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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:
2856500
负责人:
Alnawaz Rehemtulla
金额:
$15.5万
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

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中文摘要
翻译
描述:紫外线照射细胞可引起复杂的细胞 反应,称为应激反应。根据初步数据, 有人提议用实验来检验紫外线辐射引起的假说 Fas受体和肿瘤坏死因子受体等膜受体的激活 I,导致类似于Fas配体的细胞凋亡减少 和TNF2诱导的细胞凋亡。研究将检验紫外线的假说 辐射通过激活Fas受体诱导细胞凋亡 与FADD的相互作用是紫外线诱导细胞凋亡的一条途径。随后的 将测试在激活FLICE中的作用,随后将调查 冰样蛋白水解酶在紫外线诱导细胞凋亡中的作用这些研究将 提供紫外线诱导的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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