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Regulatory mechanism of expression of ETS transcription factor Myeloid elf-1-like factor (MEF) by tumor suppressors
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- SUICO Mary Ann Soten
- Principal Investigator
- 熊本大学
About This Project
- Japan Grant Number
- JP23590082 (JGN)
- Funding Program
- Grants-in-Aid for Scientific Research
- Funding Organization
- Japan Society for the Promotion of Science
Kakenhi Information
- Project/Area Number
- 23590082
- Research Category
- Grant-in-Aid for Scientific Research (C)
- Allocation Type
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- Multi-year Fund
- Review Section / Research Field
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- Biological Sciences > Medicine, Dentistry, and Pharmacy > Pharmacy > Biological pharmacy
- Research Institution
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- Kumamoto University
- Project Period (FY)
- 2011 〜 2013
- Project Status
- Completed
- Budget Amount*help
- 5,330,000 Yen (Direct Cost: 4,100,000 Yen Indirect Cost: 1,230,000 Yen)
Research Abstract
Myeloid elf-1-like factor (MEF) functions as transcriptional factor and plays critical roles in development, cellular differentiation, proliferation, transformation and immune responses. In the present study, we aim to determine the regulatory mechanisms of MEF expression by several cellular factors. First, we demonstrated that tumor suppressor p53 decreases the level of MEF protein through the induction of transcription of MDM2, an E3 ubiquitin ligase. Moreover, the findings also revealed that another tumor suppressor Rb increases the MEF protein level possibly by stabilizing its protein expression. Finally, our data further showed that hypoxia increases both the mRNA and protein levels of MEF through HIF1alpha, the main effector molecule of hypoxia. On the whole, the findings revealed in these studies provide a better understanding of how the transcriptional regulator MEF is influenced by tumor suppressors such as p53 and Rb, and by hypoxia-related protein HIF1alpha.