REVERSE TRANSCRIPTASE TEMPLATE SWITCHING AND FIDELITY

逆转录酶模板切换和保真度

基本信息

  • 批准号:
    2462203
  • 负责人:
  • 金额:
    $ 18.02万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1993
  • 资助国家:
    美国
  • 起止时间:
    1993-01-01 至 2002-12-31
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (Adapted from the applicant's abstract): Genetic variation in the retroviral populations depend on the mutation and recombination rates/replication cycle, the rate of replication/time and the selective forces that exist on the population. The high mutational rate of retroviruses is due to the virally encoded reverse transcriptase, which lacks proofreading function and has low processivity. Mutations occur through misincorporation, dislocation mutagenesis, and intramolecular or intermolecular strand switching. The template switching, which is a process required for viral replication, can lead to deletions, duplications, and recombination. Previous studies has defined the mutation rates and the spectrum of mutations possible through viral replication. The current application aims at defining the mechanism that RT switches templates and the structural determinants of RT and the reverse transcription complex that are important for fidelity. Four specific aims are proposed: 1) Utilize retroviral vectors encoding directly repeated sequences to determine in vivo the relative rates of template switching in RNA and DNA- dependent DNA synthesis, and the effects of distance between direct repeats, RNA dimer linkage signal, and template-primer hydrogen bonding on template switching; 2) Perform targeted and random mutational analysis to define structural features of reverse transcriptase and RNase H that are important for accuracy of DNA synthesis. 3) Determine whether environmental factors such as nucleotide pool imbalances and anti-viral drugs affect retroviral mutation rates. 4) Probe the structure of the reverse transcription complex by determining whether DNA synthesis initiates on both co-packaged RNAs and whether minus-strand transfer is promoted by a putative circular structure of the viral RNAs.
描述(改编自申请人摘要):基因变异

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(2)

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VINAY K. PATHAK其他文献

VINAY K. PATHAK的其他文献

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{{ truncateString('VINAY K. PATHAK', 18)}}的其他基金

MECHANISMS OF MUTATIONS & HYPERMUTATIONS IN RETROVIRUSES
突变机制
  • 批准号:
    2099505
  • 财政年份:
    1993
  • 资助金额:
    $ 18.02万
  • 项目类别:
MECHANISMS OF MUTATIONS & HYPERMUTATIONS IN RETROVIRUSES
突变机制
  • 批准号:
    2099504
  • 财政年份:
    1993
  • 资助金额:
    $ 18.02万
  • 项目类别:
REVERSE TRANSCRIPTASE TEMPLATE SWITCHING AND FIDELITY
逆转录酶模板切换和保真度
  • 批准号:
    2856334
  • 财政年份:
    1993
  • 资助金额:
    $ 18.02万
  • 项目类别:
MECHANISMS OF MUTATIONS & HYPERMUTATIONS IN RETROVIRUSES
突变机制
  • 批准号:
    2008196
  • 财政年份:
    1993
  • 资助金额:
    $ 18.02万
  • 项目类别:
MECHANISMS OF MUTATIONS & HYPERMUTATIONS IN RETROVIRUSES
突变机制
  • 批准号:
    2099503
  • 财政年份:
    1993
  • 资助金额:
    $ 18.02万
  • 项目类别:
MECHANISMS OF MUTATIONS & HYPERMUTATIONS IN RETROVIRUSES
突变机制
  • 批准号:
    3460679
  • 财政年份:
    1993
  • 资助金额:
    $ 18.02万
  • 项目类别:
Identification of Structural Determinants of Reverse Tra
反向传输的结构决定因素的识别
  • 批准号:
    6952145
  • 财政年份:
  • 资助金额:
    $ 18.02万
  • 项目类别:
Development and Characterization of Antiviral Drugs That
抗病毒药物的开发和表征
  • 批准号:
    7338640
  • 财政年份:
  • 资助金额:
    $ 18.02万
  • 项目类别:
Replication and Pathogenic Potential of XMRV in Humans
XMRV 在人类中的复制和致病潜力
  • 批准号:
    8349482
  • 财政年份:
  • 资助金额:
    $ 18.02万
  • 项目类别:
Mechanism of APOBEC3G-Mediated Hypermutation and Inhibit
APOBEC3G 介导的超突变和抑制机制
  • 批准号:
    7064431
  • 财政年份:
  • 资助金额:
    $ 18.02万
  • 项目类别:

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