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

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

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) Interaktionspartner

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