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The protein encoded by SCN10A is a tetrodotoxin-resistant voltage-gated sodium channel alpha subunit. Additionally we are shipping Sodium Channel, Voltage-Gated, Type X, alpha Subunit Proteins (9) and many more products for this protein.
Showing 10 out of 56 products:
Human Monoclonal SCN10A Primary Antibody for ICC, IF - ABIN863135
Dray, Read: Arthritis and pain. Future targets to control osteoarthritis pain. in Arthritis research & therapy 2007
Show all 3 references for ABIN863135
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 (show ANK3 Antibodies) 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 t (show SCN5A Antibodies)hat the enhancer was essential for Scn5a expression in cardiac tissue. SCN10A variant rs6801957 modulated Scn5a expression in the heart.
Nav1.8 expression increases in dorsal root ganglion neurons following pretreatment with CC chemokine ligand 2 (show CXCL2 Antibodies).
We demonstrate that 75% of dorsal root ganglion (DRG) neurons express Na(v)1.8-Cre, including >90% of neurons expressing markers of nociceptors.
Behavioural deficits in Nav1.7 (show SCN9A Antibodies)/Nav1.8 knockout mice reflects a failure of action potential propagation in a mechanosensitive set of sensory neurons rather than a loss of primary transduction currents.
The functional presence of SCN10A/Nav1.8 in intracardiac neurons is demonstrated, indicating a novel role for this neuronal sodium channel in regulation of cardiac electric activity.
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.
study suggests that SCN10A variations are involved in the genesis of AF.
Rare SCN10A variants may contribute to atrial fibrillation susceptibility.
The rs6795970 in the SCN10A gene, which is reported to carry a high risk of heart block, might be associated with cardiac conduction abnormalities in Hypertrophic Cardiomyopathy patients.
SCN10A SNPs modulate PR interval and heart rate response during atrial fibrillation.
A single-nucleotide polymorphism (SNP) associated with alterations in cardiac conduction patterns affects the transcriptional regulation of the sodium channel genes, SCN5A (show SCN5A Antibodies) and SCN10A, predisposing for cardiac arrhythmias.
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