2002 Fiscal Year Final Research Report Summary
Analysis of tyrosine kinase chimeric gene
| Project/Area Number |
13671057
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Hematology
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
EMI Nobuhiko Nagoya University Hospital, Assistant Professor, 医学部附属病院, 講師 (30185144)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YOKOZAWA Toshiya Nagoya University Hospital, Medical Staff, 医学部附属病院, 医員
|
|---|
| Project Period (FY) |
2001 – 2002
|
| Keywords | Leukemia / SYK / Tyrosine kinase / PDGFR / CEV |
|---|
| 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.
|
Research Products
(8 results)
