| http://purl.uniprot.org/citations/31065023 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31065023 | http://www.w3.org/2000/01/rdf-schema#comment | "Helicobacter pylori infection induces a number of pro-inflammatory signaling pathways contributing to gastric inflammation and carcinogenesis. Among those, NF-κB signaling plays a pivotal role during infection and malignant transformation of the gastric epithelium. However, deficiency of the adaptor molecule myeloid differentiation primary response 88 (MyD88), which signals through NF-κB, led to an accelerated development of gastric pathology upon H. felis infection, but the mechanisms leading to this phenotype remained elusive. Non-canonical NF-κB signaling was shown to aggravate H. pylori-induced gastric inflammation via activation of the lymphotoxin β receptor (LTβR). In the present study, we explored whether the exacerbated pathology observed in MyD88-deficient (Myd88-/-) mice was associated with aberrant activation of non-canonical NF-κB. Our results indicate that, in the absence of MyD88, H. felis infection enhances the activation of non-canonical NF-κB that is associated with increase in Cxcl9 and Icam1 gene expression and CD3+ lymphocyte recruitment. In addition, activation of signal transducer and activator of transcription 3 (STAT3) signaling was higher in Myd88-/- compared to wild type (WT) mice, indicating a link between MyD88 deficiency and STAT3 activation in response to H. felis infection. Thereby, MyD88 deficiency results in accelerated and aggravated gastric pathology induced by Helicobacter through activation of non-canonical NF-κB."xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.org/dc/terms/identifier | "doi:10.1038/s41598-019-43417-x"xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/author | "Gerhard M."xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/author | "Heikenwalder M."xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/author | "Mejias-Luque R."xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/author | "Obonyo M."xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/author | "Lozano-Pope I."xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/author | "Wanisch A."xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/date | "2019"xsd:gYear |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/name | "Sci Rep"xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/pages | "7030"xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/title | "Increased LIGHT expression and activation of non-canonical NF-kappaB are observed in gastric lesions of MyD88-deficient mice upon Helicobacter felis infection."xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://purl.uniprot.org/core/volume | "9"xsd:string |
| http://purl.uniprot.org/citations/31065023 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/31065023 |
| http://purl.uniprot.org/citations/31065023 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/31065023 |
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| http://purl.uniprot.org/uniprot/#_Q0PM16-mappedCitation-31065023 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/31065023 |
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