Research Topics
Genomes and Genes
| Takashi KobayashiSummaryAffiliation: Kyushu University Country: Japan Publications
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Detail Information
Publications
TRAF6 is required for generation of the B-1a B cell compartment as well as T cell-dependent and -independent humoral immune responsesTakashi Kobayashi
Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
PLoS ONE 4:e4736. 2009..These results reveal critical roles for TRAF6 in TD and TI humoral immune responses and in inductive fate decisions necessary to generate the B-1 B cell compartment...
Loss of suppressor of cytokine signaling 1 in helper T cells leads to defective Th17 differentiation by enhancing antagonistic effects of IFN-gamma on STAT3 and SmadsKentaro Tanaka
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi ku, Fukuoka 812 8582, Japan
J Immunol 180:3746-56. 2008..SOCS1-deficient T cells will be very useful to investigate the molecular mechanism for the STAT1-mediated suppression of Th17 development...
Prostaglandin E2 is a major soluble factor produced by stromal cells for preventing inflammatory cytokine production from dendritic cellsHiroshi Shiraishi
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Int Immunol 20:1219-29. 2008....- An RNA-binding protein alphaCP-1 is involved in the STAT3-mediated suppression of NF-kappaB transcriptional activityHitomi Nishinakamura
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Int Immunol 19:609-19. 2007..7 cells, while small interfering RNA against alphaCP-1 reduced it. These data suggest that alphaCP-1 is involved in the STAT3-mediated suppression of NF-kappaB activity... - Suppressor of cytokine signaling 1 protects mice against concanavalin A-induced hepatitis by inhibiting apoptosisTakehiro Torisu
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
Hepatology 47:1644-54. 2008..Conclusion: These findings indicate that SOCS1 plays important negative roles in fulminant hepatitis and that forced expression of SOCS1 is therapeutic in preventing hepatitis... - FLN29 deficiency reveals its negative regulatory role in the Toll-like receptor (TLR) and retinoic acid-inducible gene I (RIG-I)-like helicase signaling pathwayTakahito Sanada
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
J Biol Chem 283:33858-64. 2008.... - IFNgamma-dependent, spontaneous development of colorectal carcinomas in SOCS1-deficient miceToshikatsu Hanada
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
J Exp Med 203:1391-7. 2006..These data strongly suggest that SOCS1 is a unique antioncogene which prevents chronic inflammation-mediated carcinogenesis by regulation of the IFNgamma/STAT1 pathways... - Selective expansion of foxp3-positive regulatory T cells and immunosuppression by suppressors of cytokine signaling 3-deficient dendritic cellsYumiko Matsumura
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
J Immunol 179:2170-9. 2007..These results indicate an important role of SOCS3 in determining on immunity or tolerance by DCs... - Foxp3 inhibits RORgammat-mediated IL-17A mRNA transcription through direct interaction with RORgammatKenji Ichiyama
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
J Biol Chem 283:17003-8. 2008..We propose that induction of Foxp3 is the mechanism for the suppression of Th17 and polarization into inducible Treg... - TRAF6 and MEKK1 play a pivotal role in the RIG-I-like helicase antiviral pathwayRyoko Yoshida
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
J Biol Chem 283:36211-20. 2008..These data suggest that IPS-1 requires TRAF6 and MEKK1 to activate NF-kappaB and mitogen-activated protein kinases that are critical for the optimal induction of type I interferons... - Ifi202, an IFN-inducible candidate gene for lupus susceptibility in NZB/W F1 mice, is a positive regulator for NF-kappaB activation in dendritic cellsMoriyasu Yamauchi
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
Int Immunol 19:935-42. 2007..In addition, forced expression of Ifi202 enhanced IL-12p40 mRNA induction in NZW BMDCs. Thus, Ifi202 is an important NF-kappaB activator in DCs and involved in IL-12 production, which may account for a T(h)1-prone phenotype of BWF1 mice... - Cyclic adenosine monophosphate suppresses the transcription of proinflammatory cytokines via the phosphorylated c-Fos proteinKeiko Koga
