Matches in UGent Biblio for { <https://biblio.ugent.be/publication/1891614#aggregation> ?p ?o. }
Showing items 1 to 27 of
27
with 100 items per page.
- aggregation classification "D1".
- aggregation creator person.
- aggregation date "2011".
- aggregation format "application/pdf".
- aggregation hasFormat 1891614.bibtex.
- aggregation hasFormat 1891614.csv.
- aggregation hasFormat 1891614.dc.
- aggregation hasFormat 1891614.didl.
- aggregation hasFormat 1891614.doc.
- aggregation hasFormat 1891614.json.
- aggregation hasFormat 1891614.mets.
- aggregation hasFormat 1891614.mods.
- aggregation hasFormat 1891614.rdf.
- aggregation hasFormat 1891614.ris.
- aggregation hasFormat 1891614.txt.
- aggregation hasFormat 1891614.xls.
- aggregation hasFormat 1891614.yaml.
- aggregation language "eng".
- aggregation publisher "Ghent University. Faculty of Sciences".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Molecular cloning of the X-chromosome located LPS-resistance gene of SPRET/Ei mice: Tsc22d3/Gilz as a candidate gene".
- aggregation abstract "Sepsis is an overwhelming systemic inflammatory response of the host to infection, and despite the recent advances in critical care medicine, it is still a leading cause of death in intensive care units in developed countries. Lipopolysaccharide (LPS) or endotoxin, is the principal component of the outer membrane of Gram-negative bacteria, and is per se capable of reproducing several features of a Gram-negative infection, including fever, shock and other characteristics of severe sepsis, as organ dysfunction and hypotension. SPRET/Ei, an inbred mouse strain derived from Mus spretus, is highly resistant to both LPS and Gram-negative bacterial infections, and is therefore a useful model on the discovery of new targets for sepsis treatment. In the present study we show that SPRET/Ei LPS-resistance is linked to the X chromosome, most precisely to a locus located between 55 and 70 cM. Moreover, we have recently shown that SPRET/Ei LPS-resistance can be completely abolished by blocking the signaling mediated by the glucocorticoid receptor (GR). The most well-known gene responding to the signaling initiated by the binding of glucocorticoids to its receptor, the GR, is Tsc22d3/Gilz. Gilz is an important anti-inflammatory gene, and these effects were shown to be largely mediated by repressing NF-B- and AP-1-dependent gene transcription. Gilz is located on the X chromosome in the region defined by the linkage analysis as the one containing the SPRET/Ei gene(s) responsible for its resistance to LPS. GILZ mRNA and protein induction after LPS seem to be organ-specific. For example, it seems to be upregulated by LPS in the lung and downregulated in the liver. Moreover, in both organs, but particularly in the lung, Gilz mRNA expression is higher in SPRET/Ei mice and (BxS)F1 females, when compared to C57BL/6 mice and (BxS)F1-males. Different tools are currently being developed to confirm the importance of this gene in SPRET/Ei LPS-resistance. Altogether, we believe that these results may be of potential interest for future therapeutic application for the treatment of sepsis.".
- aggregation authorList BK35726.
- aggregation aggregates 4335663.
- aggregation isDescribedBy 1891614.
- aggregation similarTo LU-1891614.