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SCN10A activates sodium(1+). 17 / 17
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"The novel sodium channel PN3/alpha-SNS, which was cloned from a rat dorsal root ganglion (DRG) cDNA library, is expressed predominantly in small sensory neurons and may contribute to the tetrodotoxin-resistant (TTXR) sodium current that is believed to be associated with central sensitization in chronic neuropathic pain states."
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"In particular, while the total density of sodium channels was suggested to increase (Gurtu and Smith, 1988), TTX-resistant sodium currents mediated by Nav1.8 and Nav1.9 appear to be down regulated (Dib-Hajj et al. 1998; Dib-Hajj et al. 1999), whereas the TTX-sensitive current is potentiated, most likely through the up-regulation of Nav1.3 sodium channels (Waxman et al. 1994)."
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"Together with the electrophysiological findings showing that the intrinsic properties, such as voltage-dependent activation and inactivation of Nav1.8 sodium channels, remained unchanged after the inoculation of tumor cells, the increased expression of Nav1.8 on the cell membrane provides a possible explanation for the enhanced density of Nav1.8- mediated sodium current in the DRG neurons of MRMT-1-treated rats, which actually represents the functional upregulation of Nav1.8 sodium channels in the DRG neurons of bone cancer rats."
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"In a paper by Wang [8], it was shown that incubation of DRG neurons of segments L4/L5 with CXCL1 significantly increased the expression of TTX-sensitive (especially Nav1.1 and Nav1.7) and, to a lesser extent, TTX-resistant sodium channels (Nav1.8), which increased sodium currents."