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Immunity 30:372-83. 2009..Multiple sites of c-Fos were phosphorylated by the IKKbeta protein. Thus, we propose that c-Fos is a substrate of IKKbeta and is responsible for the immunosuppressive effect of cAMP... - A major lipid raft protein raftlin modulates T cell receptor signaling and enhances th17-mediated autoimmune responsesKazuko Saeki
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
J Immunol 182:5929-37. 2009..These data indicate that Raftlin modulates TCR signals and is necessary for the fine-tuning of T cell-mediated immune responses... - Silencing of SOCS1 in macrophages suppresses tumor development by enhancing antitumor inflammationMasayuki Hashimoto
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Cancer Sci 100:730-6. 2009..These results suggest that inflammation induced by SOCS1-deficiency in monocytes potentiates antitumor immune responses rather than tumor-promoting inflammation... - STAT6 Inhibits TGF-beta1-mediated Foxp3 induction through direct binding to the Foxp3 promoter, which is reverted by retinoic acid receptorHiromi Takaki
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582
J Biol Chem 283:14955-62. 2008..We propose that antagonistic agents for neutralizing IL-4 could be a novel strategy to facilitate inducible Treg cell generation and the promotion of tolerance in Th2-dominated diseases such as allergy... - A novel Zinc finger protein, ZCCHC11, interacts with TIFA and modulates TLR signalingYasumasa Minoda
Division of Molecular and Cellular Immunology, The Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi, Fukuoka 812 8582, Japan
Biochem Biophys Res Commun 344:1023-30. 2006..We propose that ZCCHC11 is a unique TLR signal regulator, which interacts with TIFA after LPS treatment and suppresses the TRAF6-dependent activation of NF-kappaB... - Adaptor protein SH2-B linking receptor-tyrosine kinase and Akt promotes adipocyte differentiation by regulating peroxisome proliferator-activated receptor gamma messenger ribonucleic acid levelsDaigo Yoshiga
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Fukuoka 812 8582, Japan
Mol Endocrinol 21:1120-31. 2007..These data indicate that SH2-B is a key regulator of adipogenesis both in vivo and in vitro by regulating the insulin/IGF-I receptor-Akt-Foxo1-PPARgamma pathway... - FLN29, a novel interferon- and LPS-inducible gene acting as a negative regulator of toll-like receptor signalingRyuichi Mashima
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi ku, Fukuoka 812 8582, Japan
J Biol Chem 280:41289-97. 2005..Taken together, FLN29 is a new negative feedback regulator of TLR signaling... - Suppression of SOCS3 expression in the pancreatic beta-cell leads to resistance to type 1 diabetesHiroyuki Mori
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Biochem Biophys Res Commun 359:952-8. 2007..These results suggest that enhanced STAT3 signaling protects beta-cells from destruction induced by a genotoxic stress and that STAT3/SOCS3 can be a potential therapeutic target for the treatment of type 1 diabetes... - TGF-beta1 suppresses IFN-gamma-induced NO production in macrophages by suppressing STAT1 activation and accelerating iNOS protein degradationHiromi Takaki
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Fukuoka 812 8582, Japan
Genes Cells 11:871-82. 2006..e. suppression of IFN-gamma-induced STAT1 activation by an association of the IFNGR1 with the TGF-betaRI... - Deletion of the SOCS3 gene in liver parenchymal cells promotes hepatitis-induced hepatocarcinogenesisHisanobu Ogata
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Graduate School of Medical Science, Kyushu University, Higashiku, Fukuoka, Japan
Gastroenterology 131:179-93. 2006..We investigated the effect of deleting the SOCS3 gene on the development of hepatitis and HCC in hepatitis C virus-infected patients and mouse models... - Suppressor of cytokine signaling-1 regulates inflammatory bowel disease in which both IFNgamma and IL-4 are involvedTakatoshi Chinen
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
Gastroenterology 130:373-88. 2006..However, the role of SOCS1 in inflammatory bowel diseases (IBDs) has not been clarified. To determine the role of SOCS1 in colitis, we generated SOCS1/T-cell receptor alpha (TCRalpha) double knockout (DKO) mice... - Loss of SOCS3 gene expression converts STAT3 function from anti-apoptotic to pro-apoptoticYang Lu
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
