| Project/Area Number |
06680684
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cell biology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
GOTOH Yukiko Institute for Virus Research, Kyoto University Research associate, ウイルス研究所, 助手 (70252525)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1995: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | MAPK / MAPKK / Ras / growth stimulation / nuclear translocation / シグナル伝達 |
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| Research Abstract |
Activation of the MAPK cascade by a constitutively active form of MAPKK resulted in the stimulation of the transcription of SRE-CAT and TRE-CAT,but not CRE-CAT.The transcriptional activation of SRE-CAT and TRE-CAT was well correlated with the intensity of MAPKK activity. These results suggest that the MAPK cascade may play an important role in the regulation of transcriptional stimulation induced by mitogens and differentiating stimuli.
Activation of MAPK and its nuclear translocation are thought to be key events in various signal transduction, but the relationship between these two events has not been understood. We show that introduction of v-Ras, active STE11 or a constitutively active form of MAPKK can induce nuclear translocation of MAPK in mammalian cultured cells. Not only wild-type MAPK but also non-activatable mutants of MAPK exogenously introduced can be translocated into the nuclei by expression of the constitutively active MAPKK.Moreover, injection of anti-active MAPK antibody (neutralizing antibody) blocks nuclear translocation of wild-type and non-activatable forms of MAPKs. These results suggest that nuclear translocation of MAPK is determined by phosphorylation of critical target (s) by active MAPK.
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