| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Outline of Final Research Achievements |
JAK2V617F, a gain-of-function mutation in the tyrosine kinase JAK2, is frequently detected in myeloproliferative neoplasms (MPN), however its molecular mechanism in terms of MPN development is not fully understood. The identification of the JAK2 mutation in MPN led to the development of JAK2 inhibitors, however, treatment with these inhibitors is associated with side effects caused by blockade of function of wild-type JAK2; therefore, a new therapeutic strategy based on understanding of MPN development is required.
In this study, I found that AP-1 activation by JAK2V617F through c-FOS induction involves an unidentified molecular mechanism suggesting that deregulation of AP-1 plays a role in MPN development. Additionally, the AP-1 reporter assay system I have established should be useful not only for screening novel compounds for MPN treatment but also in studying the novel pathway regulated by JAK2V617F, which would lead to the development of a novel therapeutic strategy against MPN.
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