J Biol Chem 281:36683-90. 2006..These data suggest that prolonged activation of STAT3 could induce apoptosis/growth arrest rather than anti-apoptosis and proliferation in certain cases, and SOCS3 is a critical regulator of this balance... - Involvement of Th17 cells and the effect of anti-IL-6 therapy in autoimmune uveitisTakeru Yoshimura
Department of Ophthalmology, Graduate School of Medical Science, Kyushu University, Fukuoka, Japan
Rheumatology (Oxford) 48:347-54. 2009..We initially confirmed the significant increase of several inflammatory soluble factors including IL-6 in the vitreous fluids from refractory/chronic engogenous uveitis patients... - The dual function of hepatic SOCS3 in insulin resistance in vivoTakehiro Torisu
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, University of Kyushu, Maidashi 3 1 1, Fukuoka 812 8582, Japan
Genes Cells 12:143-54. 2007..We conclude that hepatic SOCS3 is a mediator of insulin resistance in the liver; however, lack of SOCS3 in the liver promotes systemic insulin resistance by mimicking chronic inflammation... - HTLV-1 Tax-mediated TAK1 activation involves TAB2 adapter proteinQingsheng Yu
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka, Fukuoka 812 8582, Japan
Biochem Biophys Res Commun 365:189-94. 2008..These results suggest that TAB2 may be critically involved in Tax-mediated activation of TAK1 and that NF-kappaB-activating TRAF family proteins are potential cellular E3 ubiquitin ligases toward Tax... - Aberrant IL-4 production by SOCS3-over-expressing T cells during infection with Leishmania major exacerbates disease manifestationsMako Nakaya
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
Int Immunol 23:195-202. 2011..These data suggest that tight regulation of SOCS3 expression in T(h) cells is crucial for disease control during infection by L. major... - An F-box protein, FBXW5, negatively regulates TAK1 MAP3K in the IL-1beta signaling pathwayYasumasa Minoda
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812 8582, Japan
Biochem Biophys Res Commun 381:412-7. 2009..Conversely, knockdown of FBXW5 resulted in the prolonged activation of TAK1 upon IL-1beta stimulation. These results suggest that FBXW5 negatively regulates TAK1 in the IL-1beta signaling pathway... - Induction of hyper Th1 cell-type immune responses by dendritic cells lacking the suppressor of cytokine signaling-1 geneToshikatsu Hanada
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan
J Immunol 174:4325-32. 2005..We propose that reduction of the SOCS1 gene expression in DCs leads to CD8alpha(+) DC-like phenotype which promotes Th1-type hyperresponses... - Keeping DCs awake by putting SOCS1 to sleepTakashi Kobayashi
Molecular and Cellular Immunology Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan
Trends Immunol 26:177-9. 2005..This recent study demonstrates the importance of negative regulation of DC maturation and functions for DC-based immunotherapy... - Loss of SOCS3 in T helper cells resulted in reduced immune responses and hyperproduction of interleukin 10 and transforming growth factor-beta 1Ichiko Kinjyo
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Higashi ku, Fukuoka 812 8582, Japan
J Exp Med 203:1021-31. 2006..From these findings, we propose that SOCS3 regulates the production of the immunoregulatory cytokines TGF-beta1 and IL-10 through modulating STAT3 activation... - [Intracellular negative signals and allergy]Akihiko Yoshimura
Division of Molecular and Cellular Immunology Medical Institute of Bioregulation, Kyushu University, Japan
Arerugi 56:563-9. 2007 - Positive and negative roles of IL-6, STAT3, and SOCS3 in inflammatory arthritisIchiko Kinjyo
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
Adv Exp Med Biol 602:113-24. 2007 - Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasiaTakaharu Taketomi
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, 3 1 1 Maidashi, Higashi ku, Fukuoka 812 8582, Japan
Nat Neurosci 8:855-7. 2005..Anti-GDNF antibody administration corrected nerve hyperplasia in Sprouty2-deficient mice. We show Sprouty2 to be a negative regulator of GDNF for the neonatal development or survival of enteric nerve cells... - Suppressors of cytokine signaling-1 and -3 regulate osteoclastogenesis in the presence of inflammatory cytokinesMasanobu Ohishi
Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Faculty of Dental Sciences, Kyushu University, Fukuoka, Japan
J Immunol 174:3024-31. 2005..Selective suppression of SOCS1 and SOCS3 in osteoclast precursors may be a possible therapeutic strategy for inflammatory bone destruction...