| http://purl.uniprot.org/citations/22792286 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22792286 | http://www.w3.org/2000/01/rdf-schema#comment | "Homeostatic regulation of epidermal keratinocytes is controlled by the local cytokine milieu. However, a role for suppressor of cytokine signaling (SOCS), a negative feedback regulator of cytokine networks, in skin homeostasis remains unclear. Keratinocyte specific deletion of Socs3 (Socs3 cKO) caused severe skin inflammation with hyper-production of IgE, epidermal hyperplasia, and S100A8/9 expression, although Socs1 deletion caused no inflammation. The inflamed skin showed constitutive STAT3 activation and up-regulation of IL-6 and IL-20 receptor (IL-20R) related cytokines, IL-19, IL-20 and IL-24. Disease development was rescued by deletion of the Il6 gene, but not by the deletion of Il23, Il4r, or Rag1 genes. The expression of IL-6 in Socs3 cKO keratinocytes increased expression of IL-20R-related cytokines that further facilitated STAT3 hyperactivation, epidermal hyperplasia and neutrophilia. These results demonstrate that skin homeostasis is strictly regulated by the IL-6-STAT3-SOCS3 axis. Moreover, the SOCS3-mediated negative feedback loop in keratinocytes has a critical mechanistic role in the prevention of skin inflammation caused by hyperactivation of STAT3."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0040343"xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Kubo M."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Miyauchi K."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Suzuki Y."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Suzuki S."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Ozaki N."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Yoshimura A."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Motomura Y."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Cua D."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/author | "Uto-Konomi A."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/pages | "e40343"xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/title | "Dysregulation of suppressor of cytokine signaling 3 in keratinocytes causes skin inflammation mediated by interleukin-20 receptor-related cytokines."xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://purl.uniprot.org/core/volume | "7"xsd:string |
| http://purl.uniprot.org/citations/22792286 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22792286 |
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| http://purl.uniprot.org/uniprot/#_A0A0G2JFG1-mappedCitation-22792286 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22792286 |
| http://purl.uniprot.org/uniprot/#_A0A0G2JFT1-mappedCitation-22792286 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22792286 |
| http://purl.uniprot.org/uniprot/#_A0A0U1RPZ6-mappedCitation-22792286 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/22792286 |