CIS ACTNG REG ELEMENT: ATRIAL NATRIURETIC FACTOR GENE IN ACUTE PRESSURE OVERLOAD

CIS ACTNG 调节元件:急性压力超负荷时的心房利尿钠因子基因

基本信息

  • 批准号:
    6277848
  • 负责人:
  • 金额:
    $ 4.57万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    1998
  • 资助国家:
    美国
  • 起止时间:
    1998-05-01 至 1999-04-30
  • 项目状态:
    已结题

项目摘要

To identify the cis-acting regulatory element(s) which control the induction of the atrial natriuretic factor (ANF) gene in acute pressure overload, DNA constructs consisting of promoter elements linked to a reporter gene were injected into the myocardium of dogs, which underwent aortic banding or were sham-operated. Expression of a reporter gene construct harboring the ANF promoter (-34OOANF) was induced 6-12 fold after 7 d of pressure overload. An internal deletion of 556 bp (nucleotide sequence -693 to -137) completely abrogated the inducibility of the ANF reporter gene construct. An activator protein-1 (AP1)-like site (-496 to -489) and a cAMP regulatory element (CRE) (-602 to -596) are located within the deleted sequence. Site-directed mutagenesis of the AP1-like site but not the CRE completely prevented the induction of this construct to acute pressure overload. Further, the AP1-like site was able to confer inducibility of a heterologous promoter ( -myosin heavy chain) to higher values than controls. Gel mobility shift assay (GMSA) supershift analysis was performed using a radiolabeled probe of the ANF promoter (-506/-483) that included the AP1-like site (ATGAATCA) sequence, as well as a probe converted to contain an AP1 consensus sequence (ATGACTCA). GMSA analysis demonstrated that the ANF AP1-like element could bind both a constitutively expressed factor and the AP1 proteins, and conversion to a true AP1 site increased its affinity for AP1. However, 7 d after the onset of pressure overload, the AP1 proteins were present only at low levels, and the major complex formed by the ANF AP1-like probe was not supershifted by a jun antibody. Using a large animal model of pressure overload, we have demonstrated that a unique cis-acting element was primarily responsible for the overload induction of the ANF gene.
识别控制的顺式调控元件

项目成果

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Dorothy Eileen Vatner其他文献

Dorothy Eileen Vatner的其他文献

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{{ truncateString('Dorothy Eileen Vatner', 18)}}的其他基金

Adenylyl Cyclase Type 5 Inhibition to Treat Myocardial Infarction
腺苷酸环化酶 5 型抑制治疗心肌梗死
  • 批准号:
    9764847
  • 财政年份:
    2018
  • 资助金额:
    $ 4.57万
  • 项目类别:
INHIBITION OF ADENYLYL CYCLASE TYPE 5: HEALTHFUL AGING PROTECTION
抑制 5 型腺苷酸环化酶:健康的抗衰老保护
  • 批准号:
    9321949
  • 财政年份:
    2016
  • 资助金额:
    $ 4.57万
  • 项目类别:
Mechanisms of myocardial ischemia and reperfusion
心肌缺血和再灌注的机制
  • 批准号:
    8774406
  • 财政年份:
    2013
  • 资助金额:
    $ 4.57万
  • 项目类别:
SFRP2, cell survival, and coronary vascular angiogenesis
SFRP2、细胞存活和冠状血管生成
  • 批准号:
    8875747
  • 财政年份:
    2013
  • 资助金额:
    $ 4.57万
  • 项目类别:
SFRP2, cell survival, and coronary vascular angiogenesis
SFRP2、细胞存活和冠状血管生成
  • 批准号:
    8563199
  • 财政年份:
    2013
  • 资助金额:
    $ 4.57万
  • 项目类别:
AC5 inhibitor for heart failure
AC5抑制剂治疗心力衰竭
  • 批准号:
    8695476
  • 财政年份:
    2012
  • 资助金额:
    $ 4.57万
  • 项目类别:
AC5 Inhibitor for Obesity
AC5 肥胖抑制剂
  • 批准号:
    7807877
  • 财政年份:
    2010
  • 资助金额:
    $ 4.57万
  • 项目类别:
Rescue of Beta-Adrenergic Cardiomyopathy by Inhibition of Adenylyl Cyclase
通过抑制腺苷酸环化酶来挽救β-肾上腺素能心肌病
  • 批准号:
    7638978
  • 财政年份:
    2009
  • 资助金额:
    $ 4.57万
  • 项目类别:
Pre-emptive conditioning of the ischemic heart
缺血性心脏的先发性调理
  • 批准号:
    8725012
  • 财政年份:
    2009
  • 资助金额:
    $ 4.57万
  • 项目类别:
Rescue of Beta-Adrenergic Cardiomyopathy by Inhibition of Adenylyl Cyclase
通过抑制腺苷酸环化酶来挽救β-肾上腺素能心肌病
  • 批准号:
    7787533
  • 财政年份:
    2009
  • 资助金额:
    $ 4.57万
  • 项目类别:

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