Point mutations of single amino acids abolish ability of alpha(3) NC1 domain to elicit experimental autoimmune glomerulonephritis in rats
We previously showed concordance between Goodpasture syndrome antibody binding and production of experimental glomerulonephritis using human chimeric proteins. We now examine a more limited aminoterminal region of alpha(3)( IV) non- collagenous domain ( NC1) and the impact of single amino acid ( AA) mutations of this region on glomerulonephritis induction. Rats were immunized with collagenase- sol