Analysis of signal transduction of Polycythemia vera-associated JAK2 V617F mutant
| Project/Area Number |
21790090
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Keio University |
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Principal Investigator |
TAGO Megumi Keio University, 薬学部, 講師 (30445192)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | JAK2 / V617F点変異 / 真性赤血球増加症 / STAT5 / Akt / Aurora kinase A / V617F変異体 / 抗アポトーシス作用 / 腫瘍形成 / シグナル伝達 / エリスロポエチン |
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| Research Abstract |
The constitutively activated mutation of tyrosine kinase JAK2 (V617F) is found in the majority of the patients with polycythemia vera. We found that JAK2 mutant induces transformation through aberrant activation of STAT5. Interestingly, it was found that the expression of Aurora kinase A and activation of Akt were significantly induced by JAK2 mutant. We showed that Aurora kinase A was critical for JAK2 mutant-induced resistance to cisplatin-induced DNA damage. Furthermore, we clarified that Akt activation induced the downregulation of anti-apoptotic proteins, leading to anti-apoptotic activity.
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Report
(3 results)
Research Products
(50 results)
