Molecular mechanism of cellular senescence in oral precancerous
Project/Area Number |
20689035
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Research Category |
Grant-in-Aid for Young Scientists (A)
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Allocation Type | Single-year Grants |
Research Field |
Pathobiological dentistry/Dental radiology
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Research Institution | Japanese Foundation For Cancer Research |
Principal Investigator |
IMAI Akiko Japanese Foundation For Cancer Research, 癌研究所がん生物部, 研究員 (60380052)
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Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥24,310,000 (Direct Cost: ¥18,700,000、Indirect Cost: ¥5,610,000)
Fiscal Year 2010: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
Fiscal Year 2009: ¥7,410,000 (Direct Cost: ¥5,700,000、Indirect Cost: ¥1,710,000)
Fiscal Year 2008: ¥9,490,000 (Direct Cost: ¥7,300,000、Indirect Cost: ¥2,190,000)
|
Keywords | 実験腫瘍学 / 細胞老化 / 癌 / p16^<INK4a> |
Research Abstract |
Cellular senescence, an irreversible form of cell cycle arrest, is known to be acting as an important safeguard against neoplasia. However, it remains largely unclear how irreversibility of cell cycle arrest is established in cellular senescence. Here, we discovered that continuous production of reactive oxygen species (ROS) is essential for irreversibility of cellular senescence and that several genes are involved in this mechanism. Furthermore, we identified a series of proteins controlled by a proteasomal-dependent protein degradation pathway activated by ROS. These results unveil a novel pathway regulating the irreversibility of cellular senescence.
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Report
(4 results)
Research Products
(29 results)
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[Journal Article] Intrinsic cooperation between p16^<INK4a> and p21^<Waf1/Cip1> in the onset of cellular senescence and tumor suppression in vivo.2010
Author(s)
Takeuchi, S., Takahashi, A., Motoi, N., Tajima, T., Yamakoshi, K., Yoshimoto, S., Hirao, A., Yanagi, S., Fukami, K., Ishikawa, Y., Sone, S., Hara, E.
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Journal Title
Cancer Res. 70
Pages: 9381-9390
Related Report
Peer Reviewed
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[Journal Article] Real-time in vivo imaging of p16^<Ink4a> reveals crosstalk with p532009
Author(s)
Yamakoshi, K., Takahashi, A., Hirose, F., Nakayama, R., Ishimaru, N., Kubo, Y., Mann, D.J., Ohmura, M., Hirao, A., Saya, H., Arase, S., Hayashi, Y., Nakao, K., Matsumoto, M., Ohtani, N., Hara, E.
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Journal Title
J.Cell Biol. 186
Pages: 393-407
Related Report
Peer Reviewed
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[Presentation] DNA damage dependent degradation of histone methyltransferase in cellular senescence.2010
Author(s)
Takahashi, A., Yamakoshi, K., Imai, Y., Ohtani, N., Hara, E.
Organizer
Cold Spring Harbor Laboratory Meeting : Molecular Genetics of Aging
Place of Presentation
New York, U.S.A.
Related Report
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[Presentation] Intrinsic cooperation between p16^<INK4a> and p21^<Waf1/Cip1> in the onset of cellular senescence and tumor suppression in vivo.2010
Author(s)
Takeuchi, S., Takahashi, A., Motoi, N., Yoshimoto, S., Tajima, T., Yamakoshi, K., Ishikawa, Y., Sone, S., Hara, E., Ohtani, N.
Organizer
Cold Spring Harbor Laboratory Meeting : Molecular Genetics of Aging
Place of Presentation
New York, U.S.A.
Related Report
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