Project/Area Number |
09470043
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pathological medical chemistry
|
Research Institution | KOBE UNIVERSITY |
Principal Investigator |
YAMAMURA Hirohei KOBE UNIV., MED., PROF., 医学部, 教授 (90030882)
|
Co-Investigator(Kenkyū-buntansha) |
TAKANO Tomoko KOBE UNIV., MED., ASSISTANT, 医学部, 助手 (30226807)
SADA Kiyonao KOBE UNIV., MED., ASSISTANT, 医学部, 助手 (10273765)
YANAGI Shigeru KOBE UNIV., MED., ASSISTANT, 医学部, 助手 (60252003)
|
Project Period (FY) |
1997 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥15,100,000 (Direct Cost: ¥15,100,000)
Fiscal Year 1998: ¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1997: ¥8,700,000 (Direct Cost: ¥8,700,000)
|
Keywords | Protein-tyrosine / Syk / vascular endothelial cells / smooth muscle cells / neurons / tyrosine phosphorylated / non-hematopoietic cells / 血管 / 平滑筋細胞 / ZAP-70 / 神経成長円錐 |
Research Abstract |
Protein-tyrosine kinase Syk has been implicated in a variety of hematopoietic cell responses including immunoreceptor and integrin signaling. However, so far, there is no evidence of the expression and function of Syk in the non-hematopoietic tissues. in this study, we have purified 72kDa cytoplasmic protein-tyrosine kinase, having cross-reactivity with anti-Syk antibody, as a major cytosolic protein-tyrosine kinase from rat brain and blood cells-depleted rat liver. Partial sequence analysis of purified p72 kDa protein-derived peptides revealed that this protein is identical with Syk protein-tyrosine kinase. Immunohistochemical and RT-PCR northern analysis further demonstrated that Syk is expressed widely distributed in non-hematopoietic cells including vascular endothelial cells, smooth muscle cells, fibroblasts and neurons. Furthermore, Syk was significantly activated and tyrosine phosphorylated in response to a variety of ligands in non-hematopoietic cells. Thus, our results suggest the ubiquitous role of Syk in the signaling transduction of non-hematopoietic cells. We are currently attempting to establish several primary cultured cell lines derived from Syk-deficient mice. The genetic analysis of this mutant will provide a major tool in the physiological investigation of the functions of Syk. In addition to these results we studied about Syk from hematopoietic cells. The results obtained using hematopietic cells are quite useful to analyze the function of Syk in non-hematopoietic cells.
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