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rdf:type |
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lifeskim:mentions |
umls-concept:C0021311,
umls-concept:C0021747,
umls-concept:C0026809,
umls-concept:C0035647,
umls-concept:C0036126,
umls-concept:C0037083,
umls-concept:C0279516,
umls-concept:C0332307,
umls-concept:C1415900,
umls-concept:C1710082,
umls-concept:C2349975
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pubmed:issue |
2
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pubmed:dateCreated |
2005-7-8
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pubmed:abstractText |
ISG15 is an IFN-inducible ubiquitin-like protein and its expression and conjugation to target proteins are dramatically induced upon viral or bacterial infection. We have generated a UBP43 knockout mouse model that is lacking an ISG15-specific isopeptidase to study the biological role of the protein ISGylation system. We report that UBP43-deficient mice are hypersensitive to LPS-induced lethality and that TIR domain-containing adapter inducing IFN-beta --> IFN regulatory factor 3 --> type I IFN is the major axis to induce protein ISGylation and UBP43 expression in macrophages upon LPS treatment. In ubp43(-/-) macrophages, upon LPS treatment we detected increased expression of IFN-stimulated genes, including genes for several cytokines and chemokines involved in the innate immune response. The ubp43(-/-) mice were able to restrict the growth of Salmonella typhimurium more efficiently than wild-type mice. These results clearly demonstrate two aspects of IFN-signaling, a beneficial effect against pathogens but a detriment to the body without strict control.
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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 |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Vesicular...,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/G1p2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Jak1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Janus Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/TICAM-1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Tlr4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4,
http://linkedlifedata.com/resource/pubmed/chemical/Ubiquitins,
http://linkedlifedata.com/resource/pubmed/chemical/Usp18 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-1767
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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 |
175
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
847-54
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16002682-Adaptor Proteins, Vesicular Transport,
pubmed-meshheading:16002682-Animals,
pubmed-meshheading:16002682-Bone Marrow Cells,
pubmed-meshheading:16002682-Cells, Cultured,
pubmed-meshheading:16002682-Cytokines,
pubmed-meshheading:16002682-Endopeptidases,
pubmed-meshheading:16002682-Interferon Type I,
pubmed-meshheading:16002682-Janus Kinase 1,
pubmed-meshheading:16002682-Ligands,
pubmed-meshheading:16002682-Lipopolysaccharides,
pubmed-meshheading:16002682-MAP Kinase Signaling System,
pubmed-meshheading:16002682-Macrophages,
pubmed-meshheading:16002682-Mice,
pubmed-meshheading:16002682-Mice, Inbred C57BL,
pubmed-meshheading:16002682-Mice, Knockout,
pubmed-meshheading:16002682-Protein-Tyrosine Kinases,
pubmed-meshheading:16002682-Receptors, Immunologic,
pubmed-meshheading:16002682-Salmonella Infections, Animal,
pubmed-meshheading:16002682-Salmonella typhimurium,
pubmed-meshheading:16002682-Shock, Septic,
pubmed-meshheading:16002682-Toll-Like Receptor 4,
pubmed-meshheading:16002682-Ubiquitins,
pubmed-meshheading:16002682-Up-Regulation
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pubmed:year |
2005
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pubmed:articleTitle |
Enhanced antibacterial potential in UBP43-deficient mice against Salmonella typhimurium infection by up-regulating type I IFN signaling.
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pubmed:affiliation |
Departments of Molecular and Experimental Medicine and Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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