IndraLab

Statements


TNF activates SCN8A. 14 / 15
1 | 14

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"TNF-α treatment induced a significant upregulation of Nav1.6 and Nav1.7 (Figure 6, C–G)."

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"In this study, we show that TNF-α enhanced RGC excitability by upregulating Nav1.6 channels through activating TNFR1, thus contributing to RGC apoptosis."

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"These results further verify that TNF-α selectively enhances Nav1.6 currents."

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"Overall, Nav1.6 isoforms appear to be promising as diagnostic markers and therapeutic targets in the treatment of clinical metastatic tumors, but further research is required to determine their usefulness in clinical practice.Through an extensive literature review, it was found that Cheng et al (31) indicated that TNF-α upregulated Nav1.6 currents in retinal cells; Ding et al (38) also found that the TNF-α/STAT3 signalling pathway upregulated Nav1.6 expression in the dorsal root ganglion."

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"TNF-alpha promotes the combination of p-STAT3/p300 and Scn8a promoter in DRG."

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"In the present study, it was demonstrated that TNF-α promotes the production of Nav1.6 protein and mRNA, and si-Nav1.6 could partially block the induction of TNF-α in glioma, suggesting that TNF-α is associated with malignant progression of tumors in glioma.Subsequently, a number of drugs that have potential therapeutic value for gliomas were screened."

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"TNF-alpha selectively upregulates Nav1.6 currents in RGCs."

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"These results suggest that TNF-α may selectively enhance Nav1.6 currents."

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"Considering the TNF-α-mediated regulation of the p-STAT3 activity, these studies suggested an enhanced interaction between p-STAT3 and p300, possibly mediated by TNF-α, in the Scn8a promoter region, which increased the histone H4 acetylation and facilitated the Nav1.6 expression in the rodents with L5-VRT."

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"TNF-alpha induces RGC hyperexcitability by selectively upregulating Nav1.6 currents."

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"One of the major findings in this study is that TNF-α induced RGC hyperexcitability was mediated by selectively upregulating Nav1.6 currents although RGCs express the other subtypes of Na channels, such as Nav1.1 and Nav1.2 [45–47]."

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"Further analysis revealed that TNF-alpha selectively upregulated Nav1.6 subtype of Na + currents in RGCs."

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"Altogether, our study showed that TNF-α, via activating STAT3, mediated epigenetic upregulation of Nav1.6 in DRG and contributed to L5-VRT-induced mechanical allodynia, which provided a novel potential target for the treatment of nerve injury-induced neuropathic pain."

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"Taken together, all these results demonstrated that proinflammatory cytokine TNF-α induced the hyperexcitability of RGCs by enhancing Nav1.6 currents and protein expression through activating TNFR1, thus contributing to RGC apoptosis in glaucoma."