Search Results - (Author, Cooperation:S. Koyasu)
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1A. R. Forrest ; H. Kawaji ; M. Rehli ; J. K. Baillie ; M. J. de Hoon ; V. Haberle ; T. Lassmann ; I. V. Kulakovskiy ; M. Lizio ; M. Itoh ; R. Andersson ; C. J. Mungall ; T. F. Meehan ; S. Schmeier ; N. Bertin ; M. Jorgensen ; E. Dimont ; E. Arner ; C. Schmidl ; U. Schaefer ; Y. A. Medvedeva ; C. Plessy ; M. Vitezic ; J. Severin ; C. Semple ; Y. Ishizu ; R. S. Young ; M. Francescatto ; I. Alam ; D. Albanese ; G. M. Altschuler ; T. Arakawa ; J. A. Archer ; P. Arner ; M. Babina ; S. Rennie ; P. J. Balwierz ; A. G. Beckhouse ; S. Pradhan-Bhatt ; J. A. Blake ; A. Blumenthal ; B. Bodega ; A. Bonetti ; J. Briggs ; F. Brombacher ; A. M. Burroughs ; A. Califano ; C. V. Cannistraci ; D. Carbajo ; Y. Chen ; M. Chierici ; Y. Ciani ; H. C. Clevers ; E. Dalla ; C. A. Davis ; M. Detmar ; A. D. Diehl ; T. Dohi ; F. Drablos ; A. S. Edge ; M. Edinger ; K. Ekwall ; M. Endoh ; H. Enomoto ; M. Fagiolini ; L. Fairbairn ; H. Fang ; M. C. Farach-Carson ; G. J. Faulkner ; A. V. Favorov ; M. E. Fisher ; M. C. Frith ; R. Fujita ; S. Fukuda ; C. Furlanello ; M. Furino ; J. Furusawa ; T. B. Geijtenbeek ; A. P. Gibson ; T. Gingeras ; D. Goldowitz ; J. Gough ; S. Guhl ; R. Guler ; S. Gustincich ; T. J. Ha ; M. Hamaguchi ; M. Hara ; M. Harbers ; J. Harshbarger ; A. Hasegawa ; Y. Hasegawa ; T. Hashimoto ; M. Herlyn ; K. J. Hitchens ; S. J. Ho Sui ; O. M. Hofmann ; I. Hoof ; F. Hori ; L. Huminiecki ; K. Iida ; T. Ikawa ; B. R. Jankovic ; H. Jia ; A. Joshi ; G. Jurman ; B. Kaczkowski ; C. Kai ; K. Kaida ; A. Kaiho ; K. Kajiyama ; M. Kanamori-Katayama ; A. S. Kasianov ; T. Kasukawa ; S. Katayama ; S. Kato ; S. Kawaguchi ; H. Kawamoto ; Y. I. Kawamura ; T. Kawashima ; J. S. Kempfle ; T. J. Kenna ; J. Kere ; L. M. Khachigian ; T. Kitamura ; S. P. Klinken ; A. J. Knox ; M. Kojima ; S. Kojima ; N. Kondo ; H. Koseki ; S. Koyasu ; S. Krampitz ; A. Kubosaki ; A. T. Kwon ; J. F. Laros ; W. Lee ; A. Lennartsson ; K. Li ; B. Lilje ; L. Lipovich ; A. Mackay-Sim ; R. Manabe ; J. C. Mar ; B. Marchand ; A. Mathelier ; N. Mejhert ; A. Meynert ; Y. Mizuno ; D. A. de Lima Morais ; H. Morikawa ; M. Morimoto ; K. Moro ; E. Motakis ; H. Motohashi ; C. L. Mummery ; M. Murata ; S. Nagao-Sato ; Y. Nakachi ; F. Nakahara ; T. Nakamura ; Y. Nakamura ; K. Nakazato ; E. van Nimwegen ; N. Ninomiya ; H. Nishiyori ; S. Noma ; T. Noazaki ; S. Ogishima ; N. Ohkura ; H. Ohimiya ; H. Ohno ; M. Ohshima ; M. Okada-Hatakeyama ; Y. Okazaki ; V. Orlando ; D. A. Ovchinnikov ; A. Pain ; R. Passier ; M. Patrikakis ; H. Persson ; S. Piazza ; J. G. Prendergast ; O. J. Rackham ; J. A. Ramilowski ; M. Rashid ; T. Ravasi ; P. Rizzu ; M. Roncador ; S. Roy ; M. B. Rye ; E. Saijyo ; A. Sajantila ; A. Saka ; S. Sakaguchi ; M. Sakai ; H. Sato ; S. Savvi ; A. Saxena ; C. Schneider ; E. A. Schultes ; G. G. Schulze-Tanzil ; A. Schwegmann ; T. Sengstag ; G. Sheng ; H. Shimoji ; Y. Shimoni ; J. W. Shin ; C. Simon ; D. Sugiyama ; T. Sugiyama ; M. Suzuki ; N. Suzuki ; R. K. Swoboda ; P. A. t Hoen ; M. Tagami ; N. Takahashi ; J. Takai ; H. Tanaka ; H. Tatsukawa ; Z. Tatum ; M. Thompson ; H. Toyodo ; T. Toyoda ; E. Valen ; M. van de Wetering ; L. M. van den Berg ; R. Verado ; D. Vijayan ; I. E. Vorontsov ; W. W. Wasserman ; S. Watanabe ; C. A. Wells ; L. N. Winteringham ; E. Wolvetang ; E. J. Wood ; Y. Yamaguchi ; M. Yamamoto ; M. Yoneda ; Y. Yonekura ; S. Yoshida ; S. E. Zabierowski ; P. G. Zhang ; X. Zhao ; S. Zucchelli ; K. M. Summers ; H. Suzuki ; C. O. Daub ; J. Kawai ; P. Heutink ; W. Hide ; T. C. Freeman ; B. Lenhard ; V. B. Bajic ; M. S. Taylor ; V. J. Makeev ; A. Sandelin ; D. A. Hume ; P. Carninci ; Y. Hayashizaki
