| http://purl.uniprot.org/citations/30139740 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/30139740 | http://www.w3.org/2000/01/rdf-schema#comment | "Brain-derived neurotrophic factor (BDNF) is a master regulator of synaptic plasticity in various neural circuits of the mammalian central nervous system. Neuron activity-induced BDNF gene expression is regulated through the Ca2+/CREB pathway, but other regulatory factors may also be involved in controlling BDNF levels. We report here that Wnt/β-catenin signaling plays a key role in controlling neuron activity-regulated BDNF expression. Using primary cortical cultures, we show that blockade of Wnt/β-catenin signaling inhibits the BDNF up-regulation that is induced by activation of the N-methyl-d-aspartic acid (NMDA) receptor and that activation of the Wnt/β-catenin signaling pathway stimulates BDNF expression. In vivo, Wnt/β-catenin signaling activated BDNF expression and was required for peripheral pain-induced up-regulation of BDNF in the mouse spine. We also found that conditional deletion of one copy of either Wntless (Wls) or β-catenin by Nestin-Cre-mediated recombination is sufficient to inhibit the pain-induced up-regulation of BDNF. We further show that the Wnt/β-catenin/BDNF axis in the spinal neural circuit plays an important role in regulating capsaicin-induced pain. These results indicate that neuron activity-induced Wnt signaling stimulates BDNF expression in the pain neural circuits. We propose that pain-induced Wnt secretion may provide an additional mechanism for intercellular coordination of BDNF expression in the neural circuit."xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.ra118.002840"xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/author | "Shi Y."xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/author | "Zhang W."xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/author | "Zhong L."xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/author | "Zhu S."xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/author | "Tang S.J."xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/author | "Peng Y."xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/author | "Zhang W.'"xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/pages | "15641-15651"xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/title | "Neuron activity-induced Wnt signaling up-regulates expression of brain-derived neurotrophic factor in the pain neural circuit."xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://purl.uniprot.org/core/volume | "293"xsd:string |
| http://purl.uniprot.org/citations/30139740 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/30139740 |
| http://purl.uniprot.org/citations/30139740 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/30139740 |
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