IndraLab

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SCN8A activates MCF2L2. 9 / 9
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"All these results suggested that activation of STAT3 signaling was involved in TNF-α-induced Nav1.6 upregulation in DRG neurons."
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"TNF-alpha promotes the combination of p-STAT3/p300 and Scn8a promoter in DRG."
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"Here, to determine whether the activated STAT3 signaling transcriptionally regulated the expression of Nav1.6, we first observed the binding of STAT3 in the Scn8a promoter in DRG using a ChIP-PCR assay."
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"Moreover, our recent study shows that upregulation of Nav1.6 increased the DRG neuron excitability and contributed to the development of neuropathic pain [7]."
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"Moreover, IP and ChIP assays showed that L5-VRT enhanced the interaction between p-STAT3 and p300 and increased the recruitment of p-STAT3 and histone H4 acetylation on the Scn8a promoter in DRG."
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"However, it remains unknown whether activation of the TNF-α/STAT3 pathway mediates the Nav1.6 upregulation in DRG following lumbar 5 ventral root transection (L5-VRT)."
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"Suppression of STAT3 activation with local knockdown or inhibitor S3I-201 significantly attenuated H4 acetylation, and Nav1.6 upregulation in DRG, and relieved mechanical allodynia induced by L5-VRT."
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"Intraperitoneal injection of the TNF-α inhibitor thalidomide reduced the phosphorylation of STAT3 and decreased the recruitment of STAT3 and histone H4 hyper-acetylation in the Scn8a promoter, and subsequently attenuated Nav1.6 upregulation in DRG neurons and mechanical allodynia induced by L5-VRT."
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"The STAT3 activation mediated by TNF-alpha participates in Nav1.6 upregulation in DRG."
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