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Restoration of lipopolysaccharide-mediated B-cell response after expression of a cDNA encoding a GTP-binding protein
1Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
Previous analysis of hybrid progeny derived from lipopolysaccharide (LPS) responder and nonresponder inbred mouse strains demonstrated that a single genetic locus controlled responsiveness to LPS. Using a differential functional screening approach, we report the isolation of a cDNA that has sequence homology to a GTP-binding protein. Expression of the cDNA in splenic B cells of C3H/HeJ nonresponder, endotoxin-resistant mice resulted in polyclonal B-cell activation in response to LPS stimulation. Thus a GTP-binding protein may be involved in LPS stimulation in B cells and perhaps other cell types.
Previous analysis of hybrid progeny derived from lipopolysaccharide (LPS) responder and nonresponder inbred mouse strains demonstrated that a single genetic locus controlled responsiveness to LPS. Using a differential functional screening approach, we report the isolation of a cDNA that has sequence homology to a GTP-binding protein. Expression of the cDNA in splenic B cells of C3H/HeJ nonresponder, endotoxin-resistant mice resulted in polyclonal B-cell activation in response to LPS stimulation. Thus a GTP-binding protein may be involved in LPS stimulation in B cells and perhaps other cell types.