Physiological role and clinical significance of platelet apoptotis
Project/Area Number |
23591420
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Hematology
|
Research Institution | Ehime University |
Principal Investigator |
HATO TAKAAKI 愛媛大学, 医学部附属病院, 准教授 (30172943)
|
Co-Investigator(Kenkyū-buntansha) |
YASUKAWA Masaki 愛媛大学, 大学院医学系研究科, 教授 (60127917)
YAMANOUCHI Jun 愛媛大学, 医学部附属病院, 講師 (10423451)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 血小板減少 / 血小板増加 / アポトーシス / 造血器腫瘍 / 血小板 / 骨髄異形成症候群 |
Research Abstract |
We examined if the Bak and Bcl-XL genes that are regulators for platelet apoptosis have mutations in patients with thrombocytopenia or thrombocytosis. The direct sequencing of these genes in patients with myelodysplastic syndrome (MDS) found 5 point mutations in the Bcl-XL gene. Transfection of each mutant gene into human cell lines did not induce cell apoptosis, suggesting no involvement of these mutations in the pathogenesis of thrombocytopenia. We also determined the sequences of Bak and Bcl-XL genes in patients with essential thrombocythemia (ET). However, no patient had mutations in these genes. These results suggest that the Bak and Bcl-XL mutations are not responsible for thrombocytopenia or thrombocytosis in hematological malignancies including MDS and ET.
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Report
(4 results)
Research Products
(31 results)