The analysis of mechanism of interferon-induced IP-10 production in monocytes with proteasome deficiency.
| Project/Area Number |
15K19700
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Dermatology
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
INABA YUTAKA 和歌山県立医科大学, 医学部, 助教 (00647571)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 自己炎症性疾患 / インターフェロン / JAK / STAT / 中條-西村症候群 / プロテアソーム / 中條－西村症候群 / IP-10 / 中條ー西村症候群 / JAK/STAT / 自己炎症疾患 / プロテアソ-ム |
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| Outline of Final Research Achievements |
Nakajo-Nishimura syndrome (NNS) patients derived peripheral blood monocytes produced larger amount of IP-10 than control cells after IFNγ stimulation. However, it remains unclear how proteasome disability enhances IFN signaling. By western blotting, IFNγ-induced phosphorylated JAK1 level in immortalized B cells was higher in NNS patients-derived cells than in control cells. In contrast, phosphorylated STAT1 level did not change after IFNγ stimulation in either of NNS patients-derived immortalized B cells and control cells. These results suggest that proteasome degradation of phosphorylated JAK1 is critical for IFN signaling in NNS.
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Report
(4 results)
Research Products
(10 results)
