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

This protein mediates the voltage-dependent sodium ion permeability of excitable membranes. Zusätzlich bieten wir Ihnen Sodium Channel, Voltage-Gated, Type XI, alpha Subunit Antikörper (22) und viele weitere Produktgruppen zu diesem Protein an.

alle Proteine anzeigen Gen GeneID UniProt
SCN11A 24046 Q9R053
Ratte SCN11A SCN11A 29701 O88457
SCN11A 11280 Q9UI33
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Top Sodium Channel, Voltage-Gated, Type XI, alpha Subunit Proteine auf antikoerper-online.de

Showing 5 out of 11 products:

Katalog Nr. Origin Quelle Konjugat Bilder Menge Anbieter Lieferzeit Preis Details
Escherichia coli (E. coli) Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Anmelden zum Anzeigen 30 bis 35 Tage
$5,370.21
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Insektenzellen Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Anmelden zum Anzeigen 50 Days
$6,749.58
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Escherichia coli (E. coli) Maus His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Anmelden zum Anzeigen 30 bis 35 Tage
$5,370.21
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Insektenzellen Maus His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Anmelden zum Anzeigen 50 Days
$6,749.58
Details
Wheat germ Human GST tag 10 μg Anmelden zum Anzeigen 11 bis 12 Tage
$414.29
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SCN11A Proteine nach Spezies und Herkunft

Origin Exprimiert in Konjugat
Mouse (Murine) ,

Human , ,
,

Weitere Proteine zu Sodium Channel, Voltage-Gated, Type XI, alpha Subunit (SCN11A) Interaktionspartnern

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

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

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

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

  4. 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.

  5. 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.

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

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

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

  9. 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.

  10. 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.

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

  12. 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.

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

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

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

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

  17. 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.

  18. 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.

  19. 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.

  20. Na(v)1.9 is expressed by photoreceptors and Muller glia in retina f mice.

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

  1. 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.

  2. 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.

  3. 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.

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

  5. 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.

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

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

  8. 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.

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

  10. 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.

  11. 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.

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

  13. 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.

  14. 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) Protein Überblick

Protein Überblick

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).

Genbezeichner und Symbole assoziert mit SCN11A

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

Bezeichner auf Proteinebene für 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 SPEZIES
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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