Search Results - (Author, Cooperation:T. W. Huizinga)
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1Y. Okada ; D. Wu ; G. Trynka ; T. Raj ; C. Terao ; K. Ikari ; Y. Kochi ; K. Ohmura ; A. Suzuki ; S. Yoshida ; R. R. Graham ; A. Manoharan ; W. Ortmann ; T. Bhangale ; J. C. Denny ; R. J. Carroll ; A. E. Eyler ; J. D. Greenberg ; J. M. Kremer ; D. A. Pappas ; L. Jiang ; J. Yin ; L. Ye ; D. F. Su ; J. Yang ; G. Xie ; E. Keystone ; H. J. Westra ; T. Esko ; A. Metspalu ; X. Zhou ; N. Gupta ; D. Mirel ; E. A. Stahl ; D. Diogo ; J. Cui ; K. Liao ; M. H. Guo ; K. Myouzen ; T. Kawaguchi ; M. J. Coenen ; P. L. van Riel ; M. A. van de Laar ; H. J. Guchelaar ; T. W. Huizinga ; P. Dieude ; X. Mariette ; S. L. Bridges, Jr. ; A. Zhernakova ; R. E. Toes ; P. P. Tak ; C. Miceli-Richard ; S. Y. Bang ; H. S. Lee ; J. Martin ; M. A. Gonzalez-Gay ; L. Rodriguez-Rodriguez ; S. Rantapaa-Dahlqvist ; L. Arlestig ; H. K. Choi ; Y. Kamatani ; P. Galan ; M. Lathrop ; S. Eyre ; J. Bowes ; A. Barton ; N. de Vries ; L. W. Moreland ; L. A. Criswell ; E. W. Karlson ; A. Taniguchi ; R. Yamada ; M. Kubo ; J. S. Liu ; S. C. Bae ; J. Worthington ; L. Padyukov ; L. Klareskog ; P. K. Gregersen ; S. Raychaudhuri ; B. E. Stranger ; P. L. De Jager ; L. Franke ; P. M. Visscher ; M. A. Brown ; H. Yamanaka ; T. Mimori ; A. Takahashi ; H. Xu ; T. W. Behrens ; K. A. Siminovitch ; S. Momohara ; F. Matsuda ; K. Yamamoto ; R. M. Plenge
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-01-07Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Alleles ; Animals ; Arthritis, Rheumatoid/*drug therapy/*genetics/metabolism/pathology ; Asian Continental Ancestry Group/genetics ; Case-Control Studies ; Computational Biology ; *Drug Discovery ; Drug Repositioning ; European Continental Ancestry Group/genetics ; Female ; Genetic Predisposition to Disease/*genetics ; Genome-Wide Association Study ; Hematologic Neoplasms/genetics/metabolism ; Humans ; Male ; Mice ; Mice, Knockout ; *Molecular Targeted Therapy ; Polymorphism, Single Nucleotide/geneticsPublished by: -
2WINKEL, J. G. J. ; TAX, W. J. M ; JACOBS, C. W. M. ; HUIZINGA, T. W. J. ; WILLEMS, P. H. G. M.
Oxford, UK : Blackwell Publishing Ltd
Published 1990Staff ViewISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: We have studied the effects of Fc receptor triggering on the free cytosolic Ca2+ concentration, [Ca2+]i, in U937. These cells express two types of IgG Fc receptors, FcγRI and FcγRII. Binding of several anti-FcγRI and anti-FcγRII mouse monoclonal antibodies (MoAb) to Quin2- or Indo-I-loaded U937 cells had no direct effect on [Ca2+]i. After addition of a bridging anti-mouse Ig antibody however, transient increases in [Ca2+]i were observed for both types of FcγR. One of the anti-FcγRII MoAb, CIKM5, was exceptional in that it could induce Ca2+ increases in U937 cells by itself. Studies with F(ab′)2 fragments of CIK M5 revealed that this MoAb simultaneously binds to FcγRII, via both its Fab and Fc fragments, which might induce cross-linking of two FcγRII molecules. One anti-FcγRI MoAb, 197, a mouse (m)IgG2a antibody directed to an epitope outside the IgG-binding region, remarkably also caused an immediate increase in [Ca2+]i, but only when added to U937 precultured with gamma interferon (IFN-γ). FcγRI can bind monomeric human IgG as well as mIgG2a, and cross-linking of cytophilic Ig induced an increase in [Ca2+]i. Our results show that [Ca2+]i increases can be induced only after cross-linking of FcγR, either via anti-FcγR MoAb or via Fc-FcR interactions. Furthermore, we show that FcγR cross-linking results in activation of the Ca2+/phosphatidylinositol (PI) signal transduction pathway.Type of Medium: Electronic ResourceURL: -
3ten Bokkel Huinink, D. ; Veltman, G. A. M. ; Huizinga, T. W. J. ; Roelfsema, F. ; Keizer, H. J.
Springer
Published 2000Staff ViewISSN: 1569-8041Keywords: cancer ; diabetes insipidus ; metastases ; pituitary glandSource: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: -
4Brinkman, Brigitta M. N. ; Huizinga, T. W. J. ; Breedveld, Ferdinand C. ; Verweij, C. L.
Springer
Published 1996Staff ViewISSN: 1432-1203Source: Springer Online Journal Archives 1860-2000Topics: BiologyMedicineNotes: Abstract Clinical and laboratory studies have suggested a pivotal role for tumor necrosis factor alpha (TNFA) in the pathogenesis of rheumatoid arthritis (RA). Interindividual variation in the expression of TNFA indicates the existence of functionally distinct TNFA alleles that could play a role in susceptibility to TNFA-associated diseases such as RA. In order to determine whether differential TNFA gene expression is present in RA, we studied the relative contribution of TNFA alleles to the total amount of steady-state mRNA in peripheral blood mononuclear cells of RA patients and healthy individuals. Moreover, allelic TNFA mRNA expression was analyzed in synovial biopsy material of RA patients. For this purpose, we used the recently identified C-insertion polymorphism located in the 5′ untranslated region of the first exon. The location of this polymorphism within a part of the gene that is transcribed into mRNA allowed us to discriminate between the contribution of each allele to the total amount of TNFA mRNA in heterozygous individuals. The results of this study do not indicate the existence of variation at the level of mRNA transcribed from each TNFA allele by in vitro and physiological stimulation conditions in RA patients. Therefore, our data do not suggest a role for transcriptionally distinct TNFA alleles in the susceptibility to RA.Type of Medium: Electronic ResourceURL: -
5Rood, M. J. ; Verschuuren, J. J. G.M. ; van Duinen, S. G. ; Maat-Schieman, M. L. ; Hegeman-Kleinn, I. M. ; van Buchem, M. A. ; Breedveld, F. C. ; Huizinga, T. W. J.
Springer
Published 2000Staff ViewISSN: 1432-1459Source: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: