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• W1969946369 abstract "In mammals, pain sensation is initiated by the detection of noxious stimuli through specialized transduction ion channels and receptors in nociceptive sensory neurons. Transient receptor potential (TRP) channels are the key sensory transducers that confer nociceptors distinct sensory modalities. However, the regulatory mechanisms about their expression are poorly defined. Here we show that the zinc-finger protein ZBTB20 regulates TRP channels expression in nociceptors. ZBTB20 is highly expressed in nociceptive sensory neurons of dorsal root ganglia. Disruption of ZBTB20 in nociceptors led to a marked decrease in the expression levels of TRPV1, TRPA1 and TRPM8 and the response of calcium flux and whole-cell currents evoked by their respective specific agonists. Phenotypically, the mice lacking ZBTB20 specifically in nociceptors showed a defect in nociception and pain sensation in response to thermal, mechanical and inflammatory stimulation. Our findings point to ZBTB20 as a critical regulator of nociception and pain sensation by modulating TRP channels expression in nociceptors. The upregulation of TRP ion channels is implicated in pain processing. In this study, the authors show that the zinc-finger protein ZBTB20 is responsible for TRP channel upregulation, and eliminating ZBTB20 from pain-sensing neurons in mouse models of pain results in the reduction of pain-like sensation." @default.
• W1969946369 created "2016-06-24" @default.
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• W1969946369 date "2014-11-05" @default.
• W1969946369 modified "2023-09-27" @default.
• W1969946369 title "ZBTB20 regulates nociception and pain sensation by modulating TRP channel expression in nociceptive sensory neurons" @default.
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• W1969946369 doi "https://doi.org/10.1038/ncomms5984" @default.
• W1969946369 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6687506" @default.
• W1969946369 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25369838" @default.
• W1969946369 hasPublicationYear "2014" @default.
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