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-03-29Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; *Atlases as Topic ; Cell Line ; Cells, Cultured ; Cluster Analysis ; Conserved Sequence/genetics ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Genes, Essential/genetics ; Genome/genetics ; Humans ; Mice ; *Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Promoter Regions, Genetic/*genetics ; RNA, Messenger/analysis/genetics ; Transcription Factors/metabolism ; Transcription Initiation Site ; Transcription, Genetic/genetics ; Transcriptome/*geneticsPublished by: -
2Koga, S., Hozumi, K., Hirano, K.-i., Yazawa, M., Terooatea, T., Minoda, A., Nagasawa, T., Koyasu, S., Moro, K.
Rockefeller University Press
Published 2018Staff ViewPublication Date: 2018-06-05Publisher: Rockefeller University PressPrint ISSN: 0022-1007Electronic ISSN: 1540-9538Topics: MedicinePublished by: -
3Proby, C.M. ; Ota, T. ; Suzuki, H. ; Koyasu, S. ; Gamou, S. ; Shimizu, N. ; Wahl, J.K. ; Wheelock, M.J. ; Nishikawa, T. ; Amagai, M.
Oxford, UK : Blackwell Science Ltd
Published 2000Staff ViewISSN: 1365-2133Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Pemphigus vulgaris (PV) is an autoimmune blistering disease characterized by circulating pathogenic IgG antibodies against desmoglein 3 (Dsg3). The purpose of this study was to develop chimeric molecules for specific recognition and elimination of autoimmune B cells in PV. Mouse hybridoma cell lines producing anti-Dsg3 antibody (5H10, 12A2) were developed as an in vitro model system for targeting B cells. Dsg3-GFP, a baculoprotein containing the entire extracellular domain of Dsg3 fused with green fluorescence protein, recognized and targeted the hybridoma cells through their surface immunoglobulin receptors in an antigen-specific way. The epitopes of these monoclonal antibodies were mapped on the amino terminal EC1 and part of EC2, a region considered functionally important in cadherins. Chimeric toxin molecules containing the mapped region (Dsg3ΔN1) and modified Pseudomonas exotoxin were produced in bacteria (Dsg3ΔN1-PE40-KDEL, PE37-Dsg3ΔN1-KDEL) and tested in vitro on hybridoma cell lines. The chimeric toxins, but not Dsg3ΔN1 alone, showed dose-dependent toxic activity with a reduction in hybridoma cell number to 40–60% of toxin-negative control cultures, compared with little or no effect on anti-Dsg3-negative hybridoma cells. Furthermore, these toxins showed toxic effects on anti-Dsg3 IgG-producing B cells from Dsg3ΔN1-immunized mice, with a 60% reduction in cell number compared with Dsg3ΔN1 alone. Thus, specific recognition and targeting of antigen-specific B cells in PV was demonstrated; this strategy may hold promise as a future therapeutic option for PV and other autoimmune diseases.Type of Medium: Electronic ResourceURL: -
4Aoki-Ota, M. ; Tsunoda, K. ; Ota, T. ; Iwasaki, T. ; Koyasu, S. ; Amagai, M. ; Nishikawa, T.
