| Project/Area Number |
13671057
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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 | Nagoya University |
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Principal Investigator |
EMI Nobuhiko Nagoya University Hospital, Assistant Professor, 医学部附属病院, 講師 (30185144)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOZAWA Toshiya Nagoya University Hospital, Medical Staff, 医学部附属病院, 医員
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Leukemia / SYK / Tyrosine kinase / PDGFR / CEV / TEL / STAT5 / PI3K |
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| Research Abstract |
We here investigate the intracellular signal transduction of the stable transfectants. TEL-Syk fusion protein was associated with p85 subunit of phosphatidyl inositol 3 kinase (PI3-K) followed by the activation of Akt in the absence of IL-3. Vav, phospholipase C-γ2 (PLC-γ2) and mitogen-activated protein kinase (MAPK) were also constitutively activated. TEL-Syk also activated signal transducer and activator of transcription (STAT) 5 in the absence of Janus kinase 2 (JAK2) activation. None of these kinases were phosphorylated in the BaF3 cell transfected with TELΔPNT-Syk in which the oligomerization domain of TEL was deleted. Piceatannol, the Syk specific kinase inhibitor, inhibited the activation of STAT5 and the growth of the TEL-Syk transformed cell. These data suggest that TEL-Syk fusion protein in cytoplasm leads to constitutive activation of PI3-K, PLC-γ, MAPK and STAT5 signal pathways which are closely involved in IL-3 independent cell proliferation of BaF3 cells.
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