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• W2091713887 endingPage "11548" @default.
• W2091713887 startingPage "11543" @default.
• W2091713887 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." @default.
• W2091713887 created "2016-06-24" @default.
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• W2091713887 date "1999-09-28" @default.
• W2091713887 modified "2023-10-14" @default.
• W2091713887 title "Lps^d/Ran of endotoxin-resistant C3H/HeJ mice is defective in mediating lipopolysaccharide endotoxin responses" @default.
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• W2091713887 doi "https://doi.org/10.1073/pnas.96.20.11543" @default.
• W2091713887 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/18070" @default.
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• W2091713887 hasPublicationYear "1999" @default.
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