课题基金 / 基金详情

FEN-1/WRN Complex in Prevention of Genetic Diseases

FEN-1/WRN Complex in Prevention of Genetic Diseases
FEN-1/WRN 复合物预防遗传病
批准号：
7459899
负责人：
L DAVID FINGER
金额：
$5.2万
依托单位：
BECKMAN RESEARCH INSTITUTE/CITY OF HOPE
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
项目状态：
已结题
起止时间：
2006-06-26 至 2009-06-25
来源：
https://reporter.nih.gov/project-details/7459899
关键词：
AmidesBindingBiochemicalCatalysisChemicalsCleaved cellComplexCritiquesDNADNA BindingDNA SequenceDNA StructureDNA biosynthesisDNA chemical synthesisDNA-Binding ProteinsDNA-Protein InteractionExcisionExhibitsFlap EndonucleasesGenesGenomeGenomicsGoalsHereditary DiseaseHeteronuclear NMRHomologous GeneHumanHuman GenomeHuntington DiseaseIncidenceKineticsKnock-in MouseKnock-outMaintenanceMammalsMapsMetabolic PathwayModelingMolecularMyotonic DystrophyNatureNitrogenNucleotidesOkazaki fragmentsPathway interactionsPhenotypePolymerasePreventionProcessPropertyProteinsProtonsRNA primersRTH-1 NucleaseRecruitment ActivityResolutionSiteSpinocerebellar AtaxiasStructureSurfaceSurgical FlapsTertiary Protein StructureTestingTrinucleotide RepeatsYeastsendonucleasehuman diseasein vivomutantnucleasepol genesyeast genetics

项目摘要

项目成果

L DAVID FINGER的其他基金

相似基金

相关文献

中文摘要
翻译
点击翻译按钮获取中文摘要
英文摘要
DESCRIPTION (provided by applicant): Tri-nucleotide repeat (TNR) DNA sequences occur throughout the human genome and have an intrinsic propensity to expand during replication. Expansion of such sequences is known to result in several human diseases, including Huntington's disease, spinocerebellar ataxia, and myotonic dystrophy. Errors in several DNA metabolic pathways due to the nature of TNR sequences have been implicated as the cause for TNR expansion. One mechanism for TNR expansion involves errors in Okazaki fragment maturation. Normally, 5'-flap endonuclease (FEN-1) cleaves the single stranded 5'-flap DNA structures generated during lagging-strand DNA synthesis. However, when the flap contains a TNR sequence, the flap can fold into a hairpin structure that has been shown to inhibit FEN-1 cleavage of the flap structures. Therefore, the inability of FEN-1 to process TNR 5'-hairpin-flaps is proposed to be one cause of TNR expansion. FEN-1 has recently been shown in vivo to proc similarities in TNR hairpin flap and fork DNA structures, it is hypothesized that the FEN-1 /WRN complex processes TNR hairpin flap structures in vivo, thereby suppressing TNR expansions in mammals. This hypothesis is consistent with the observation that deletion of the yeast FEN-1 gene results in critique one a two orders of magnitude difference in the incidence of TNR expansions. Furthermore, it is hypothesized that the unique DNA binding properties of WRN guide FEN-1 activity to TNR hairpin flap sites in addition to stimulating catalytic activity.
期刊论文(0)
专著(0)
科研奖励(0)
会议论文
FEN-1/WRN Complex in Prevention of Genetic Diseases
FEN-1/WRN Complex in Prevention of Genetic Diseases
国内基金
海外基金
帽结合蛋白(cap binding protein)调控乙烯信号转导的分子机制
  • 批准号：
    32170319
  • 项目类别：
    面上项目
  • 资助金额：
    58.00万元
  • 批准年份：
    2021
  • 负责人：
    董春海
  • 依托单位：
    青岛农业大学
帽结合蛋白（cap binding protein）调控乙烯信号转导的分子机制
  • 批准号：
    --
  • 项目类别：
    --
  • 资助金额：
    58万元
  • 批准年份：
    2021
  • 负责人：
    董春海
  • 依托单位：
    青岛农业大学
ID1 (Inhibitor of DNA binding 1) 在口蹄疫病毒感染中作用机制的研究
番茄EIN3-binding F-box蛋白2超表达诱导单性结实和果实成熟异常的机制研究
  • 批准号：
    31372080
  • 项目类别：
    面上项目
  • 资助金额：
    80.0万元
  • 批准年份：
    2013
  • 负责人：
    杨迎伍
  • 依托单位：
    重庆大学