/CaMKII pathway in human brain low-grade astrocytoma, providing new potential targets for molecular therapies of this disease.

  9. analysis of how ion permeation of Nav1.2 involves complexation with carboxylates and lysine

  10. Review: Dysfunction in SCN2A has been recently recognized as a major cause of neurodevelopmental disorders (NDDs), including epilepsy, intellectual disability (ID), and autism spectrum disorder (ASD). Loss of NaV1.2 function contributes to ASD and ID, whereas gain of function contributes to early onset epilepsy. Sodium channel function can be enhanced or suppressed using pharmacology.

  11. SCN1A and SCN2A mutations and clinical/EEG features in Chinese patients from epilepsy or severe seizures

  12. We utilized a targeted next generation sequencing (NGS) approach on a girl with early-onset seizures and Rett-like features, including autistic behavior, limited hand function with chorea, and profound intellectual disability, to identify novel missense mutation (c.1270G>A; p.V424M) in the SCN2A gene, which encodes the alphaII-subunit of the voltage-gated Na+ channel (Nav1.2).

  13. SCN2A autism spectrum disorder (ASD)-associated variants dampened or eliminated channel function in transfected HEK293 cells. A compartmental model of developing excitatory neurons demonstrated that all ASD variants, regardless of their mechanism of action, resulted in deficits in neuronal excitability. Corresponding analysis of mature neurons predicted minimal change in neuronal excitability.

  14. clinical and experimental data suggest a correlation between age at disease onset, response to sodium channel blockers and the functional properties of mutations in children with SCN2A-related epilepsy.

  15. The most frequently mutated gene in early-onset seizure and severe developmental delay disorders was SCN2A (11 patients, 3%), occurring de novo in all patients.

  16. Pathogenic, likely pathogenic, and benign variants in SCNs were identified using databases of sodium channel variants. Benign variants were also identified from population-based databases. Eight algorithms commonly used to predict pathogenicity were compared. In addition, logistic regression was used to determine if a combination of algorithms could better predict pathogenicity.

  17. Data indicate eight new cases with overlapping duplications at 2q24 and SCN3A was not involved in duplication, suggesting that having an extra copy of SCN2A has an effect on epilepsy pathogenesis.

  18. This study demonstrated the association of SCN2A rs1864885 A > G, in Japanese childhood encephalopathy patients.

  19. Our findings broaden the clinical spectrum observed with SCN2A gain-of-function mutations, showing that fairly different biophysical mechanisms can cause a convergent clinical phenotype of neonatal seizures and later onset episodic ataxia.

  20. We argue that very rare, loss-of-function mutations at SCN2A act in a moderately penetrant manner to increase the risk of developing several neuropsychiatric disorders including seizure disorders, intellectual disability, autism and schizophrenia.

SCN2A profil antigène

Profil protéine

Voltage-gated sodium channels are transmembrane glycoprotein complexes composed of a large alpha subunit with 24 transmembrane domains and one or more regulatory beta subunits. They are responsible for the generation and propagation of action potentials in neurons and muscle. This gene encodes one member of the sodium channel alpha subunit gene family. It is heterogeneously expressed in the brain, and mutations in this gene have been linked to several seizure disorders. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined.

Gene names and symbols associated with SCN2A

  • sodium voltage-gated channel alpha subunit 2 (SCN2A) anticorps
  • sodium channel protein type 2 subunit alpha (LOC100217927) anticorps
  • sodium channel protein type 2 subunit alpha (LOC100389294) anticorps
  • sodium channel protein type 2 subunit alpha (LOC100484218) anticorps
  • sodium channel, voltage-gated, type II, alpha (Scn2a) anticorps
  • sodium voltage-gated channel alpha subunit 2 (Scn2a) anticorps
  • sodium channel protein type 2 subunit alpha (LOC478773) anticorps
  • sodium channel, voltage-gated, type II, alpha subunit (SCN2A) anticorps
  • 6430408L10 anticorps
  • A230052E19Rik anticorps
  • BFIC3 anticorps
  • BFIS3 anticorps
  • BFNIS anticorps
  • EIEE11 anticorps
  • HBA anticorps
  • HBSCI anticorps
  • HBSCII anticorps
  • Na(v)1.2 anticorps
  • NAC2 anticorps
  • NachII anticorps
  • Nav1.2 anticorps
  • RII/RIIA anticorps
  • RNSCPIIR anticorps
  • SCN anticorps
  • SCN2A anticorps
  • SCN2A1 anticorps
  • Scn2a2 anticorps
  • ScpII anticorps

Protein level used designations for SCN2A

sodium channel, voltage-gated, type II, alpha subunit , sodium channel protein type 2 subunit alpha-like , sodium channel, voltage-gated, type II, alpha polypeptide 1 , RIIA sodium channel protein , alternative product , sodium channel protein brain II subunit alpha , sodium channel protein type 2 subunit alpha , sodium channel protein type II subunit alpha , sodium channel protein, brain II subunit alpha , sodium channel voltage-gated type II alpha polypeptide , sodium channel, voltage-gated, type 2, alpha 1 polypeptide , sodium channel, voltage-gated, type 2, alpha 1 subunit , voltage-gated sodium channel subunit alpha Nav1.2 , HBSC II , sodium channel protein, brain type 2 alpha subunit , sodium channel, voltage-gated, type II, alpha 1 polypeptide , sodium channel, voltage-gated, type II, alpha 2 polypeptide , voltage-gated sodium channel subtype II , voltage-gated sodium channel II , sodium channel protein , sodium channel, type II, alpha polypeptide , sodium channel, voltage-gated, type II, alpha 1

GENE ID SPECIES
459700 Pan troglodytes
703298 Macaca mulatta
100016409 Monodelphis domestica
100051816 Equus caballus
100217927 Taeniopygia guttata
100389294 Callithrix jacchus
100484218 Ailuropoda melanoleuca
110876 Mus musculus
24766 Rattus norvegicus
6326 Homo sapiens
395945 Gallus gallus
478773 Canis lupus familiaris
396588 Sus scrofa
539718 Bos taurus
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