anti-Sodium Channel, Voltage-Gated, Type XI, alpha Subunit (SCN11A) Antibodies

This protein mediates the voltage-dependent sodium ion permeability of excitable membranes. Additionally we are shipping Sodium Channel, Voltage-Gated, Type XI, alpha Subunit Proteins (11) and many more products for this protein.

list all antibodies Gene Name GeneID UniProt
SCN11A 24046 Q9R053
SCN11A 29701 O88457
SCN11A 11280 Q9UI33
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Top anti-Sodium Channel, Voltage-Gated, Type XI, alpha Subunit Antibodies at antibodies-online.com

Showing 10 out of 19 products:

Catalog No. Reactivity Host Conjugate Application Images Quantity Supplier Delivery Price Details
Human Rabbit Un-conjugated ELISA, WB Western blot analysis SCN11A using 293 whole cell lysates 100 μL Log in to see 11 to 12 Days
$390.77
Details
Human Mouse Un-conjugated ELISA, WB Detection limit for recombinant GST tagged SCN11A is approximately 0.03ng/ml as a capture antibody. Western Blot detection against Immunogen (33 KDa) . 100 μg Log in to see 11 to 12 Days
$440.00
Details
Human Rabbit Un-conjugated WB Western blot analysis SCN11A using 293 whole cell lysates. 100 μg Log in to see 11 to 16 Days
$454.83
Details
Human Rabbit Un-conjugated IHC, WB   100 μL Log in to see 7 to 8 Days
$454.67
Details
Mouse Rabbit Un-conjugated IHC   100 μL Log in to see 7 to 8 Days
$454.67
Details
Human Rabbit Un-conjugated IHC, WB   100 μL Log in to see 11 to 14 Days
$551.83
Details
Human Rabbit HRP ELISA   100 μg Log in to see 11 to 16 Days
$412.19
Details
Human Rabbit FITC ELISA   100 μg Log in to see 11 to 16 Days
$412.19
Details
Human Rabbit Biotin ELISA   100 μg Log in to see 11 to 16 Days
$412.19
Details
Human Rabbit Un-conjugated ELISA, IF/ICC, IHC   100 μg Log in to see 11 to 16 Days
$412.19
Details

More Antibodies against Sodium Channel, Voltage-Gated, Type XI, alpha Subunit Interaction Partners

Mouse (Murine) Sodium Channel, Voltage-Gated, Type XI, alpha Subunit (SCN11A) interaction partners

  1. Two missense var- iants, p.R222S and p.R222H of Nav1.9, were identified in SCN11A by linkage analysis and exome analy- sis

  2. This study demonstrated that NaV1.9 presumably contributes to acute thermal and mechanical nociception in mice.

  3. Recently Nav1.9, a voltage-gated sodium channel subtype, has been established as a genetic influence for certain peripheral pain syndromes.

  4. A missense mutation (p.V1184A) in NaV1.9 leads to cold-aggravated peripheral pain.

  5. We conclude that Nav1.9 acts as a subthreshold amplifier in cold-sensitive nociceptive neurons and is required for the perception of cold pain under normal and pathological conditions.

  6. NaV1.9 is required for persistence of responses to intense mechanical stimulation, contributes to inflammatory mechanical hypersensitivity, and is essential for activation by noxious inflammatory mediators, including those from diseased human bowel.

  7. The results strongly suggested that Nav1.9 was expressed and functionally contributed to the signaling processing in the central auditory pathway.

  8. Axon growth of NaV1.9-deficient motoneurons in cell culture is drastically reduce.

  9. In the stable NaV1.9-deficient cells we successfully constructed, proliferation, phagocytosis and migration were obviously inhibited.

  10. Na(V)1.9 function appears to be essential for activity-dependent axon growth in motor neurons, acting upstream of spontaneous Ca(2+) elevation through voltage-gated calcium channels.

  11. Results provide evidence that Nav1.9 plays a crucial role in the generation of heat and mechanical pain hypersensitivity, both in subacute and chronic inflammatory pain models.

  12. results indicate that the spontaneous augmentation of Na(V)1.9 was regulated directly by protein kinase A, and indirectly by protein kinase C

  13. The present study provides evidence for a modulatory role of Na(v)1.9 also indicate that Na(v)1.9 signaling might be involved in visceral pain.

  14. inflammatory mediators modify the function of NaV1.9 to maintain inflammation-induced hyperalgesia

  15. Hyperexcitability was maintained in Na(v)1.9(-/-) mice, but hyperexcitability was absent and APs were blunted in Na(v)1.8(-/-) mice.

  16. Nav1.9 is an effector of the hyperalgesia produced by inflammatory mediators and plays a role in mediating peripheral sensitization.

  17. potential role of Nav1.9 in the transmission of trigeminal pain and the regulation of intestinal reflexes

  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. Na(V)1.9 underlies the G-protein pathway-regulated TTX-r persistent Na(+) current in small diameter sensory neurones that may drive spontaneous discharge in nociceptive nerve fibres during inflammation.

  20. Na(v)1.9 channels do not significantly contribute to normal visceral pain responses to acute colonic mechanical stimulation but may be important for the development of inflammation-related acute visceral hyperalgesic responses.

