REGULATION OF TRANSCRIPTIONAL ELONGATION BY HIV1 TAT

HIV1 TAT 对转录延伸的调节

基本信息

  • 批准号:
    6170603
  • 负责人:
  • 金额:
    $ 23.51万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1997
  • 资助国家:
    美国
  • 起止时间:
    1997-08-01 至 2002-07-31
  • 项目状态:
    已结题

项目摘要

Control of transcriptional elongation has been recognized as an important step in gene regulation, but mechanisms regulating the efficiency of elongation by RNA polymerase II have not been extensively studied. The goal of the proposed research is to elucidate mechanisms regulating elongation using HIV-l Tat as a model system. Tat stimulates the efficiency of elongation by recognizing the trans-acting-response (TAR) RNA element located at the 5' end of the nascent viral transcript. Tat trans-activation requires specific cellular cofactors. The applicant has recently isolated and cloned a cellular cofactor, Tat-SFI, which is specifically required for Tat activation of elongation and is a substrate of an associated linase. Tat-SFI is distantly related to EWS and FUS/TLS, which are members of a novel class of putative transcription factors with RNA recognition motifs and are frequently associated with sarcomas. Preliminary studies suggest that Tat may stimulate the efficiency of elongation by recruiting a preformed complex containing Tat-SFI and its kinase to the HIV promoter and by enhancing the effect of an elongation factor, Elongin (Sill). This proposal seeks to further dissect the function of Tat-SFI in Tat activation through analyzing the sequence specificity of the various interactions among Tat, Tat-SFI, the Tat- SFI kinase, and TAR, and through mapping the and amino acid residues critical for Tat-SFI activity. One important objective is to assess the intriguing functional significance of Tat-SFI phosphorylation in Tat activation and to isolate, clone, and characterize its kinase. A significant effort will also be devoted to the investigation of the mechanisms by which Tat and Tat SFI stimulate the efficiency of elongation and the identification of components of a Tat-stimulated elongating polymerase complex. Finally, the relationship between Tat and cellular elongation factors such as Elongin and TFIIS in activation of polymerase processivity will be studied. Further analysis of Tat activation of the efficiency of elongation and the role of the cellular cofactors in this process will likely reveal general mechanisms of gene regulation at the stage of elongation.
控制转录伸长已被认为是一种有效的方法

项目成果

期刊论文数量(0)
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专利数量(0)

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QIANG ZHOU其他文献

QIANG ZHOU的其他文献

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{{ truncateString('QIANG ZHOU', 18)}}的其他基金

Tat cofactors and control of HIV-1 latency
Tat辅助因子和HIV-1潜伏期的控制
  • 批准号:
    8434937
  • 财政年份:
    2011
  • 资助金额:
    $ 23.51万
  • 项目类别:
Tat cofactors and control of HIV-1 latency
Tat辅助因子和HIV-1潜伏期的控制
  • 批准号:
    8139592
  • 财政年份:
    2011
  • 资助金额:
    $ 23.51万
  • 项目类别:
Tat cofactors and control of HIV-1 latency
Tat辅助因子和HIV-1潜伏期的控制
  • 批准号:
    8236887
  • 财政年份:
    2011
  • 资助金额:
    $ 23.51万
  • 项目类别:
Tat cofactors and control of HIV-1 latency
Tat辅助因子和HIV-1潜伏期的控制
  • 批准号:
    8811092
  • 财政年份:
    2011
  • 资助金额:
    $ 23.51万
  • 项目类别:
Input competition and synaptic modification during developmental remodeling
发育重塑过程中的输入竞争和突触修饰
  • 批准号:
    7568566
  • 财政年份:
    2009
  • 资助金额:
    $ 23.51万
  • 项目类别:
Regulation of Transcriptional Elongation by HIV-1 Tat
HIV-1 Tat 对转录延伸的调节
  • 批准号:
    7925117
  • 财政年份:
    2009
  • 资助金额:
    $ 23.51万
  • 项目类别:
Activity-dependent Plasticity of Retinotectal Synapses
视网膜顶盖突触的活动依赖性可塑性
  • 批准号:
    6525067
  • 财政年份:
    2002
  • 资助金额:
    $ 23.51万
  • 项目类别:
Activity-dependent Plasticity of Retinotectal Synapses
视网膜顶盖突触的活动依赖性可塑性
  • 批准号:
    6784202
  • 财政年份:
    2002
  • 资助金额:
    $ 23.51万
  • 项目类别:
Activity-dependent Plasticity of Retinotectal Synapses
视网膜顶盖突触的活动依赖性可塑性
  • 批准号:
    6405058
  • 财政年份:
    2001
  • 资助金额:
    $ 23.51万
  • 项目类别:
Regulation of Transcriptional Elongation by HIV-1 TAT
HIV-1 TAT 对转录延伸的调节
  • 批准号:
    7190551
  • 财政年份:
    1997
  • 资助金额:
    $ 23.51万
  • 项目类别:

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