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Scn9a  -  sodium channel, voltage-gated, type IX, alpha

Mus musculus

Synonyms: Kiaa4197, Nav1.7, PN1, Peripheral sodium channel 1, Sodium channel protein type 9 subunit alpha, ...
 
 
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Disease relevance of Scn9a

  • Decrease in inflammatory hyperalgesia by herpes vector-mediated knockdown of Nav1.7 sodium channels in primary afferents [1].
  • Together, these observations show that PN-1 promotes neurite outgrowth from neuroblastoma cells by inhibiting thrombin and suggest that this depends on the ability of thrombin to retract neurites [2].
 

Psychiatry related information on Scn9a

  • Double knockouts of both Nav1.7 and Nav1.8 also develop normal levels of neuropathic pain, despite a lack of inflammatory pain symptoms and altered mechanical and thermal acute pain thresholds [3].
 

High impact information on Scn9a

  • Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain [4].
  • Induction of peripheral inflammation increases the expression of the Nav1.7 sodium channel in sensory neurons, potentially increasing their excitability [1].
  • Development of closed-state inactivation was also much faster for Nav1.6 currents than for Nav1.7 currents [5].
  • A recent study demonstrated that Nav1.7 expression is negatively correlated with conduction velocity and DRG cell size, while the Nav1.6 voltage-gated sodium channel has been implicated as the predominant isoform present at nodes of Ranvier of myelinated fibres [5].
  • Among subpopulations of granulosa cells, the expression of PN-1 and uPA was heterogeneous and complementary [6].
 

Biological context of Scn9a

  • Linkage analysis established that Scn9a mapped to the proximal segment of mouse chromosome 2 [7].
  • Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons [5].
  • In LRP1-/- MEF cells, inhibitor sensitivity and kinetic values (t(1/2) at 45 min) of PN-1 uptake showed a similarity to syndecan-1-mediated endocytosis [8].
  • In these cells, PN-1 uptake was increased by overexpression of full-length syndecan-1 and decreased by RNA interference targeting this proteoglycan [8].
  • Protease nexin-1 (PN-1), an inhibitor of serine proteases, contributes to tissue homeostasis and influences the behavior of some tumor cells [8].
 

Anatomical context of Scn9a

  • We have used a total of 27 AXB/BXA recombinant inbred mouse strains to determine the chromosomal location of a newly identified gene encoding an alpha-subunit isoform of the sodium channel from Schwann cells, Scn9a [7].
  • To test whether NT-3 could prevent muscle spindle degeneration, spindle number and morphology were assessed 3 weeks after sciatic nerve crush or section on PN1 [9].
  • Mis-expression of voltage-gated sodium channels by damaged sensory neurons has also been implicated in the development of neuropathic pain, but the role of Nav1.7 and Nav1.8 is uncertain [3].
  • Two voltage gated sodium channel alpha-subunits, Nav1.7 and Nav1.8, are expressed at high levels in nociceptor terminals and have been implicated in the development of inflammatory pain [3].
  • It has been suggested that PN-1:thrombin complexes might mediate the neurite outgrowth activity of PN-1 [2].
 

Associations of Scn9a with chemical compounds

  • In contrast, ACh treatment in the presence of TTX had no effect on PN1 gene expression compared to treatment with TTX alone [10].
 

Other interactions of Scn9a

  • The segregation of restriction fragment length polymorphisms in 145 progeny from a Mus spretus x C57BL/6J backcross indicates that Scn9a is very tightly linked to Scn1a (gene encoding the type I sodium channel alpha-subunit of the brain) and forms part of a cluster of four Scna genes located on mouse chromosome 2 [7].
  • Genetic mapping of the peripheral sodium channel genes, Scn9a and Scn10a, in the mouse [11].
 

Analytical, diagnostic and therapeutic context of Scn9a

  • The changes in mRNA levels of the three genes after denervation indicated that these genes were regulated in a innervation-dependent manner and that nerve activity may play an important regulatory role in the expression of prothrombin, ThR, and PN-1 [12].

References

  1. Decrease in inflammatory hyperalgesia by herpes vector-mediated knockdown of Nav1.7 sodium channels in primary afferents. Yeomans, D.C., Levinson, S.R., Peters, M.C., Koszowski, A.G., Tzabazis, A.Z., Gilly, W.F., Wilson, S.P. Hum. Gene Ther. (2005) [Pubmed]
  2. Neurite outgrowth activity of protease nexin-1 on neuroblastoma cells requires thrombin inhibition. Gurwitz, D., Cunningham, D.D. J. Cell. Physiol. (1990) [Pubmed]
  3. Neuropathic pain develops normally in mice lacking both Nav1.7 and Nav1.8. Nassar, M.A., Levato, A., Stirling, L.C., Wood, J.N. Molecular pain [electronic resource] (2005) [Pubmed]
  4. Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Nassar, M.A., Stirling, L.C., Forlani, G., Baker, M.D., Matthews, E.A., Dickenson, A.H., Wood, J.N. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  5. Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons. Herzog, R.I., Cummins, T.R., Ghassemi, F., Dib-Hajj, S.D., Waxman, S.G. J. Physiol. (Lond.) (2003) [Pubmed]
  6. Coordinated and cell-specific induction of both physiological plasminogen activators creates functionally redundant mechanisms for plasmin formation during ovulation. Hägglund, A.C., Ny, A., Liu, K., Ny, T. Endocrinology (1996) [Pubmed]
  7. A new sodium channel alpha-subunit gene (Scn9a) from Schwann cells maps to the Scn1a, Scn2a, Scn3a cluster of mouse chromosome 2. Beckers, M.C., Ernst, E., Belcher, S., Howe, J., Levenson, R., Gros, P. Genomics (1996) [Pubmed]
  8. Activation of ERK signaling upon alternative protease nexin-1 internalization mediated by syndecan-1. Li, X., Herz, J., Monard, D. J. Cell. Biochem. (2006) [Pubmed]
  9. Muscle-derived neurotrophin-3 reduces injury-induced proprioceptive degeneration in neonatal mice. Wright, D.E., Williams, J.M., McDonald, J.T., Carlsten, J.A., Taylor, M.D. J. Neurobiol. (2002) [Pubmed]
  10. Cholinergic stimulation increases thrombin activity and gene expression in cultured mouse muscle. Glazner, G.W., Yadav, K., Fitzgerald, S., Coven, E., Brenneman, D.E., Nelson, P.G. Brain Res. Dev. Brain Res. (1997) [Pubmed]
  11. Genetic mapping of the peripheral sodium channel genes, Scn9a and Scn10a, in the mouse. Kozak, C.A., Sangameswaran, L. Mamm. Genome (1996) [Pubmed]
  12. Regulation of prothrombin, thrombin receptor, and protease nexin-1 expression during development and after denervation in muscle. Kim, S., Buonanno, A., Nelson, P.G. J. Neurosci. Res. (1998) [Pubmed]
 
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