| http://purl.uniprot.org/citations/29444433 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29444433 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29444433 | http://www.w3.org/2000/01/rdf-schema#comment | "MicroRNA-223 is known as a myeloid-enriched anti-inflammatory microRNA that is dysregulated in numerous inflammatory conditions. Here, we report that neutrophilic inflammation (wound response) is augmented in miR-223-deficient zebrafish, due primarily to elevated activation of the canonical nuclear factor κB (NF-κB) pathway. NF-κB over-activation is restricted to the basal layer of the surface epithelium, although miR-223 is detected throughout the epithelium and in phagocytes. Not only phagocytes but also epithelial cells are involved in miR-223-mediated regulation of neutrophils' wound response and NF-κB activation. Cul1a/b, Traf6, and Tab1 are identified as direct targets of miR-223, and their levels rise in injured epithelium lacking miR-223. In addition, miR-223 is expressed in cultured human bronchial epithelial cells, where it also downregulates NF-κB signaling. Together, this direct connection between miR-223 and the canonical NF-κB pathway provides a mechanistic understanding of the multifaceted role of miR-223 and highlights the relevance of epithelial cells in dampening neutrophil activation."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.celrep.2018.01.058"xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Zhu X."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Zhu X."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Zhou W."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Zhou W."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Deng Q."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Deng Q."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Hsu A.Y."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Hsu A.Y."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Freeman J.L."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Freeman J.L."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Gurol T."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Gurol T."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Wirbisky-Hershberger S.E."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Wirbisky-Hershberger S.E."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Kasinski A.L."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Kasinski A.L."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Pal A.S."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/author | "Pal A.S."xsd:string |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29444433 | http://purl.uniprot.org/core/name | "Cell Rep."xsd:string |