1996 Fiscal Year Final Research Report Summary
Regulatory mechanism of Ras in intracellular Signal Transduction
| Project/Area Number |
07680677
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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 |
Functional biochemistry
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| Research Institution | TOKYO INSTITUTE OF TECHNOLOGY |
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Principal Investigator |
SATO Takaya TOKYO INSTITUTE OF TECHNOLOGY,Biosci.& Biotech., Assistant, 生命理工学部, 寄附講座教員 (20251655)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Ras / GTP-binding protein / signal transduction / IL-3 |
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| Research Abstract |
Regulatory mechanisms and the physiological role of the Ras-mediated signaling pathway in hematopoietic BaF3 cells were analyzed. Involvement of the Ras-guanine nucleotide exchange factor mSos in IL-3-induced Ras activation was examined by the use of a stable transfectant that conditionally expresses dominant-negative mSos. We found that the dominant-negative mSos mutant inhibited Ras-regulated kinases such as ERK2, suggesting an important role of mSos in IL-3 signal transduction. Furthermore, Ras-dependent activation of JNK1 in response to IL-3 stimulation was observed. We also analyzed the roles of small GTP-binding proteins, Cdc42, Rac, and Rho in signaltransduction leading to JNK1 activation in a transient expression system. In regard with the tyrosine kinase ACK,a target of Cdc42, enhanced tyrosine phosphorylation of this protein was detected following temperature shift-down, hyperosmotic shock, and EGF treatment.
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