2017 Fiscal Year Final Research Report
Roles of tyrosine phosphorylation of KAP1 in leukemogenesis
Project/Area Number |
15K19545
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Hematology
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Research Institution | Kumamoto University |
Principal Investigator |
Kubota Sho 熊本大学, 国際先端医学研究機構, 特別研究員(PD・RPD) (70747831)
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Research Collaborator |
Sashida Goro 熊本大学, 国際先端医学研究機構, 特別招聘教授 (70349447)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | BCR-ABL / CML / KAP1 / TIF1beta / エピジェネティクス |
Outline of Final Research Achievements |
BCR-ABL, which is a highly activated oncogenic fusion tyrosine kinase in chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive acute lymphocytic leukemia (Ph+ ALL). Although it is well known that tyrosine phosphorylation is important for signal transduction in cytoplasm, roles of nuclear tyrosine phosphorylation in nuclear events is poorly understood. We generated a new BCR-ABL knock-in mice model, and we mated mice with conditional KAP1 knockout mice. Using these mice model, we analyzed the function of tyrosine phosphorylation of KAP1 in normal hematopoiesis and leukemogenesis. Analysis for moceluclar mechanism of tyrosine phosphorylation of KAP1 was performed in K562 CML cell line.
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Free Research Field |
造血器腫瘍
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