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
- 来源:
- 关键词:
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
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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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:
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:
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:
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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