ArticleProceedings of the National Academy of Sciences of the United States of America1999
Lps(d)/Ran of endotoxin-resistant C3H/HeJ mice is defective in mediating lipopolysaccharide endotoxin responses.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 45 citations in OpenAlex.
- The Calm after the Storm: Implications of Sepsis Immunoparalysis on Host Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Sepsis-induced suppression of lung innate immunity is mediated by IRAK-M.The Journal of clinical investigation · 2006Article
- Mannan derivatives induce phenotypic and functional maturation of mouse dendritic cells.Immunology · 2006Article
- Quantitative aspects of lipopolysaccharide and cytokine requirements to generate nitric oxide in macrophages from LPS-hyporesponsive (Lps(d)) C3H/HeJ mice.Folia microbiologica · 2004Article
- Presence of Lps(d) mutation influences cytokine regulation in vivo by the Mycoplasma arthritidis mitogen superantigen and lethal toxicity in mice infected with M. arthritidis.Infection and immunity · 2001Article
- Specific association of Type I c-Abl with Ran GTPase in lipopolysaccharide-mediated differentiation.Oncogene · 2001Article
- Differential expression of caveolin-1 in lipopolysaccharide-activated murine macrophages.Infection and immunity · 2000Article
- Toll-like receptor 4-deficient mice have reduced bone destruction following mixed anaerobic infection.Infection and immunity · 2000Article
- Regulation of matrix metalloproteinases and their inhibitor genes in lipopolysaccharide-induced endotoxemia in mice.The American journal of pathology · 2000Article
- Dominant negative down-regulation of endotoxin-induced tumor necrosis factor alpha production by Lps(d)/Ran.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
C3H/HeJ inbred mice are defective in that they are highly resistant to endotoxic shock as compared with normal responder mice. Their B cells and macrophages do not respond significantly when exposed to lipopolysaccharide (LPS), whereas cells from the responder mice do. Using a functional assay, we previously isolated a cDNA, which encodes for Ran/TC4 GTPase. We now show that this gene is mutated in C3H/HeJ mice, which accounts for their resistance to endotoxin stimulation. Sequence analysis of independent mutant Lps(d)/Ran cDNAs isolated from splenic B cells of C3H/HeJ mice reveals a consistent single base substitution at position 870, where a thymidine is replaced with a cytidine. In situ hybridization maps the Lps(d)/Ran cDNA to mouse chromosome 4. By retroviral gene transfer, the wild-type Lps(n)/Ran cDNA but not the mutant Lps(d)/Ran cDNA can restore LPS responsiveness of C3H/HeJ cells. Adenoviral gene transfer in vivo with the mutant Lps(d)/Ran cDNA but not the wild-type Lps(n)/Ran cDNA rescues endotoxin-sensitive mice from septic shock. Thus Lps/Ran is an important target for LPS-mediated signal transduction, and the Lps(d)/Ran gene may be useful as a therapeutic sequence in gene therapy for endotoxemia and septic shock.
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