{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hsieh MC"],"funding":["Mackay Memorial Hospital","Ministry of Science and Technology, Taiwan"],"pagination":["1295-1315"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8423947"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(2)"],"pubmed_abstract":["Many epigenetic regulators are involved in pain-associated spinal plasticity. Coactivator-associated arginine methyltransferase 1 (CARM1), an epigenetic regulator of histone arginine methylation, is a highly interesting target in neuroplasticity. However, its potential contribution to spinal plasticity-associated neuropathic pain development remains poorly explored. Here, we report that nerve injury decreased the expression of spinal CARM1 and induced allodynia. Moreover, decreasing spinal CARM1 expression by Fbxo3-mediated CARM1 ubiquitination promoted H3R17me2 decrement at the K<sup>+</sup> channel promoter, thereby causing K<sup>+</sup> channel epigenetic silencing and the development of neuropathic pain. Remarkably, in naïve rats, decreasing spinal CARM1 using CARM1 siRNA or a CARM1 in"],"journal":["Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics"],"pubmed_title":["Blocking the Spinal Fbxo3/CARM1/K<sup>+</sup> Channel Epigenetic Silencing Pathway as a Strategy for Neuropathic Pain Relief."],"pmcid":["PMC8423947"],"funding_grant_id":["MOST 108-2320-B-715-002-MY3 and 108-2314-B-715-004-MY3","MMH-MM-10705 and MMH-MM-10803","MOST 108-2320-B-038-028","MOST 108-2320-B-715-004-MY3","MMH-MM-108-87"],"pubmed_authors":["Chen GD","Lai CY","Cheng JK","Lin TB","Hsieh MC","Ho YC","Peng HY","Lee AS","Tseng KW","Wang HH","Yang PS","Ng SC"],"additional_accession":[]},"is_claimable":false,"name":"Blocking the Spinal Fbxo3/CARM1/K<sup>+</sup> Channel Epigenetic Silencing Pathway as a Strategy for Neuropathic Pain Relief.","description":"Many epigenetic regulators are involved in pain-associated spinal plasticity. Coactivator-associated arginine methyltransferase 1 (CARM1), an epigenetic regulator of histone arginine methylation, is a highly interesting target in neuroplasticity. However, its potential contribution to spinal plasticity-associated neuropathic pain development remains poorly explored. Here, we report that nerve injury decreased the expression of spinal CARM1 and induced allodynia. Moreover, decreasing spinal CARM1 expression by Fbxo3-mediated CARM1 ubiquitination promoted H3R17me2 decrement at the K<sup>+</sup> channel promoter, thereby causing K<sup>+</sup> channel epigenetic silencing and the development of neuropathic pain. Remarkably, in naïve rats, decreasing spinal CARM1 using CARM1 siRNA or a CARM1 in","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2025-04-22T09:15:35.617Z","creation":"2025-04-05T22:59:28.742Z"},"accession":"S-EPMC8423947","cross_references":{"pubmed":["33415686"],"doi":["10.1007/s13311-020-00977-5"]}}