J. J. Yang

发表

Circumvention of normal constraints on granule protein gene expression in peripheral blood neutrophils and monocytes of patients with antineutrophil cytoplasmic autoantibody-associated glomerulonephritis.

D. Alcorta, R. Falk, J. Jennette, 2004, Journal of the American Society of Nephrology : JASN.

Novel effects of neutrophil-derived proteinase 3 and elastase on the vascular endothelium involve in vivo cleavage of NF-kappaB and proapoptotic changes in JNK, ERK, and p38 MAPK signaling pathways.

R. Falk, J. Jennette, W. Pendergraft, 2002, Journal of the American Society of Nephrology : JASN.

Understanding the pathogenesis of ANCA: where are we today?

R. Falk, Hong Xiao, G. Preston, 2002, Cleveland Clinic journal of medicine.

Are ANCA pathogenetic? Pros and cons

R. Falk, J. Jennette, J. J. Yang, 1997 .

Antibodies with dual reactivity to plasminogen and complementary PR3 in PR3-ANCA vasculitis.

A. Wolberg, R. Falk, J. Jennette, 2008, Journal of the American Society of Nephrology : JASN.

Animal models in ANCA‐vasculitis

R. Kettritz, R. Falk, J. Jennette, 1995, Clinical and experimental immunology.

Expression profile of leukocyte genes activated by anti-neutrophil cytoplasmic autoantibodies (ANCA).

D. Alcorta, R. Falk, J. Jennette, 2002, Kidney international.

Microarray Studies of Gene Expression in Circulating Leukocytes in Kidney Diseases

D. Alcorta, R. Falk, J. Jennette, 2002, Nephron Experimental Nephrology.

Epigenetic basis for aberrant upregulation of autoantigen genes in humans with ANCA vasculitis.

T. Magnuson, D. Ciavatta, R. Falk, 2010, The Journal of clinical investigation.

ANCA antigens, proteinase 3 and myeloperoxidase, are not expressed in endothelial cells.

D. Alcorta, R. Falk, J. Jennette, 2000, Kidney international.

Internalization of proteinase 3 is concomitant with endothelial cell apoptosis and internalization of myeloperoxidase with generation of intracellular oxidants.

P. Heeringa, R. Falk, J. Jennette, 2001, The American journal of pathology.

Apoptosis of endothelial cells induced by the neutrophil serine proteases proteinase 3 and elastase.

R. Kettritz, R. Falk, J. Jennette, 1996, The American journal of pathology.