Molecular Mechanisms of Genomic Instability and DNA Repair

基因组不稳定性和DNA修复的分子机制

• 批准号: 08280103
• 负责人: HANAOKA Fumio
• 金额: $ 133.7万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research on Priority Areas (A)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08280103/
• 关键词: DNA repair; Nucleotide excision repair; Recombination repair; Homologous recombination; Mutagenesis; Carcinogenesis; Genetic disease; 組換之修復; 相同的組換之

We have studied various DNA repair mechanisms and the consequence of their defects from molecular to organism level. We categorized our studies into the following three subjects.1. Mechanisms of excision repair and molecular consequence of their defects.2. Mechanisms of homologous recombination and recombination repair.3. Molecular mechanisms of mutagenesis.In order to support this research project effectively, the advisory committee has conducted the following activities.1. We have financially supported a couple of research groups, when we found that it is better to support them with respect to the progress bf those research areas.2. We have published research forums and had meetings with all the members in order to facilitate exchange of information.3. We have financially supported related two workshops, which have been held annually. One is "Workshop on Genetic Recombination and Its Regulation", and the other is "Workshop on DNA Repair and Mutagenesis".4. We have held advisory committee twice per year in order to evaluate the outcomes of the research groups and to obtain suggestions for future research direction.5. We have supported researchers to attend international meetings. We have also invited foreign researchers to Japan in order to facilitate the exchange of information.6. We have published at the final year a book, which describes research activities of all the members of this project including the list of related publications and copies of their representative paper.

我们从分子到生物体水平研究了各种DNA修复机制及其缺陷的后果。我们将我们的研究分为以下三个主题： 1．切除修复机制及其缺陷的分子后果。 2．同源重组及重组修复机制3．诱变的分子机制。为了有效支持本研究项目，咨询委员会开展了以下活动： 1．当我们发现在这些研究领域的进展方面支持他们更好时，我们已经在经济上支持了几个研究小组。2。我们出版了研究论坛，并与所有成员举行了会议，以促进信息交流。 3．我们资助了每年举办的两次相关研讨会。一是“基因重组及其调控研讨会”，二是“DNA修复与突变研讨会”。 4．我们每年召开两次顾问委员会，以评估研究小组的成果并获取对未来研究方向的建议。 5．我们支持研究人员参加国际会议。我们还邀请外国研究人员来日本，以促进信息交流。6．我们在最后一年出版了一本书，描述了该项目所有成员的研究活动，包括相关出版物的清单和他们的代表性论文的副本。

项目成果

Matsuda,T.: "Low fidelity DNA synthesis by human DNA polymeraseη"Nature. 404. 1011-1013 (2000)

Matsuda, T.：“通过人类 DNA 聚合酶进行低保真 DNA 合成”，《自然》404. 1011-1013 (2000)。

Sugasawa,K.et al.: "HHR23B,a human Red23 homolog,stimulates XPC protoein in nucleotide excision rapair in vitro." Mol.Cell.Biol.16. 4852-4861 (1996)

Sugasawa, K. 等人：“HHR23B，一种人类 Red23 同源物，在体外核苷酸切除修复中刺激 XPC 蛋白。”

Miyauchi-hashimoto, H.: "Ultraviolet radiation-induced suppression of natural killer cell activity is enhanced in xeroderma pigmentosum group A (XPA) model mice"J. Invest. Dermatol.. 112. 965-970 (1999)

Miyauchi-hashimoto, H.：“紫外线辐射诱导的自然杀伤细胞活性抑制在着色性干皮病 A 组 (XPA) 模型小鼠中得到增强”J.

Takeuchi,S.: "Strand specificity and absewe of hot spots for p53 mutations in ultravidet B-induced skin tumors of XPA-deficient mice." Cancer Res.58. 641-646 (1998)

Takeuchi,S.：“在 Ultravidet B 诱导的 XPA 缺陷小鼠皮肤肿瘤中，p53 突变的链特异性和热点消除。”

Ishioka,K.: "Abortive recombination in Escherichia colirur mutants blocks chromosome partitioning" Genes Cells. 3. 209-220 (1998)

Ishioka,K.：“大肠杆菌突变体中的失败重组会阻止染色体分配”Genes Cells。