| http://purl.uniprot.org/citations/23583459 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23583459 | http://www.w3.org/2000/01/rdf-schema#comment | "When transmembrane form of tumor necrosis factor (mTNF) interacts with its cognate receptors or agonistic antibodies signaling pathways are activated in the ligand expressing cells. This "reverse signaling" appears a fine-tuning control mechanism in the immune response. Despite a clinical relevance key molecules of TNF reverse signaling and their functions remain elusive. We examined the role of CKIP-1, an interacting partner of the N terminal fragment of mTNF in inflammation and TNF reverse signaling. We found that CKIP-1 expression was elevated upon LPS challenge in THP-1 human monocyte model cells. Overexpression of CKIP-1 triggered classical activation of THP-1 cells and transactivated the human TNF promoter when co-expressed with c-Jun in the HEK293 model system. TNF reverse signaling induced a massive translocation of CKIP-1 from the plasma membrane to intracellular compartments in THP-1 cells. Expression of the N terminal fragment of mTNF in HEK293 cells resembled the effects of TNF reverse signaling with respect to relocalization of CKIP-1. In parallel with the translocation, CKIP-1-triggered activation of THP-1 cells was antagonized by TNF reverse signaling. Similarly, the presence of the N terminal fragment of mTNF inhibited CKIP-1 mediated TNF promoter activation in HEK293 cells. Both TNF reverse signaling in THP-1 cells and expression of the N terminal fragment of mTNF in HEK293 cells were found to induce apoptosis that could be prevented by overexpression of CKIP-1. Our findings demonstrate that CKIP-1 activates pro-inflammatory pathways and interferes with TNF reverse signaling induced apoptosis in human model cells."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.imlet.2013.04.001"xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/author | "Juhasz K."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/author | "Sonnleitner A."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/author | "Duda E."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/author | "Zvara A."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/author | "Balogi Z."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/author | "Nimmervoll B."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/author | "Lipp A.M."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/name | "Immunol Lett"xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/pages | "55-64"xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/title | "Casein kinase 2-interacting protein-1, an inflammatory signaling molecule interferes with TNF reverse signaling in human model cells."xsd:string |
| http://purl.uniprot.org/citations/23583459 | http://purl.uniprot.org/core/volume | "152"xsd:string |
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