| Project/Area Number |
21591197
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hematology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
KIRITO Keita 山梨大学, 大学院・医学工学総合研究部, 教授 (90306150)
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| Co-Investigator(Kenkyū-buntansha) |
KOMATSU Norio 順天堂大学, 医学部, 教授 (50186798)
SAKOE Kumi 自治医科大学, 医学部, 研究員 (10398505)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 骨髄増殖性腫瘍 / JAK2V617F / SHP-2 / 低酸素環境 / JAK2変異 / 造血幹細胞 / 骨髄増殖性疾患 / 低酸素 / JAK2 / HIF-1 |
|---|
| Research Abstract |
We found that hypoxia suppressed activity of JAK2V617F and induced growth arrest in JAK2V617F-positive MPN cells. SHP-2 plays important roles in these process. Interestingly, several studies have reported that SHP-2 is required for the activation of JAK2 by cytokines. In addition, recent studies have revealed that the activity of SHP-2 is increased in platelets from MPN patients. In conclusion, hypoxic environment may modulate fate of JAK2-positive MPN cells through suppression of SHP-2 levels and subsequent suppression of JAK2V617F activity.
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