Oxford, UK : Blackwell Science Ltd
Published 2004Staff ViewISSN: 1365-2133Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background Pemphigus vulgaris (PV) is an autoimmune blistering disease caused by antidesmoglein3 (anti-Dsg3) IgG autoantibodies. Recently, we developed a PV mouse model by adoptive transfer of splenocytes from recombinant Dsg3-immunized Dsg3–/– mice to Rag2–/– immunodeficient mice that expressed Dsg3.Objectives We determined whether the adoptive transfer of naive splenocytes from nonimmunized Dsg3–/– mice induces the anti-Dsg3 IgG production and the PV phenoytpe in recipient mice.Methods We adoptively transferred naive Dsg3–/– splenocytes into Rag2–/– mice and compared their PV phenoytpe with those mice receiving immunized Dsg3–/– splenocytes. The numbers of splenocytes and their subpopulations required for anti-Dsg3 IgG production were examined.Results Mice that received naive Dsg3–/– splenocytes produced anti-Dsg3 IgG, which bound to keratinocyte cell surfaces in vivo, and developed the PV phenotype, including oral erosions with suprabasilar acantholysis. Antibody production and the appearance of the PV phenotype were delayed by approximately 2 weeks in mice that received naive splenocytes compared with mice that received immunized splenocytes. However, once the PV phenotypes developed, there were no apparent differences in disease severity between the two models. Interestingly, the anti-Dsg3 IgG titres were significantly lower in mice that received naive splenocytes than in mice that received immunized splenocytes, suggesting that the former antibodies were more potent than the latter. The frequency of anti-Dsg3 IgG production depended on the number of transferred naive splenocytes. Both CD4+ T cells and B220+ B cells from naive Dsg3–/– mice were essential for the production of anti-Dsg3 IgG antibodies.Conclusions Dsg3-specific naive lymphocytes in Dsg3–/– mice can be primed and activated by the endogenous Dsg3 in recipient mice to produce pathogenic anti-Dsg3 IgG without active immunization. This approach using naive lymphocytes provides a unique model to dissect immunological mechanisms of tolerance against peripheral autoimmune targets.Type of Medium: Electronic ResourceURL: -
5Kadowaki, T. ; Kasuga, M. ; Tobe, K. ; Takaku, F. ; Nishida, E. ; Sakai, H. ; Koyasu, S. ; Yahara, I. ; Toyoshima, K. ; Akiyama, T. ; Yamamoto, T.
Amsterdam : ElsevierStaff ViewISSN: 0006-291XSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
6Koyasu, S. ; Kadowaki, T. ; Nishida, E. ; Tobe, K. ; Abe, E. ; Kasuga, M. ; Sakai, H. ; Yahara, I.
Amsterdam : ElsevierStaff ViewISSN: 0014-4827Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyMedicineType of Medium: Electronic ResourceURL: -
7Miyata, Y. ; Hoshi, M. ; Koyasu, S. ; Kadowaki, T. ; Kasuga, M. ; Yahara, I. ; Nishida, E. ; Sakai, H.
Amsterdam : ElsevierStaff ViewISSN: 0014-4827Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyMedicineType of Medium: Electronic ResourceURL: -
8Staff View
ISSN: 0014-5793Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
9Kadowaki, T. ; Kasuga, M. ; Tobe, K. ; Takaku, F. ; Nishida, E. ; Sakai, H. ; Koyasu, S. ; Yahara, I. ; Toyoshima, K. ; Akiyama, T. ; Yamamoto, T.
Amsterdam : ElsevierStaff ViewISSN: 0006-291XSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
10Staff View
ISSN: 0014-4827Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyMedicineType of Medium: Electronic ResourceURL: