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- aggregation classification "A1".
- aggregation creator B674513.
- aggregation creator B674514.
- aggregation creator person.
- aggregation creator person.
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- aggregation date "2013".
- aggregation format "application/pdf".
- aggregation hasFormat 3182293.bibtex.
- aggregation hasFormat 3182293.csv.
- aggregation hasFormat 3182293.dc.
- aggregation hasFormat 3182293.didl.
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- aggregation hasFormat 3182293.yaml.
- aggregation isPartOf urn:issn:1757-4676.
- aggregation language "eng".
- aggregation rights "I have retained and own the full copyright for this publication".
- aggregation subject "Medicine and Health Sciences".
- aggregation title "LPS resistance of SPRET/Ei mice is mediated by Gilz, encoded by the Tsc22d3 gene on the X chromosome".
- aggregation abstract "Natural variation for LPS-induced lethal inflammation in mice is useful for identifying new genes that regulate sepsis, which could form the basis for novel therapies for systemic inflammation in humans. Here we report that LPS resistance of the inbred mouse strain SPRET/Ei, previously reported to depend on the glucocorticoid receptor (GR), maps to the distal region of the X-chromosome. The GR-inducible gene Tsc22d3, encoding the protein Gilz and located in the critical region on the X-chromosome, showed a higher expressed SPRET/Ei allele, regulated in cis. Higher Gilz levels were causally related to reduced inflammation, as shown with knockdown and overexpression studies in macrophages. Transient overexpression of Gilz by hydrodynamic plasmid injection confirmed that Gilz protects mice against endotoxemia Our data strongly suggest that Gilz is responsible for the LPS resistance of SPRET/Ei mice and that it could become a treatment option for sepsis.".
- aggregation authorList BK1036166.
- aggregation endPage "470".
- aggregation issue "3".
- aggregation startPage "456".
- aggregation volume "5".
- aggregation aggregates 3182377.
- aggregation isDescribedBy 3182293.
- aggregation similarTo emmm.201201683.
- aggregation similarTo LU-3182293.