Complement receptor 2 polymorphisms associated with systemic lupus erythematosus modulate alternative splicing
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P. Gaffney | M. Petri | J. Reveille | C. Langefeld | G. Alarcón | T. Vyse | J. Harley | C. Jacob | K. Kaufman | R. Kimberly | K. Moser | G. Gilkeson | J. Edberg | B. Tsao | E. Brown | J. Merrill | R. Ramsey‐Goldman | L. Vilá | J. James | J. Ziegler | S. Boackle | D. Ulgiati | K. B. Douglas | D. Windels | A. V. Gadeliya | Jian Zhao | Hui Wu | M. Alarcón-Riquelme | E. Brown
[1] B. Frey,et al. Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing , 2008, Nature Genetics.
[2] Jyoti K. Shah,et al. Differential expression of 24 , 426 human alternative splicing events and predicted cis-regulation in 48 tissues and cell lines , 2011 .
[3] Eric T. Wang,et al. Alternative Isoform Regulation in Human Tissue Transcriptomes , 2008, Nature.
[4] Marta E Alarcón-Riquelme,et al. Genome-wide association scan in women with systemic lupus erythematosus identifies susceptibility variants in ITGAM, PXK, KIAA1542 and other loci , 2008, Nature Genetics.
[5] Jacek Majewski,et al. Genome-wide analysis of transcript isoform variation in humans , 2008, Nature Genetics.
[6] T. Shimoda,et al. Association of polymorphisms in complement component C3 gene with susceptibility to systemic lupus erythematosus. , 2008, Rheumatology.
[7] K. J. Hertel,et al. Combinatorial Control of Exon Recognition* , 2008, Journal of Biological Chemistry.
[8] Rolf Backofen,et al. Pre-mRNA Secondary Structures Influence Exon Recognition , 2007, PLoS genetics.
[9] Guey-Shin Wang,et al. Splicing in disease: disruption of the splicing code and the decoding machinery , 2007, Nature Reviews Genetics.
[10] Manuel A. R. Ferreira,et al. PLINK: a tool set for whole-genome association and population-based linkage analyses. , 2007, American journal of human genetics.
[11] B. Croker,et al. Augmentation of NZB Autoimmune Phenotypes by the Sle1c Murine Lupus Susceptibility Interval1 , 2007, The Journal of Immunology.
[12] R. Cantor,et al. Association of a common complement receptor 2 haplotype with increased risk of systemic lupus erythematosus , 2007, Proceedings of the National Academy of Sciences.
[13] A. Kornblihtt. Chromatin, transcript elongation and alternative splicing , 2006, Nature Structural &Molecular Biology.
[14] M. Farrall,et al. Integrating Case‐control and TDT Studies , 2005 .
[15] M Farrall,et al. Integrating case-control and TDT studies. , 2005, Annals of human genetics.
[16] V. Holers,et al. Complement receptors and the shaping of the natural antibody repertoire , 2005, Springer Seminars in Immunopathology.
[17] B. Tsao. Update on human systemic lupus erythematosus genetics , 2004, Current opinion in rheumatology.
[18] S. Gallati,et al. The role of common single‐nucleotide polymorphisms on exon 9 and exon 12 skipping in nonmutated CFTR Alleles , 2004, Human mutation.
[19] G. Tsokos,et al. NF-κB Regulates the Expression of the Human Complement Receptor 2 Gene1 , 2002, The Journal of Immunology.
[20] L. Morel,et al. A Role for the Cr2 Gene in Modifying Autoantibody Production in Systemic Lupus Erythematosus1 , 2002, The Journal of Immunology.
[21] V. Holers,et al. Functional Analysis of the Human Complement Receptor 2 (CR2/CD21) Promoter: Characterization of Basal Transcriptional Mechanisms1 , 2002, The Journal of Immunology.
[22] V. Holers,et al. CR2/CD21 Proximal Promoter Activity Is Critically Dependent on a Cell Type-Specific Repressor1 , 2001, The Journal of Immunology.
[23] D. Karp,et al. Cr2, a candidate gene in the murine Sle1c lupus susceptibility locus, encodes a dysfunctional protein. , 2001, Immunity.
