Regulation of cell proliferation and cell death by stress signaling in cancer

癌症中应激信号对细胞增殖和细胞死亡的调节

• 批准号: 17014013
• 负责人: ICHIJO Hidenori
• 金额: $ 35.2万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research on Priority Areas
• 财政年份: 2005
• 资助国家: 日本
• 起止时间: 2005 至 2009
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17014013/
• 关键词: ASK1; ASK2; MAPキナーゼ; アポトーシス; ASKファミリー; ASKI

This study aimed at analyzing the mechanisms by which cancer cells acquire abnormal proliferation and death-resistant phenotypes in the context of perturbation of stress signaling. By using ASK family knockout mice, we found that stress-activated MAP kinases play pivotal roles in development and expansion of human cancer.

这项研究旨在分析在压力信号扰动的背景下，癌细胞获得异常增殖和抗死亡表型的机制。通过使用ASK家族基因敲除小鼠，我们发现应激激活的MAP激酶在人类癌症的发生和扩展中发挥着关键作用。

项目成果

Hyperactivity in novel environment with increased dopamine and impaired novelty preference in apoptosis signal-regulating kinase 1 (ASK1)-deficient mice

• DOI: 10.1016/j.neures.2009.12.003
• 发表时间: 2010-03-01
• 期刊: NEUROSCIENCE RESEARCH
• 影响因子: 2.9
• 作者: Kumakura, Karen;Nomura, Hiroshi;Matsuki, Norio
• 通讯作者: Matsuki, Norio

Identification of Op18/stathmin as a potential target of ASK1-p38 MAP kinase cascade

• DOI: 10.1002/jcp.20465
• 发表时间: 2006-02-01
• 期刊: JOURNAL OF CELLULAR PHYSIOLOGY
• 影响因子: 5.6
• 作者: Mizumura, K;Takeda, K;Ichijo, H
• 通讯作者: Ichijo, H

Requirement of reactive oxygen species-dependent activation of ASK1-p38 MAP kinase pathway for extracelluler ATP-induced apoptosis in macrophage

细胞外 ATP 诱导巨噬细胞凋亡需要活性氧依赖的 ASK1-p38 MAP 激酶途径激活

• 发表时间: 2008
• 期刊: J. Biol. Chem 283
• 作者: Noguchi;T.;et. al.
• 通讯作者: et. al.

Serine 58 of 14-3-3{zeta} is a molecular switch regulating ASK1 and oxidant stress-induced cell death

14-3-3{zeta} 的丝氨酸 58 是调节 ASK1 和氧化应激诱导的细胞死亡的分子开关

• 发表时间: 2009
• 期刊: Mol.Cell.Biol. 29
• 作者: Zhou;J.;et al.
• 通讯作者: et al.

Signaling pathways in invertebrate immune and stress response

无脊椎动物免疫和应激反应中的信号通路

• 发表时间: 2009
• 期刊: Invertebrate Survival Journal 6
• 作者: Hatanaka;R.;et al.
• 通讯作者: et al.