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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007600,
umls-concept:C0016006,
umls-concept:C0017262,
umls-concept:C0021760,
umls-concept:C0033268,
umls-concept:C0033713,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0086418,
umls-concept:C0185117,
umls-concept:C0205225,
umls-concept:C0227525,
umls-concept:C0597357,
umls-concept:C0677626,
umls-concept:C1749467,
umls-concept:C2911684
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pubmed:issue |
8
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pubmed:dateCreated |
1998-11-24
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pubmed:abstractText |
Interleukin 6 (IL-6) belongs to a family of cytokines using receptors sharing a common signal-transducing chain, gp130 and containing a specific ligand-binding chain (IL-6R alpha). It was shown that both the membrane-bound and the soluble form (sIL-6R) of this ligand specific receptor chain occurs naturally. The soluble form of IL-6 receptor was found to be able to associate with the membrane-bound gp130 and to generate active IL-6 receptor complex capable of inducing signal transduction. This study on a human hepatoma cell line and primary rat hepatocytes examined how the effectiveness of IL-6 is modified by the presence of soluble IL-6 receptor and whether the sIL-6R in the absence of IL-6 acts on hepatocytes. The authors studied the gene expression of junB, a member of the Jun family of transcription factors, and the production of fibrinogen in response to IL-6 and sIL-6R. The data show that in hepatic cells, endogeneously expressing IL-6R, the IL-6 induced junB and fibrinogen expression is inhibited by the presence of sIL-6R. In addition we found that sIL-6R alone (in the absence of IL-6) induced junB mRNA expression, but had no effect on fibrinogen production.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1043-4666
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
620-6
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9722935-Animals,
pubmed-meshheading:9722935-Carcinoma, Hepatocellular,
pubmed-meshheading:9722935-Cells, Cultured,
pubmed-meshheading:9722935-Fibrinogen,
pubmed-meshheading:9722935-Gene Expression Regulation,
pubmed-meshheading:9722935-Humans,
pubmed-meshheading:9722935-Liver,
pubmed-meshheading:9722935-Polymerase Chain Reaction,
pubmed-meshheading:9722935-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:9722935-RNA, Messenger,
pubmed-meshheading:9722935-Rats,
pubmed-meshheading:9722935-Receptors, Interleukin-6,
pubmed-meshheading:9722935-Solubility,
pubmed-meshheading:9722935-Tumor Cells, Cultured
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pubmed:year |
1998
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pubmed:articleTitle |
Soluble interleukin 6 (IL-6) receptor influences the expression of the protooncogene junB and the production of fibrinogen in the HepG2 human hepatoma cell line and primary rat hepatocytes.
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pubmed:affiliation |
Department of Genetics, Cell- and Immunobiology, Semmelweis University Medical School, Budapest, Hungary.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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