Regulation of cell death and proliferation by the MTK1 SAPKKK and its failure in cancer
Project/Area Number |
21390090
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pathological medical chemistry
|
Research Institution | Nagoya University |
Principal Investigator |
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2011: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2009: ¥8,060,000 (Direct Cost: ¥6,200,000、Indirect Cost: ¥1,860,000)
|
Keywords | 分子病態学 / 分子腫瘍学 / シグナル伝達 / MAPキナーゼ / ストレス応答 / がん / 蛋白質リン酸化 |
Research Abstract |
Stress-responsive MAPK pathways are activated by a wide array of stress stimuli such as DNA-damage, and play pivotal roles in the regulation of cellular stress responses, ranging from survival to apoptotic cell death. Perturbation of these critical signaling systems is involved in a variety of life-threatening disorders including cancer. In this study, we investigated physiological functions of a stress-responsive MAPKKK, MTK1. We found that, under stress conditions, MTK1 participated in down-regulation of cyclin expression. Furthermore, we screened for molecules that interact with MTK1, and identified a protein kinase(termed Mip1) as a novel substrate of MTK1. In response to stress, Mip1 was phosphorylated and activated by MTK1, thereby inhibiting stress-induced apoptosis. Interestingly, we confirmed that Mip1 expression was aberrantly regulated in human cancer.
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Report
(4 results)
Research Products
(69 results)