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1 Goodpasture (GP) autoimmune disease is caused by autoant
2 Goodpasture (GP) disease is an autoimmune disorder in wh
3 Goodpasture antibodies only breach the quaternary struct
4 Goodpasture antigen-binding protein (GPBP), a BM protein
5 Goodpasture autoantibodies bind two conformational epito
6 Goodpasture autoantibodies, which bound to murine alpha3
7 Goodpasture autoantigen [collagen alpha3(IV)NC1; approxi
8 Goodpasture disease is an autoimmune kidney disease medi
9 Goodpasture epitopes in the native autoantigen are crypt
10 Goodpasture syndrome is an autoimmune disease of the kid
11 Goodpasture syndrome is an autoimmune vascular disease a
12 Goodpasture's (GP) disease is caused by autoantibodies t
15 ing type I diabetes, multiple sclerosis, and Goodpasture disease, is associated with particular human
17 la melanogaster, and Danio rerio do not bind Goodpasture autoantibodies, while Xenopus laevis, chicke
19 nforced M-alpha3alpha4alpha5(IV) hexamers by Goodpasture antibodies is a novel mechanism whereby path
20 to ROS specifically enhanced recognition by Goodpasture antibodies in a sequential and time-dependen
21 itions, like bronchiectasis, coagulopathies, Goodpasture's syndrome, and acute bronchopulmonary infec
24 with glomerular basement membrane diseases, Goodpasture's disease (GP) and Alport syndrome (AS), and
25 with glomerular basement membrane diseases, Goodpasture's disease and Alport syndrome, and determine
26 In contrast, alpha3NC1 monomers elicited Goodpasture-like murine antibodies, targeting the E(A) a
27 to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for
28 stration to rodents was sufficient to expose Goodpasture epitope in vivo and initiate autoantibody pr
29 y of reactive oxygen species (ROS) to expose Goodpasture epitopes buried within NC1 hexamers obtained
30 n probably contains one recognition site for Goodpasture autoantibodies, and an algorithm analysis of
31 opsy are essential to distinguish PICGN from Goodpasture syndrome and other immune-mediated renal dis
34 ) NC1 antibodies that cross-react with human Goodpasture [anti-GBM/anti-alpha3(IV) NC1] autoantibodie
39 reditary leiomyomatosis, and autoimmunity in Goodpasture syndrome; however, the transcriptional and d
40 he conformations of the antibody epitopes in Goodpasture's disease and Alport's post-transplantation
41 Rapidly progressive glomerulonephritis in Goodpasture disease is mediated by autoantibodies bindin
43 inst these two putative regions co-inhibited Goodpasture autoantibodies binding to denatured human al
44 contributes to the emergence of the 2 major Goodpasture epitopes on the human alpha3(IV)NC1 domain,
45 mergence and divergence of a multifunctional Goodpasture antigen-binding protein (GPBP), a basement m
46 phritis, diabetes mellitus, IgA nephropathy, Goodpasture's syndrome, and Alport syndrome renal epithe
49 erdin reductase (hBVR) and the expression of Goodpasture antigen-binding protein (GPBP), a nonconvent
50 re we investigate the molecular mechanism of Goodpasture disease, an HLA-linked autoimmune renal diso
51 glomerulonephritis (EAG), an animal model of Goodpasture's disease, can be induced in Wistar Kyoto (W
52 glomerulonephritis (EAG), an animal model of Goodpasture's disease, can be induced in Wistar Kyoto (W
53 glomerulonephritis (EAG), an animal model of Goodpasture's disease, can be induced in Wistar Kyoto (W
54 glomerulonephritis (EAG), an animal model of Goodpasture's disease, can be induced in Wistar Kyoto (W
55 nephritis (EAG), which is an animal model of Goodpasture's disease, can be induced in Wistar Kyoto ra
56 oimmune glomerulonephritis (EAG), a model of Goodpasture's disease, Wistar Kyoto (WKY) rats immunized
59 bunits were identified as a native target of Goodpasture autoantibodies in the GBM of squirrel monkey
60 rular basement membrane (GBM) are targets of Goodpasture autoantibodies or Alport posttransplant neph
61 antation nephritis was compared with that of Goodpasture autoantibodies from patients with autoimmune
62 lomerular basement membrane (GBM) disease or Goodpasture's syndrome is among the earliest recognized
63 ot from healthy controls or col(IV)-reactive Goodpasture's syndrome patients after renal transplant,
70 e's disease are specific for epitopes in the Goodpasture antigen (the NC1 domain of the alpha3 chain
71 by 30-50%, respectively, thereby keeping the Goodpasture epitopes largely concealed when compared wit
74 is for the crypticity of the epitopes of the Goodpasture autoantigen, the alpha3alpha4alpha5 noncolla
75 pical protein kinase that phosphorylates the Goodpasture auto-antigen, the alpha3 chain of collagen I
76 y demonstrates, for the first time, that the Goodpasture antigen-binding protein (GPBP) binds to huma
77 pends on both Ab and T cell responses to the Goodpasture Ag noncollagenous domain 1 of the alpha3-cha
79 In summary, our findings characterize two Goodpasture epitopes confined to each end of the alpha3
81 145-specific T cells expand in patients with Goodpasture disease and, in alpha3135-145-immunized HLA-
84 antibodies were analyzed in 14 patients with Goodpasture's disease and 2 patients with Alport's post-
85 new therapeutic strategies for patients with Goodpasture's disease and other autoimmune disorders.
87 undant autoreactive T cells in patients with Goodpasture's disease are specific for peptides in the a
88 antibodies were analyzed in 57 patients with Goodpasture's disease, and kidney-bound antibodies were