| http://purl.uniprot.org/citations/31627033 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31627033 | http://www.w3.org/2000/01/rdf-schema#comment | "Recently, we reported that HaCaT human keratinocytes secreted leucine-rich repeat LGI family member 3 (LGI3) protein after exposure to ultraviolet B (UVB) irradiation. In the present study, we aimed to determine whether LGI3 is also released in response to stimulation by lipopolysaccharides (LPS), membrane components of gram-negative bacteria. Our results showed that LGI3 was indeed secreted by LPS-stimulated HaCaT cells. We also found that LPS potently stimulated the induction of cycloxygenase-2 (COX-2), which is involved in the inflammatory response. In addition, LPS-induced LGI3 secretion and COX-2 expression were blocked by NS-398, a selective COX-2 inhibitor. Moreover, LPS activated nuclear factor-κB (NF-κB) via a TRIF-dependent pathway, and activated NF-κB led to LGI3 production in HaCaT cells. For the first time, we predicted the LGI3 promoter sequence and demonstrated that NF-κB bound to the LGI3 gene promoter region. LPS treatment also increased the expression of a disintegrin and metalloproteinase domain-containing protein 22 (ADAM22), a candidate LGI3 receptor. Furthermore, co-immunoprecipitation, flow cytometry, and immunocytochemistry revealed that LGI3 associated with ADAM22 in LPS-treated keratinocytes. Thus, ADAM22 may be an LGI3 receptor in human keratinocytes. Taken together, these data suggest that the TRIF-dependent pathway is a novel regulator of LGI3 secretion in response to LPS stimulation in HaCaT cells and that keratinocyte-derived LGI3 interacts with ADAM22 and mediates LPS-induced inflammation."xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.cyto.2019.154872"xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/author | "Lee S.H."xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/author | "Kim D.S."xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/author | "Yun H.Y."xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/author | "Baek K.J."xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/author | "Kwon N.S."xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/name | "Cytokine"xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/pages | "154872"xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/title | "LGI3 is secreted and binds to ADAM22 via TRIF-dependent NF-kappaB pathway in response to LPS in human keratinocytes."xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://purl.uniprot.org/core/volume | "126"xsd:string |
| http://purl.uniprot.org/citations/31627033 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/31627033 |
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