MAD DATA COLLECTION OF XRCC4/LIGASEIV
XRCC4/LIGASEIV 的疯狂数据收集
基本信息
- 批准号:7602315
- 负责人:
- 金额:$ 1.71万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2007
- 资助国家:美国
- 起止时间:2007-07-01 至 2008-06-30
- 项目状态:已结题
- 来源:
- 关键词:ApoptosisCell CycleCellsComplexComputer Retrieval of Information on Scientific Projects DatabaseDNADNA Double Strand BreakDNA ligase IVData CollectionDouble Strand Break RepairDrug DesignEukaryotaEukaryotic CellFundingGenetic RecombinationGrantHumanInstitutionIonizing radiationLightMetabolismNonhomologous DNA End JoiningPathway interactionsPharmaceutical PreparationsProcessRadiation therapyResearchResearch PersonnelResourcesSourceStructureUnited States National Institutes of Healthbasecancer therapyinhibitor/antagonistinsightnovelrepaired
项目摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
DNA double stranded breaks are often encountered within a cell as intermediates of particular recombination processes or can be induced by external agents such as ionizing radiation and radiomimetic drugs. In addition, double strand breaks can also occur as a result of the by-products released during metabolism. It is crucial to repair double strand breaks effectively and this is carried out by two distinct repair mechanisms, one of which is non-homologous end joining repair pathway. Although the other repair mechanism exists, NHEJ is predominant in higher eukaryotes and prevails all through out the cell cycle. Xrcc4-DNA ligase IV complex is an absolutely essential component of NHEJ pathway and is responsible for carrying out the final step of ligating the broken DNA ends. Solving the crystal structure of this human complex could provide us with great insights and revelations that could shed light on the actual mechanism of this pathway, which is currently unclear. Also, since the lack of proper double strand break repair causes apoptosis in a cell, developing inhibitors of this complex through structure-based drug design could provide a novel treatment for cancer that can be used in combination with radiation therapy.
这个子项目是众多研究子项目之一
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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MURRAY JUNOP其他文献
MURRAY JUNOP的其他文献
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{{ truncateString('MURRAY JUNOP', 18)}}的其他基金
STRUCTURAL STUDIES OF PROTEINS INVOLVED IN THE LPS BIOSYNTHETIC PATHWAY
LPS 生物合成途径相关蛋白质的结构研究
- 批准号:
8363381 - 财政年份:2011
- 资助金额:
$ 1.71万 - 项目类别:
STRUCTURAL STUDIES OF PROTEINS INVOLVED IN THE LPS BIOSYNTHETIC PATHWAY
LPS 生物合成途径相关蛋白质的结构研究
- 批准号:
8170632 - 财政年份:2010
- 资助金额:
$ 1.71万 - 项目类别:
STRUCTURAL STUDIES OF PROTEINS INVOLVED IN THE LPS BIOSYNTHETIC PATHWAY
LPS 生物合成途径相关蛋白质的结构研究
- 批准号:
7957304 - 财政年份:2009
- 资助金额:
$ 1.71万 - 项目类别:
STRUCTURAL STUDIES OF PROTEINS INVOLVED IN THE LPS BIOSYNTHETIC PATHWAY
LPS 生物合成途径相关蛋白质的结构研究
- 批准号:
7726202 - 财政年份:2008
- 资助金额:
$ 1.71万 - 项目类别:
STRUCTURAL STUDIES OF PROTEINS INVOLVED IN THE LPS BIOSYNTHETIC PATHWAY
LPS 生物合成途径涉及的蛋白质的结构研究
- 批准号:
7602269 - 财政年份:2007
- 资助金额:
$ 1.71万 - 项目类别:
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