IndraLab

Statements


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"Nav1.7 and Nav1.8 channels cannot mediate sodium influx, which hinders the formation of action potentials, and ultimately leads to insensitivity to pain [55]."

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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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"SCN10A and Nav1.8 modulation of peak and late sodium currents in patients with early onset atrial fibrillation."

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"Genetic knockout of murine Scn10a also attenuate late sodium current in mouse cardiomyocytes."

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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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"Heterologous co-expression of wild-type (WT) SCN10A with WT-SCN5A in HEK cells caused a near doubling of sodium channel current (I Na) compared with WT-SCN5A alone."

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"We hypothesize that SCN10A modulates the activity of the canonical cardiac sodium channel encoded by SCN5A in the heart."

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"(2) SNS/PN3, M 1 2 3 4 5 6 7 8 9 M 200 which is expressed preferentially in small DRG and trigeminal neurons, produces a sodium current that is relatively resistant to TTX (Akopian et al., 1996; Sanga[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Nav alpha subunits may also interact with each other and it was shown that Nav1.8 is in direct physical contact with Nav1.5, thereby enhancing sodium current density [42])."

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"Nav1.8 contributes most of the sodium current underlying the action potential upstroke in neurons that expresses the channel [8], [9]."

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"We show that in male rat dorsal root ganglion (DRG) neurons these mutations, which impair inactivation, significantly increase TTX-resistant resurgent sodium currents mediated by Nav1.8."

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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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"Nav1.8 has been shown to contribute most of the sodium current underlying the upstroke of action potentials [8], [9], [29], [34], and thus its modulation can significantly influence neuronal excitability."

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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."

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"64 More recently rare variants in SCN10A, encoding the Nav1.8 sodium channel, have not only been associated with AF but also shown to modulate both the peak and late sodium current (I Na-L) (XREF_TABLE)."

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"In summary, these findings underscored the significant suppressive impact of HJ-69 on the excitability of nociceptive DRG neurons.Nav channels are essential in generation and transmission of pain sign[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Blocking SCN10A channels in heart reduces late sodium current and is antiarrhythmic."