Cutting edge: functional characterization of the effect of the C3H/HeJ defect in mice that lack an Lpsn gene: in vivo evidence for a dominant negative mutation.

Abstract excerpt

A point mutation in the Tlr4 gene, which encodes Toll-like receptor 4, has recently been proposed to underlie LPS hyporesponsiveness in C3H/HeJ mice (Lpsd). The data presented herein demonstrate that F1 progeny from crosses between mice that carry a approximately 9-cM deletion of chromosome 4 (including deletion of LpsTlr4) and C3H/HeJ mice (i.e., Lps0 x Lpsd F1 mice) exhibit a pattern of LPS sensitivity,...

Topics

• Animals
• Chromosome Mapping
• Crosses, Genetic
• Drosophila Proteins
• Genotype
• Haplotypes
• Lipopolysaccharides
• Macrophages
• Membrane Glycoproteins
• Mice
• Mice, Inbred C3H
• Mutation, Missense
• NF-kappa B