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MOLECULAR MEDIATORS OF RADIATION-INDUCED APOPTOSIS

MOLECULAR MEDIATORS OF RADIATION-INDUCED APOPTOSIS
辐射诱导细胞凋亡的分子介质
批准号：
2647826
负责人：
Alnawaz Rehemtulla
金额：
$16.01万
依托单位：
UNIVERSITY OF MICHIGAN AT ANN ARBOR
依托单位国家：
美国
项目类别：
财政年份：
1998
资助国家：
美国
项目状态：
已结题
起止时间：
1998-01-01 至 2000-12-31
来源：
https://reporter.nih.gov/project-details/2647826
关键词：
apoptosis biological signal transduction cytokine receptors endopeptidases enzyme activity immunofluorescence technique immunoprecipitation protease inhibitor radiobiology receptor expression stainings tissue /cell culture tumor necrosis factor alpha ultraviolet radiation western blottings

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中文摘要
翻译
描述：紫外线照射细胞， 反应，称为应激反应。 根据初步数据， 实验提出了检验的假设，紫外线照射引起的 膜受体如Fas受体和TNF受体的活化 I，其导致类似于Fas配体的凋亡减少 和TNF 2诱导的细胞凋亡。 研究将检验紫外线 辐射通过激活Fas受体诱导细胞凋亡， 与FADD相互作用作为UV诱导的细胞凋亡的途径。 随后的 在激活FLICE中的作用将被测试，然后调查 ICE样蛋白酶在紫外线诱导的细胞凋亡中的作用。 这些研究将 提供了紫外线诱导细胞凋亡途径的详细图片。
英文摘要
DESCRIPTION: UV irradiation of cells elicits complicated cellular responses, called the stress response. Based on Preliminary Data, experiments are proposed to test the hypothesis that UV irradiation causes activation of membrane receptors such as the Fas receptor and TNF receptor I, which results in reduction of apoptosis that is analogous to Fas ligand and TNF2-induced apoptosis. Studies will test the hypothesis that UV irradiation induces apoptosis by activating Fas receptor and subsequent interaction with FADD as a pathway to UV-induced apoptosis. The subsequent role in activation of FLICE will be tested followed by investigation of the role of ICE-like proteases in UV-induced apoptosis. These studies will provide a detailed picture of the pathway for UV-induced apoptosis.
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Core C: Radiosensitization Core
Task Specific Project 3
HTS for FADD kinase inhibitors using molecular imaging
Proj 2: Molecular Imaging of Cell Surface Receptors in Cancer
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