Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H
Author:
Publisher
Springer Science and Business Media LLC
Subject
Genetics
Link
http://www.nature.com/articles/ng912z.pdf
Reference30 articles.
1. Pangburn, M.K. & Muller-Eberhard, H.J. Relation of putative thioester bond in C3 to activation of the alternative pathway and the binding of C3b to biological targets of complement. J. Exp. Med. 152, 1102–1114 (1980).
2. Pangburn, M.K. & Muller-Eberhard, H.J. Complement C3 convertase: cell surface restriction of β1H control and generation of restriction on neuraminidase-treated cells. Proc. Natl Acad. Sci. USA 75, 2416–2420 (1978).
3. Weiler, J.M., Daha, M.R., Austen, K.F. & Fearon, D.T. Control of the amplification convertase of complement by the plasma protein β1H. Proc. Natl Acad. Sci. USA 73, 3268–3272 (1976).
4. Pangburn, M.K., Schreiber, R.D. & Muller-Eberhard, H.J. Human complement C3b inactivator: isolation, characterization, and demonstration of an absolute requirement for the serum protein β1H for cleavage of C3b and C4b in solution. J. Exp. Med. 146, 257–270 (1977).
5. Vogt, B.A., Wyatt, R.J., Burke, B.A., Simonton, S.C. & Kashtan, C.E. Inherited factor H deficiency and collagen type III glomerulopathy. Pediatr. Nephrol. 9, 11–15 (1995).
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