| Project/Area Number |
02454152
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
KIKUCHI Kunimi Hokkaido Univ., Inst. Immunol. Sci., Prof., 免疫科学研究所, 教授 (20006117)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUNO Yusuke Hokkaido Univ., Inst. Immunol. Sci., Assoc. Prof., 免疫科学研究所, 助教授 (00002121)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥5,800,000 (Direct Cost: ¥5,800,000)
Fiscal Year 1991: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1990: ¥4,600,000 (Direct Cost: ¥4,600,000)
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| Keywords | Protein Phosphatase / MRL / lpr Mice / Spleen / Thymus / PP1 / PP2A / PP2C / Signal Transduction / T細胞 / B細胞 / 分別定量 |
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| Research Abstract |
The differential assay conditions for protein phoshatases PP1, PP2A and PP2C were extensively studied by using crude extracts from mouse lymphoid tissues as enzyme sources. Under these conditions, the protein phosphatase activities were measured in MRL/lpr mice, autoimmune prone mice, and the control. In MRL/lpr mice, significant alterations in protein phosphatase activities were demonstrated. In spleen and liver from MRL/lpr mice, activities of PP1 and PP2A were distinctively elevated than those of the control mice. The increases in PP2A activity of MRL/lpr spleen and liver were taken to be due to accumulation of the abnormal lymphocytes emerged in MRL/lpr mice. Although the PP1 activity in MRL/lpr lymph nodes was nodes lower than those of normal spleen and thymus, it was greatly increased by Co^<2+>-trypsin treatment so that the PP1 activity of MRL/lpr lymph nodes was the highest among those all the tissues examined. In contrast, PP2C activities showed no remarkable alterations in the autoimmune disease model mice. Then, the protein phosphatase activities were measured by using T, B, Mphi cells prepared from mouse lymphoid tissues, and the alterations in PP1 activity was also confirmed. These results demonstrated a specific elevation in potency of protein dephosphorylation in the tissues with this disease, a new possibility to explain the defect in signal transduction in the MRL/lpr mice.
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