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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
49
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pubmed:dateCreated |
1993-1-21
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pubmed:databankReference |
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pubmed:abstractText |
C4b-binding protein (C4BP) is involved in the fluid-phase regulation of the classical pathway of complement. During an acute-phase response, we have shown that hepatic levels of murine C4BP mRNA are elevated 2.5-fold while rat liver C4BP gene expression exhibits a 4-fold induction. Furthermore, a survey of different mouse tissues showed that during acute inflammation C4BP gene expression was confined to the liver. To gain a better understanding of the acute-phase regulation of C4BP gene expression we utilized the rat hepatoma cell line FAO in which tumor necrosis factor-alpha (TNF-alpha) produced a 2.7-fold induction of C4BP mRNA levels. In the absence of TNF-alpha, interleukin-1 alpha (IL-1 alpha) and interleukin-6 (IL-6) had little effect on C4BP gene expression but when all three cytokines were used together a synergistic 4-fold induction of C4BP mRNA levels was observed. In contrast the synthetic glucocorticoid dexamethasone inhibited TNF-alpha-induced C4BP gene expression. Cycloheximide-mediated inhibition of inducible C4BP gene expression demonstrated the requirement for ongoing protein synthesis. Rapid induction of C4BP mRNA levels by TNF-alpha and IL-6 (within 1 h) and the observation that stimulation was inhibited by actinomycin D provided evidence that regulation of C4BP gene expression during the acute-phase response is regulated at the transcriptional level. Isolation of a genomic clone extending into the 5' regulatory region of the rat C4BP gene enabled us to identify the major transcriptional start site and putative response elements through which TNF-alpha, IL-6, IL-1 alpha, and dexamethasone may exert their effects on C4BP gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0006-2960
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
12376-84
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1339286-Acute-Phase Reaction,
pubmed-meshheading:1339286-Animals,
pubmed-meshheading:1339286-Base Sequence,
pubmed-meshheading:1339286-Carrier Proteins,
pubmed-meshheading:1339286-Complement Inactivator Proteins,
pubmed-meshheading:1339286-Cycloheximide,
pubmed-meshheading:1339286-Female,
pubmed-meshheading:1339286-Gene Expression Regulation,
pubmed-meshheading:1339286-Glycoproteins,
pubmed-meshheading:1339286-Interleukin-1,
pubmed-meshheading:1339286-Interleukin-6,
pubmed-meshheading:1339286-Male,
pubmed-meshheading:1339286-Mice,
pubmed-meshheading:1339286-Mice, Inbred CBA,
pubmed-meshheading:1339286-Molecular Sequence Data,
pubmed-meshheading:1339286-RNA, Messenger,
pubmed-meshheading:1339286-Rats,
pubmed-meshheading:1339286-Rats, Inbred F344,
pubmed-meshheading:1339286-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:1339286-Sequence Homology, Nucleic Acid,
pubmed-meshheading:1339286-Transcription, Genetic,
pubmed-meshheading:1339286-Tumor Cells, Cultured,
pubmed-meshheading:1339286-Tumor Necrosis Factor-alpha
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pubmed:year |
1992
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pubmed:articleTitle |
Regulation of C4b-binding protein gene expression by the acute-phase mediators tumor necrosis factor-alpha, interleukin-6, and interleukin-1.
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pubmed:affiliation |
Department of Immunology, Scripps Research Institute, La Jolla, California 92037.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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