OCULAR LENS STUDIES
眼晶状体研究
基本信息
- 批准号:2157911
- 负责人:
- 金额:$ 22.13万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1978
- 资助国家:美国
- 起止时间:1978-12-01 至 1997-06-30
- 项目状态:已结题
- 来源:
- 关键词:DNA damage antioxidants catalase cataract crystallins epithelium free radical scavengers gene expression genetic enhancer element glutathione peroxidase hydrogen peroxide laboratory rat lens oxidation reduction reaction oxidative stress phorbols phosphorylation photochemistry radiation genetics reducing agents regulatory gene reporter genes tissue /cell culture transcription factor transfection
项目摘要
The work described in this application is designed to explore the premise
that the lens epithelial cell redox status may regulate gene expression.
There are a number of genes whose products regulate the expression of
other genes. It is proposed that some of these regulatory genes such as
fos, jun and NF-kappaB are themselves controlled by redox in lens systems.
These regulatory genes have been chosen since they are widely distributed,
are effected by redox and binding sites for their products have been
reported to be associated with certain crystallin genes. The experimental
work described in this application will elucidate the extent to which
oxidative stress alters the expression of these control genes and
subsequently effects the expression of a reporter gene and of lens genes.
The demonstration of the disruption of normal cellular gene regulation by
oxidative stress would provide a new fundamental aspect to the mechanism
by which oxidative stress can cause cataract and place greater emphasis on
events occurring in the epithelial cells. Specifically, it is planned to
determine the expression of fos, jun and NF-kappaB in the lens in resting
and dividing cell lines under normal and oxidative stress conditions. The
regulation by fos, jun and NF-kappaB of a reporter gene and certain lens
genes containing AP-1 enhancer sites and NF-kappaB binding sites will be
examined. Cellular redox set points will be determined based on GSH/GSSG,
NADH/NAD and NADPH/NADP. The effect of agents which eliminate aspects of
oxidative stress such as AL-3823A, desferoxamine and Tempo will also be
investigated. Preliminary observations are reported indicating the
feasibility of this approach.
本申请中描述的工作旨在探索前提
透镜上皮细胞氧化还原状态可能调节基因表达。
有许多基因,其产物调节
其他基因有人提出,这些调控基因中的一些,如
在透镜系统中,fos、jun和NF-κ B本身受氧化还原控制。
选择这些调控基因是因为它们分布广泛,
受氧化还原作用的影响,其产物的结合位点
据报道与某些晶体蛋白基因有关。实验
本申请中描述的工作将阐明
氧化应激改变了这些控制基因的表达,
随后影响报道基因和透镜基因的表达。
正常细胞基因调控被破坏的证明,
氧化应激将为该机制提供一个新的基本方面,
氧化应激可导致白内障,
发生在上皮细胞中的事件。具体而言,计划在
测定静息状态下透镜中fos、jun和NF-κ B的表达
以及在正常和氧化应激条件下的分裂细胞系。的
fos、jun和NF-κ B对报告基因和某些透镜的调控
含有AP-1增强子位点和NF-κ B结合位点的基因将被
考察细胞氧化还原设定点将根据GSH/GSSG确定,
NADH/NAD和NADPH/NADP。消除某些方面的药剂的效果
氧化应激如AL-3823 A、去铁胺和克里思也将
研究了初步观察报告表明,
这种做法的可行性。
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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ABRAHAM SPECTOR其他文献
ABRAHAM SPECTOR的其他文献
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{{ truncateString('ABRAHAM SPECTOR', 18)}}的其他基金
THE EFFECT OF OXIDATION UPON LENS TRANSPORT SYSTEMS
氧化对镜片传输系统的影响
- 批准号:
3259555 - 财政年份:1983
- 资助金额:
$ 22.13万 - 项目类别:
THE EFFECT OF OXIDATION UPON LENS TRANSPORT SYSTEMS
氧化对镜片传输系统的影响
- 批准号:
3259556 - 财政年份:1983
- 资助金额:
$ 22.13万 - 项目类别:
THE EFFECT OF OXIDATION UPON LENS TRANSPORT SYSTEMS
氧化对镜片传输系统的影响
- 批准号:
3259552 - 财政年份:1983
- 资助金额:
$ 22.13万 - 项目类别:
THE EFFECT OF OXIDATION UPON LENS TRANSPORT SYSTEMS
氧化对镜片传输系统的影响
- 批准号:
3259550 - 财政年份:1983
- 资助金额:
$ 22.13万 - 项目类别:
THE EFFECT OF OXIDATION UPON LENS TRANSPORT SYSTEMS
氧化对镜片传输系统的影响
- 批准号:
3259553 - 财政年份:1983
- 资助金额:
$ 22.13万 - 项目类别:
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