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The protein encoded by SCN10A is a tetrodotoxin-resistant voltage-gated sodium channel alpha subunit. Zusätzlich bieten wir Ihnen Sodium Channel, Voltage-Gated, Type X, alpha Subunit Proteine (9) und viele weitere Produktgruppen zu diesem Protein an.
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Mammalian Monoclonal SCN10A Primary Antibody für ISt, IHC - ABIN1304845
François, Schüetter, Laffray, Sanguesa, Pizzoccaro, Dubel, Mantilleri, Nargeot, Noël, Wood, Moqrich, Pongs, Bourinet: The Low-Threshold Calcium Channel Cav3.2 Determines Low-Threshold Mechanoreceptor Function. in Cell reports 2015
Show all 17 Pubmed References
Human Monoclonal SCN10A Primary Antibody für AA, ICC - ABIN863135
Dray, Read: Arthritis and pain. Future targets to control osteoarthritis pain. in Arthritis research & therapy 2007
Show all 3 Pubmed References
While Scn10a transcripts are not detectible in ventricular cardiomyocytes, gene deletion results in reproducible loss of late sodium current under extreme experimental conditions. However, there are no identifiable consequences of this Scn10a deletion in the intact mouse heart at usual rates.
Results suggest that Nav1.8 plays a role in modulating specific aspects of the retinal physiology and that starburst amacrine cells are a fundamental cellular contributor to the oscillatory potentials in mice, a clear demonstration of the dichotomy between electroretinogram b-wave and oscillatory potentials.
These preclinical proof-of-concept data suggest that PF-01247324, its derivatives, or other Nav1.8-selective blockers merit further study for providing symptomatic therapy for cerebellar dysfunction in MS and related disorders.
A novel splice variant of SCN10A lacking exon 11 was found in human but not detected in mouse or rat.
Nav1.8 gain-of-function point mutation contributes to intense hyperexcitability along the afferent axon within distinct sensory neuron subtypes.
Nav1.8 interacts with ankyrin G (zeige ANK3 Antikörper) and they co-localize in skin nerve fibers.
The enhanced NaV1.8 activity are essential for the development of long-lasting hyperalgesia in acid-induced, chronic, widespread muscle pain.
Analysis of BAC transgenic strains harboring an engineered deletion of the enhancer within Scn10a revealed that the enhancer was essential for Scn5a (zeige SCN5A Antikörper) expression in cardiac tissue. SCN10A variant rs6801957 modulated Scn5a (zeige SCN5A Antikörper) expression in the heart.
Nav1.8 expression increases in dorsal root ganglion neurons following pretreatment with CC chemokine ligand 2 (zeige CXCL2 Antikörper).
We demonstrate that 75% of dorsal root ganglion (DRG) neurons express Na(v)1.8-Cre, including >90% of neurons expressing markers of nociceptors.
Our findings suggest that there are interaction effects of DM and SCN10A (rs7375036) that influence the development of CAN.
This study demonstrated that at the association and mechanistic levels, the SCN10A single nucleotide polymorphism rs6795970 biases human pain sensitivity.
We investigated the association of SCN10A gene variants with 105 sporadic sudden unexplained nocturnal death syndrome victims. A total of 6 rare mutations and 16 polymorphisms were detected in SUNDS victims. This is the first report of common and rare variants of SCN10A gene in the Chinese Han population, which provides the genetic epidemiological evidence that SCN10A may be a novel susceptibility gene.
Compared with Brugada syndrome (BrS) patients carrying SCN5A (zeige SCN5A Antikörper) or CACNA1C (zeige CACNA1C Antikörper) mutations, symptomatic patients in the SCN10A group tended to be older than those in the other gene groups. In six BrS probands who carried SCN10A variants, most experienced severe arrhythmic attacks.
The p.M650K mutation shifted steady-state fast inactivation of Nav1.8 (SCN10A)to more hyperpolarized potentials and did not significantly alter any other tested gating behaviors. The AP half-width was significantly broader and the stimulated action potential firing rate was reduced for M650K transfected DRGs compared to WT.
SCN10A mutations do not play primary role in arrhythmogenic right ventricular dysplasia/cardiomyopathy.
SCN10A genetic variation substantially influences functional status in patients with multiple sclerosis.
SCN10A gene mutations that reduce sodium channel current may provide a mechanistic link between Atrioventricular nodal reentrant tachycardia and Brugada syndrome and predispose to expression of both phenotypes.
The results demonstrate distinct properties of human Na(v)1.8, which contribute to the firing properties of human DRG neurons.
The common SNP SCN10A V1073 was strongly associated with Brugada syndrome and demonstrated loss of NaV1.8 function, as did rare variants in isolated patients.
voltage-gated sodium channel that is resistant to tetrodotoxin
peripheral nerve sodium channel 3
, sensory neuron sodium channel
, sodium channel protein type 10 subunit alpha
, sodium channel protein type X subunit alpha
, voltage-gated sodium channel subunit alpha Nav1.8
, sodium channel, voltage-gated, type X, alpha polypeptide
, sodium channel type X alpha polypeptide
, sodium channel voltage-gated type X alpha polypeptide
, sodium channel, voltage-gated, type 10, alpha polypeptide
, TTX-resistant sodium channel