| Project/Area Number |
23591387
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Hematology
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| Research Institution | Osaka University |
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Principal Investigator |
SAITOH Norimitsu 大阪大学, 大学院医学(系)研究科(研究院), 特任助教(常勤) (30597399)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBAYAMA Hirohiko 大阪大学, 大学院医学系研究科, 講師 (60346202)
KANAKURA Yuzuru 大阪大学, 大学院医学系研究科, 教授 (20177489)
ORITANI Kenji 大阪大学, 大学院医学系研究科, 准教授 (70324762)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | Anamorsin / Picot / 鉄硫黄クラスター / 細胞内シグナル伝達 / Ras / Bリンパ球 / LPS / B細胞性リンパ腫 / PICOT / 鉄・硫黄クラスター / トランスジェニック / ERK1/2 / IkB / P53 / PKC / P38MAPK |
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| Research Abstract |
Anamorsin (AM) was originally isolated as a molecule that conferred resistance to apoptosis. AM deficient mice die during late gestation; AM is indispensable for embryo growth and hematopoiesis. Furthermore, our previous study showed AM overexpression in approximately 30% of B cell neoplasm cases. In this work, we focused on B cells of AM transgenic (Tg) mice. LPS-stimulated proliferation of AM Tg B cells was decreased compared with WT mice. Phosphorylation of Erk1/2 and IKBa in LPS-stimulated AM Tg B cells was also decreased. Upstream analysis based on the results of DNA micro array comparing AM Tg and WT B cells stimulated with or without LPS suggested that Ras activation was decreased in LPS-stimulated AM Tg B cells. We also confirmed impairment of LPS induced Ras activation in AM Tg mice by Ras assay. Our findings indicate the possibility that AM plays a role of negative regulation in LPS signaling pathway through the inhibition of Ras activation, which is a novel function of AM.
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