[24] Christopher J. Lee,et al. Genome-wide detection of alternative splicing in expressed sequences of human genes , 2001, Nucleic Acids Res..
[25] G. Tsokos,et al. Multiple Transcription Factors Regulate the Inducible Expression of the Human Complement Receptor 2 Promoter1 , 2001, The Journal of Immunology.
[26] K. Makar,et al. A site in the complement receptor 2 (CR2/CD21) silencer is necessary for lineage specific transcriptional regulation. , 2001, International immunology.
[27] K. Blenman,et al. Genetic reconstitution of systemic lupus erythematosus immunopathology with polycongenic murine strains. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[28] C. Goodnow,et al. A critical role for complement in maintenance of self-tolerance. , 1998, Immunity.
[29] J. Cyster,et al. Polygenic autoimmune traits: Lyn, CD22, and SHP-1 are limiting elements of a biochemical pathway regulating BCR signaling and selection. , 1998, Immunity.
[30] M. Dehoff,et al. An intronic silencer regulates B lymphocyte cell- and stage-specific expression of the human complement receptor type 2 (CR2, CD21) gene. , 1998, Journal of immunology.
[31] M. Hochberg,et al. Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. , 1997, Arthritis and rheumatism.
[32] I. Melchers,et al. Analysis of the human CD21 transcription unit reveals differential splicing of exon 11 in mature transcripts and excludes alternative splicing as the mechanism causing solubilization of CD21. , 1997, Molecular immunology.
[33] J. Banchereau,et al. Follicular Dendritic Cells Specifically Express the Long CR2/CD21 Isoform , 1997, The Journal of experimental medicine.
[34] H. Marquart,et al. Complement receptor expression and activation of the complement cascade on B lymphocytes from patients with systemic lupus erythematosus (SLE) , 1995, Clinical and experimental immunology.
[35] Y. S. Choi,et al. Activation and proliferation of follicular dendritic cell-like cells by activated T lymphocytes. , 1994, Journal of immunology.
[36] D. Fearon,et al. Functional dissection of the CD21/CD19/TAPA-1/Leu-13 complex of B lymphocytes , 1993, The Journal of experimental medicine.
[37] E. Levy,et al. T lymphocyte expression of complement receptor 2 (CR2/CD21): a role in adhesive cell‐cell interactions and dysregulation in a patient with systemic lupus erythematosus (SLE) , 1992, Clinical and experimental immunology.
[38] J. Bonnefoy,et al. CD21 is a ligand for CD23 and regulates IgE production , 1992, Nature.
[39] S. Mathur,et al. Epstein Barr virus/complement C3d receptor is an interferon alpha receptor. , 1991, The EMBO journal.
[40] M. Reth,et al. Exon trap cloning: using PCR to rapidly detect and clone exons from genomic DNA fragments. , 1990, Nucleic acids research.
[41] J. Harley,et al. Genomic organization and polymorphisms of the human C3d/Epstein-Barr virus receptor. , 1989, The Journal of biological chemistry.
[42] D. Fearon,et al. Structure of the human B lymphocyte receptor for C3d and the Epstein- Barr virus and relatedness to other members of the family of C3/C4 binding proteins [published erratum appears in J Exp Med 1988 Nov 1;168(5):1953-4] , 1988, The Journal of experimental medicine.
[43] G. Nemerow,et al. Molecular cloning of the cDNA encoding the Epstein-Barr virus/C3d receptor (complement receptor type 2) of human B lymphocytes. , 1987, Proceedings of the National Academy of Sciences of the United States of America.
[44] P. Schur,et al. Decreased expression of the C3b/C4b receptor (CR1) and the C3d receptor (CR2) on B lymphocytes and of CR1 on neutrophils of patients with systemic lupus erythematosus. , 1986, Arthritis and rheumatism.
[45] P. A. Biro,et al. Epstein-Barr virus receptor of human B lymphocytes is the C3d receptor CR2. , 1984, Proceedings of the National Academy of Sciences of the United States of America.
[46] J F Fries,et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. , 1982, Arthritis and rheumatism.