Elucidation of physiological significance of Txnip suppression and Redox regulation under innate immune response.

• Project/Area Number: 22590345
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Tohoku University
• Principal Investigator: KANARI Yasuyoshi 東北大学, 大学院・生命科学研究科, 助教 (60351590)
• Co-Investigator(Renkei-kenkyūsha): MUTA Tatsushi 東北大学, 大学院・生命科学研究科, 教授 (60222337)
• Project Period (FY): 2010 – 2012
• Project Status: Completed (Fiscal Year 2012)
• Budget Amount: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000); Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
• Keywords: 炎症 / 代謝 / Toll様受容体 / 解糖系 / 自然免疫 / TLR / 炎症性サイトカイン / Redox / Txnip / Transgenic mouse / Yeast two Hybrid法 / 生活習慣病 / Macrophage

Research Abstract

Whereas a number of inflammatory genes are induced by activation of nuclear factor-κB and other transcription factors, Txnip are dramatically suppressed by almost proinflammatory stimuli in many types of cells. Suppression of Txnip by LPS is accompanied by a decrease of the glucose sensing transcription factor MondoA in the nuclei and dissociation of the MondoA:Mlx complex that bound to the carbohydrate-response elements in the Txnip promoter in unstimulated cells. This observation links between inflammatory responses and metabolic regulation.

Research Products

• [Journal Article] Thioredoxin-Interacting Protein Gene Expression via MondoA Is Rapidly and Transiently Suppressed during Inflammatory Responses. (2013)
  • Author(s): Kanari, Y. et al.
  • Journal Title: PLoS One Volume: 8 Issue: 3 Pages: e59026-e59026
  • DOI: 10.1371/journal.pone.0059026
  • Peer Reviewed
• [Journal Article] Enhanced Apoptosis by Disruption of the STAT3-I κ B-ζ Signaling Pathway in Epithelial Cells Induces Sjogren' S Syndrome-like Autoimmune Disease. (2013)
  • Author(s): 大熊敦史
  • Journal Title: Immunity Volume: 38 Issue: 3 Pages: 450-460
  • DOI: 10.1016/j.immuni.2012.11.016
  • Peer Reviewed
• [Journal Article] Identification of interleukin-1 receptor-associated kinase 1 as a critical component that induces post-transcriptional activation of IκB-ζ (2012)
  • Author(s): Ohba T, Ariga Y, Maruyama T, Truong NK, Inoue J, Muta T
  • Journal Title: The FEBS Journal Volume: 279 Issue: 2 Pages: 211-222
  • DOI: 10.1111/j.1742-4658.2011.08416.x
  • Peer Reviewed
• [Journal Article] An evolutionary analysis of RAC2 identifies haplotypes associated with human autoimmune diseases (2011)
  • Author(s): Sironi, M., F. R. Guerini, C. Agliardi, M. Biasin, R. Cagliani, M. Fumagalli, D. Caputo, A. Cassinotti, S. Ardizzone, M. Zanzottera, E. Bolognesi, S. Riva, Y. Kanari, M. Miyazawa, M. Clerici
  • Journal Title: Mol. Biol. Evol Volume: 28 Issue: 12 Pages: 3319-3329
  • DOI: 10.1093/molbev/msr164
  • Peer Reviewed
• [Presentation] Sugahara-Tobinai A and Takai T Autoimmune disease in B6.Slam129 mice CREST Workshop on Inflammation andAutoimmunity (2012)
  • Author(s): Kanari Y
  • Organizer: Sendai
  • Year and Date: 2012-11-15
• [Book] 生態適応科学自然のしくみを活かし、持続可能な未来を拓く東北大学生態適応グローバルCOE (2013)
  • Author(s): 第II部第5章執筆担当
  • Publisher: 日経BP社
• [Book] 生態適応科学 自然のしくみを活かし、持続可能な未来を拓く (2013)
  • Author(s): 東北大学グローバルCOE
  • Total Pages: 243
  • Publisher: 日経BP