Analysis of repair systems for oxidative DNA damage in Senescence-Accelerated Mouso
加速衰老 Mouso 氧化 DNA 损伤修复系统分析
基本信息
- 批准号:11680819
- 负责人:
- 金额:$ 2.37万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:1999
- 资助国家:日本
- 起止时间:1999 至 2000
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Senescence-Accelerated Mouse Prone (SAMP) strains, show accelerated senescence coupled with a short lifespan as a genetic trait, and hence are a useful animal model to elucidate the mechanisms involved in organismal senescence process. 8-Oxoguanine is one of the major premutagenic oxidative base legions in vivo and is suspected to play a crucial role in organismal senescence. Mammalian 8-oxoguanine DNA glycosylase (OGG1) is thought to play a major role in the removal of 8-oxoguanine adducts in vivo. We have assessed the possible implication of 8-oxoguanine and OGG1 and accelerated senescence and short lifespan of SAMP mice. Examination of the Ogg1 gene of SAM strains have revealed that all SAM strains, except for SAMR3, hold R336H substitution in the OGG1. In addition, all nine SAMP strains, but none of the five SAMR strains, had the R304W substitution. We have revealed that R304W mutation caused a complete loss of OGG1 activity, while the R336H mutation led to disruption of nuclear localization of the enzyme although the activity remained normal. We have also revealed that SAMP1 retained 1.5 to 1.9-fold increase in 8-oxoguanine level of hepatic nuclear DNA as compared with normal mice. until at least 12 months of age. A genetic association study utilizing two hybrid progenies originated from SAMP1 mice, however, indicated that the mutant Ogg1 gene per se is not responsible for the accelerated senescence and short lifespan of SAMP1. These data do not preclude the possibility that retention of the high 8-oxoguanine level is associated with accelerated senescence and short lifespan of SAMP1 mice. Further study utilizing SAMP1 mice might elucidate the possible implication of 8-oxoguanine in senescence.
衰老加速小鼠倾向(SAMP)菌株,显示加速衰老加上短寿命作为一个遗传性状,因此是一个有用的动物模型,以阐明生物体衰老过程中涉及的机制。8-氧代鸟嘌呤是体内主要的致突变性氧化碱基军团之一,被怀疑在生物体衰老中起着至关重要的作用。哺乳动物8-氧代鸟嘌呤DNA糖基化酶(OGG 1)被认为在体内8-氧代鸟嘌呤加合物的去除中起主要作用。我们已经评估了8-氧代鸟嘌呤和OGG 1与SAMP小鼠的加速衰老和短寿命的可能关系。SAM菌株的Ogg 1基因的检测显示,除SAMR 3外,所有SAM菌株在OGG 1中均具有R336 H置换。此外,所有9个SAMP菌株,但没有5个SAMR菌株,有R304 W取代。我们已经发现,R304 W突变导致OGG 1活性完全丧失,而R336 H突变导致该酶的核定位中断,尽管活性保持正常。我们还发现,与正常小鼠相比,SAMP 1保留了1.5至1.9倍的肝核DNA的8-氧代鸟嘌呤水平的增加。直到至少12个月大。然而,利用源自SAMP 1小鼠的两个杂交后代进行的遗传关联研究表明,突变的Ogg 1基因本身并不导致SAMP 1的加速衰老和短寿命。这些数据并不排除高8-氧代鸟嘌呤水平的保留与SAMP 1小鼠的加速衰老和短寿命相关的可能性。利用SAMP 1小鼠的进一步研究可能阐明8-氧代鸟嘌呤在衰老中的可能意义。
项目成果
期刊论文数量(19)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Yanming Xing: "Transmission of mouse senile amyloidosis"Laboratory Investigation. (印刷中).
邢彦明:“小鼠老年淀粉样变性的传播”实验室调查(出版中)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Masayuki Mori: "Deletion in the beige gene of the beige rat owing to recombination between LINEls"Mammalian Genome. 10(7). 622-625 (1999)
Masayuki Mori:“由于 LINEls 之间的重组,导致米色大鼠的米色基因缺失”哺乳动物基因组。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
森 政之: "Deletion the beige gene of th ebeige rat owing to recombination between LINE1s"Mammalian Genome. 10・7. 622-625 (1999)
Masayuki Mori:“由于 LINE1 之间的重组而删除了米色大鼠的米色基因”《哺乳动物基因组》10・7(1999)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Yanming Xing: "Transmission of mouse senile amyloidosis"Laboratory Investigation. (in press).
邢彦明:“小鼠老年淀粉样变性的传播途径”实验室调查。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Motoyuki Shimizu: "Chromosome 13 locus,pbd2,regulates bone density in mice"Journal of Bone & Mineral Research. (印刷中).
Motoyuki Shimizu:“13 号染色体位点,pbd2,调节小鼠骨密度”《骨与矿物质研究杂志》(正在出版)。
- DOI:
- 发表时间:
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- 影响因子:0
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MORI Masayuki其他文献
Experimental Demonstration of a Hard-Type Oscillator Using a Resonant Tunneling Diode and Its Comparison with a Soft-Type Oscillator
使用谐振隧道二极管的硬型振荡器的实验演示及其与软型振荡器的比较
- DOI:
10.1587/transele.2021ecs6002 - 发表时间:
2021 - 期刊:
- 影响因子:0.5
- 作者:
MAEZAWA Koichi;ITO Tatsuo;MORI Masayuki - 通讯作者:
MORI Masayuki
Possibilities of Large Voltage Swing Hard-Type Oscillators Based on Series-Connected Resonant Tunneling Diodes
基于串联谐振隧道二极管的大电压摆幅硬型振荡器的可能性
- DOI:
10.1587/transele.e101.c.305 - 发表时间:
2018 - 期刊:
- 影响因子:0.5
- 作者:
MAEZAWA Koichi;MORI Masayuki - 通讯作者:
MORI Masayuki
MORI Masayuki的其他文献
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{{ truncateString('MORI Masayuki', 18)}}的其他基金
Identification of genes for ulcerative colitis utilizing SAM mice
利用 SAM 小鼠鉴定溃疡性结肠炎基因
- 批准号:
24500487 - 财政年份:2012
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Fabrication of InSb-based high-speed and low power devices on Si by using surface reconstruction controlled epitaxy
表面重构控制外延在Si上制备InSb基高速低功耗器件
- 批准号:
22560323 - 财政年份:2010
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Molecular genetic analysis of hybrid vigor and inbreeding depression utilizing recombinant inbred mouse strains
利用重组近交小鼠品系进行杂种优势和近交抑制的分子遗传学分析
- 批准号:
21650097 - 财政年份:2009
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Structural Insight for Ca channel Regulation by Calmodulin
钙调蛋白对 Ca 通道调节的结构洞察
- 批准号:
20770110 - 财政年份:2008
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Fabrication of InSb quantum well on Si using surface reconstruction Assisted growth method and its application for ultra-fast FET
表面重构辅助生长法在Si上制备InSb量子阱及其在超快FET中的应用
- 批准号:
19760233 - 财政年份:2007
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Characterization of SAM mice as an ulcerative colitis model
SAM 小鼠作为溃疡性结肠炎模型的表征
- 批准号:
19300145 - 财政年份:2007
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Generation of hypomorphic model mice utilizing an mRNA instability element
利用 mRNA 不稳定元件生成亚效型模型小鼠
- 批准号:
17500286 - 财政年份:2005
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Analysis and application of newly discovered rat L1 retotransposon
新发现的大鼠L1转座子的分析及应用
- 批准号:
14580796 - 财政年份:2002
- 资助金额:
$ 2.37万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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