Characterization and biological assessment of DNA-Protein crosslink repair in vertebrate cells

脊椎动物细胞 DNA-蛋白质交联修复的表征和生物学评估

• 批准号: 20510051
• 负责人: TANO Keizo
• 金额: $ 3万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20510051/
• 关键词: 修復; 生物影響

To elucidate the process of DNA-Protein Crosslink (DPC) repair, we employed reverse genetic approach using chicken DT40 cells. It has been suggested that endogenous reactive oxygen species (ROS) is involved in formation of DPC. We generated several ROS scavenge enzyme genes knock out cells to elucidate mechanism of antioxidant defense system. In addition, we try to look for the therapeutic potential of DPC producing chemical, HMTA, in mouse level. All the results so far, already published in peer reviewed journals.

为了阐明DNA-蛋白质交联(DPC)修复的过程，我们采用了鸡DT40细胞的反向遗传方法。有研究表明，内源性活性氧参与了DPC的形成。我们克隆了几个ROS清除酶基因敲除细胞，以阐明抗氧化防御系统的机制。此外，我们还试图在小鼠水平上寻找DPC产生的化学物质HMTA的治疗潜力。到目前为止，所有的结果都已经发表在同行评议的期刊上。

项目成果

Adverse effect of mild hyperthermia combined with hexyamethylenetetramine compared to its effect combined with tirapazamine in the treatment of solid tumors

温和热疗联合六次甲基四胺与联合替拉扎明治疗实体瘤的不良反应比较

• 发表时间: 2010
• 期刊: Exp.Ther.Med. 1
• 作者: Masunaga S;Tano K;Nakamura J;Watanabe M;Kashino G;Suzuki M;Kinashi Y;Ono K
• 通讯作者: Ono K

OD1枯渇細胞とPRDX1枯渇細胞の抗酸化剤に対する挙動の違い

OD1 耗尽的细胞和 PRDX1 耗尽的细胞对抗氧化剂的行为差异

• 发表时间: 2010
• 作者: 樋口優人;井上絵里;田野恵三;吉村明;渡邉正己;榎本武美;関政幸
• 通讯作者: 関政幸

Generation and characterization of cells that can be conditionally depleted of mitochondrial SOD2

可条件性去除线粒体 SOD2 的细胞的生成和表征

• 发表时间: 2009
• 期刊: Biochem.Biophys.Res.Commun. 379
• 作者: Takada;S.
• 通讯作者: S.

Usefulness of hexamethylenetetramine as an adjuvant to radiation and cisplatin in the treatment of solid tumors : its independency of p53 status

六亚甲基四胺作为放射和顺铂的佐剂在实体瘤治疗中的用途：其与p53状态的独立性

• 发表时间: 2010
• 期刊: J Radiat Res (Tokyo)
• 作者: Kim;J.W.;Masunaga S.
• 通讯作者: Masunaga S.

Cells deficient in PARP-1 show an accelerated accumulation of DNA single strand breaks, but not AP sites, over the PARP-1-proficient cells exposed to MMS.

• DOI: 10.1016/j.mrfmmm.2009.09.006
• 发表时间: 2009-12-01
• 期刊: MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
• 影响因子: 2.3
• 作者: Pachkowski, Brian F.;Tano, Keizo;Afonin, Valeriy;Elder, Rhoderick H.;Takeda, Shunichi;Watanabe, Masami;Swenberg, James A.;Nakamura, Jun
• 通讯作者: Nakamura, Jun