Matches in UGent Biblio for { <https://biblio.ugent.be/publication/211435#aggregation> ?p ?o. }
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- aggregation classification "A1".
- aggregation creator B162649.
- aggregation creator B162650.
- aggregation creator B162651.
- aggregation creator B162652.
- aggregation creator B162653.
- aggregation creator person.
- aggregation date "2001".
- aggregation format "application/pdf".
- aggregation hasFormat 211435.bibtex.
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- aggregation isPartOf urn:issn:0270-7306.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Science General".
- aggregation title "Essential role of STAT3 in the control of the acute-phase response as revealed by inducible gene activation in the liver".
- aggregation abstract "We generated mice carrying a STAT3 allele amenable to Cre-mediated deletion and intercrossed them with R-lx-Cre transgenic mice, in which the expression of Cre recombinase can be induced by type I interferon. Interferon-induced deletion of STAT3 occurred very efficiently (more than 90%) in the liver and slightly less efficiently (about 70%) in the bone marrow. Analysis of the induction of liver acute-phase genes in response to bacterial lipopolysaccharide unequivocally identifies STAT3 as a fundamental mediator of their induction. The different degrees of defectiveness displayed by the various genes allowed us to differentiate them into three separate groups according to their degree of dependence on STAT3. Induction was totally defective for group I genes, defective at 24 h but almost normal at earlier time points for group II. genes, and only slightly defective for group III genes. This division was in good agreement with the known structures of the respective promoters. We also found that the overall induction of the transcription factors C/EBP beta and -delta was only minimally defective in the absence of STAT3. Finally, even though corticosterone levels and action were found to be normal in the conditional-mutant mice, production of both proinflammatory and antiinflammatory cytokines was increased and prolonged, probably as a result of STAT3 deletion in macrophages.".
- aggregation authorList BK402901.
- aggregation endPage "1632".
- aggregation issue "5".
- aggregation startPage "1621".
- aggregation volume "21".
- aggregation aggregates 621201.
- aggregation isDescribedBy 211435.
- aggregation similarTo MCB.21.5.1621-1632.2001.
- aggregation similarTo LU-211435.