Human Sodium Channel, Voltage-Gated, Type XI, alpha Subunit (SCN11A) interaction partners

  1. A total of 11 mutations in SCN11A: p.R222H in seven families, and p.R225C, p.F814C, p.F1146S, or p.V1184A, in independent families. A founder mutation, SCN11A p.R222H was confirmed to be frequently observed in patients with Familial episodic limb pain in Japan. And identification of two novel missense variants of SCN11A, p.F814C and p.F1146S.

  2. We identified a missense mutation of p.Arg225Cys in SCN11A in a four-generation Chinese family with early-onset familial episodic pain and adult onset familial essential tremor syndrome.

  3. SCN11A single-nucleotide polymorphisms affect Postoperative pain sensitivity in Chinese Han women after Gynecological surgery. The SNP rs33985936 and rs13080116 may serve as novel predictors for Postoperative pain.

  4. a U-shaped relationship between the resting potential and the neuronal action potential threshold explains why NaV1.9 mutations that evoke small degrees of membrane depolarization cause hyperexcitability and familial episodic pain disorder or painful neuropathy, while mutations evoking larger membrane depolarizations cause hypoexcitability and insensitivity to pain.

  5. Recently Nav1.9, a voltage-gated sodium channel subtype, has been established as a genetic influence for certain peripheral pain syndromes.

  6. Results show the expression of Nav1.9 channels within the human colon for the first time. Furthermore, Nav1.9 channel expression is decreased in Hirschsprung's disease versus normal controls.

  7. autosomal dominant Congenital insensitivity to pain reflects the second gain-of-function mutation of SCN11A.

  8. A missense mutation (p.V1184A) in NaV1.9 leads to cold-aggravated peripheral pain.

  9. A G699R substitution in the Nav1.9 domain II S4-S5 linker renders dorsal root ganglion neurons hyperexcitable, via depolarized resting membrane potential, reduced current threshold and increased evoked firing in small-fiber neuropathy.

  10. missense mutations of Nav1.9 in individuals with painful peripheral neuropathy

  11. The results demonstrate that Nav1.8 and Nav1.9 are present in human lingual nerve neuromas, with significant correlations between the level of expression of Nav1.8 and symptoms of pain.

  12. we identified a specific de novo missense mutation in SCN11A in individuals with the congenital inability to experience pain who suffer from recurrent tissue damage and severe mutilations.

  13. Gain-of-function mutations in SCN11A can be causative of an autosomal-dominant episodic pain disorder.

  14. Results provide evidence that Nav1.9 plays a crucial role in the generation of heat and mechanical pain hypersensitivity, both in subacute and chronic inflammatory pain models.

  15. we demonstrate that the tetrodotoxin-insensitive sodium channel Na(V)1.9 underlies the neurotrophin-evoked excitation

Sodium Channel, Voltage-Gated, Type XI, alpha Subunit (SCN11A) Antigen Profile

Protein Summary

This protein mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which sodium ions may pass in accordance with their electrochemical gradient. It is a tetrodotoxin-resistant sodium channel isoform. Also involved, with the contribution of the receptor tyrosine kinase NTRK2, in rapid BDNF-evoked neuronal depolarization (By similarity).

Gene names and symbols associated with SCN11A

  • sodium voltage-gated channel alpha subunit 11 (SCN11A) antibody
  • sodium channel protein type 11 subunit alpha (LOC100349709) antibody
  • sodium channel, voltage-gated, type XI, alpha (Scn11a) antibody
  • sodium voltage-gated channel alpha subunit 11 (Scn11a) antibody
  • NaN antibody
  • NaT antibody
  • NAV1.9 antibody
  • NSS2 antibody
  • SCN11A antibody
  • SCN12A antibody
  • SNS-2 antibody
  • SNS2 antibody

Protein level used designations for SCN11A

sodium channel, voltage-gated, type XI, alpha subunit , sodium channel protein type 11 subunit alpha-like , sensory neuron sodium channel 2 , sodium channel protein type 11 subunit alpha , sodium channel protein type XI subunit alpha , sodium channel, voltage-gated, type XI, alpha polypeptide , voltage-gated sodium channel NAV1.9b , voltage-gated sodium channel subunit alpha Nav1.9 , sodium channel voltage-gated type 11 alpha polypeptide , sodium channel voltage-gated type XI alpha polypeptide , sodium channel, voltage-gated, type 11, alpha polypeptide , sodium channel, voltage-gated, type11, alpha polypeptide , PN5 , hNaN , peripheral nerve sodium channel 5 , sodium channel, voltage-gated, type XII, alpha polypeptide , voltage-gated sodium channel Nav1.9

GENE ID SPECIES
460275 Pan troglodytes
100349709 Oryctolagus cuniculus
100414951 Callithrix jacchus
100464374 Ailuropoda melanoleuca
100601668 Nomascus leucogenys
24046 Mus musculus
29701 Rattus norvegicus
11280 Homo sapiens
485593 Canis lupus familiaris
100739142 Sus scrofa
535956 Bos taurus
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