Association of single-nucleotide polymorphisms in the polymeric immunoglobulin receptor gene with immunoglobulin A nephropathy (IgAN) in Japanese patients

[1]  Y. Ohnishi,et al.  Single-nucleotide polymorphisms in the class II region of the major histocompatibility complex in Japanese patients with immunoglobulin A nephropathy , 2002, Journal of Human Genetics.

[2]  Yusuke Nakamura,et al.  Association between single-nucleotide polymorphisms in selectin genes and immunoglobulin A nephropathy. , 2002, American journal of human genetics.

[3]  A. Sekine,et al.  Catalog of 258 single-nucleotide polymorphisms (SNPs) in genes encoding three organic anion transporters, three organic anion-transporting polypeptides, and three NADH:ubiquinone oxidoreductase flavoproteins , 2001, Journal of Human Genetics.

[4]  Yusuke Nakamura,et al.  A high-throughput SNP typing system for genome-wide association studies , 2001, Journal of Human Genetics.

[5]  R. Lifton,et al.  IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22–23 , 2000, Nature Genetics.

[6]  W. Owen,et al.  Evidence for genetic factors in the development and progression of IgA nephropathy. , 2000, Kidney international.

[7]  J. Todd,et al.  Evaluation of single nucleotide polymorphism typing with invader on PCR amplicons and its automation. , 2000, Genome research.

[8]  Y. Iwakura,et al.  Generation of polymeric immunoglobulin receptor-deficient mouse with marked reduction of secretory IgA. , 1999, Journal of immunology.

[9]  L. Kruglyak Prospects for whole-genome linkage disequilibrium mapping of common disease genes , 1999, Nature Genetics.

[10]  M. Ehm,et al.  Detecting marker-disease association by testing for Hardy-Weinberg disequilibrium at a marker locus. , 1998, American journal of human genetics.

[11]  Masaki Kobayashi,et al.  Natural history and risk factors for immunoglobulin a nephropathy in Japan , 1997 .

[12]  J. D. de Fijter,et al.  Deficient IgA1 immune response to nasal cholera toxin subunit B in primary IgA nephropathy. , 1996, Kidney international.

[13]  S. Harper,et al.  Increased dimeric IgA producing B cells in the bone marrow in IgA nephropathy determined by in situ hybridisation for J chain mRNA. , 1996, Journal of clinical pathology.

[14]  F. Schena Immunogenetic aspects of primary IgA nephropathy. , 1995, Kidney international.

[15]  E. Lander,et al.  Genetic dissection of complex traits: guidelines for interpreting and reporting linkage results , 1995, Nature Genetics.

[16]  N. Risch,et al.  A comparison of linkage disequilibrium measures for fine-scale mapping. , 1995, Genomics.

[17]  M. Arakawa,et al.  Immunohistochemical characterization of glomerular IgA deposits in IgA nephropathy. , 1990, Clinical nephrology.

[18]  P. Krajči,et al.  Molecular cloning of the human transmembrane secretory component (poly-Ig receptor) and its mRNA expression in human tissues. , 1989, Biochemical and biophysical research communications.

[19]  M. Daha,et al.  Serum IgA and the production of IgA by peripheral blood and bone marrow lymphocytes in patients with primary IgA nephropathy: evidence for the bone marrow as the source of mesangial IgA. , 1988, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[20]  H. Prydz,et al.  Direct evidence for an integrated function of J chain and secretory component in epithelial transport of immunoglobulins , 1984, Nature.

[21]  G. Blobel,et al.  The receptor for transepithelial transport of IgA and IgM contains multiple immunoglobulin-like domains , 1984, Nature.

[22]  M. Kilian,et al.  Perturbation of mucosal immune defence mechanisms by bacterial IgA proteases. , 1983, Bulletin europeen de physiopathologie respiratoire.

[23]  J. Egido,et al.  IgA glomerulonephritis (Berger's disease): evidence of high serum levels of polymeric IgA. , 1980, Clinical and experimental immunology.