2014 Fiscal Year Final Research Report
Molecular bases of cellular stress and disease development regulated by by stress inducible molecules, TRB1 and TRB3
Project/Area Number |
24590085
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Biological pharmacy
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Research Institution | Nagoya City University |
Principal Investigator |
HAYASHI Hidetoshi 名古屋市立大学, 薬学研究科(研究院), 教授 (80198853)
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | TRB1 / TRB3 / p53 / checkpoint / HDAC1 / stress / cell cycle |
Outline of Final Research Achievements |
Environmental and metabolic changes induce various stress responses in cells and tissues to maintain the homeostasis, however uncontrollable continuous and strong stress will lead the homeostatic disorders and consequently to various diseases. We investigated that contribution of TRB1 and TRB3, which are induced by various stresses, to a variety of stress responses and onset of various diseases. Antigen-stimulation induces the TRB1 expression and it up-regulated the immune responses. One of the antiproliferative cytokines , TGF-beta also induced TRB1, which inhibited its signaling. It was known that both TRB1 and TRB3 are over expressed in a number of cancers. We clarified that TRB1 inhibited the function of typical tumor-suppressor gene, p53, and that TRB3 disturbed the cell cycle checkpoint. It was indicated that the two molecules advantageously act for the progression of cancer cells.
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Free Research Field |
生化学、細胞生物学
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