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DNMT3A activates KCNA2. 7 / 7
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"DNA methyltransferase DNMT3a contributes to neuropathic pain by repressing Kcna2 in primary afferent neurons."

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"Author Correction: DNA methyltransferase DNMT3a contributes to neuropathic pain by repressing Kcna2 in primary afferent neurons."

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"DNMT3a contributes to neuropathic pain genesis likely by repressing at least Kcna2 in the injured DRG.In summary, our study reveals a DNMT3a-triggered epigenetic mechanism of Kcna2 downregulation in the injured DRG after peripheral nerve injury."

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"it is likely that an elevation of DNA methylation within the Kcna2 gene promotor caused by the increased DNMT3a interferes with the binding of transcription factors and/or serves as docking sites for methyl-CpG-binding domain proteins, resulting in Kcna2 gene silencing in the dorsal horn neurons under CPP-induced bone cancer pain conditions, although the detailed mechanisms remain to be confirmed."

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"Although we reported that PCC injection did not alter the expression of Kcna1, Kcna4, Oprd1, Oprm1, Oprk1, Gad1, and Gad2 in dorsal horn, whether the DNMT3a-triggered changes in the expression of these potassium channels in dorsal horn post-PCC will be further examined.In conclusion, the current study demonstrates a DNMT3a-triggered epigenetic mechanism of Kcna2 downregulation in the dorsal horn under bone cancer pain conditions."

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"Contribution of DNMT3a to PCC-induced Kv1.2 downregulation in spinal cord."

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"Here, we report that blocking increased OCT1 in the injured DRG alleviated CCI-caused mechanical allodynia, heat hyperalgesia, and cold allodynia during the induction and maintenance periods through rescuing DNMT3a-triggered downregulation of DRG MOR and Kv1.2."