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REGULATION OF CBP/P300 TRANSACTIVATION BY E2FI

REGULATION OF CBP/P300 TRANSACTIVATION BY E2FI
E2FI 对 CBP/P300 交易的监管
批准号:
7562328
负责人:
ERIK K FLEMINGTON
金额:
$3.04万
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-05-01 至 2008-04-30

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中文摘要
翻译
这个子项目是众多研究子项目之一
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The Epstein-Barr virus (EBV) is a human DNA tumor virus and it has been implicated in the development of a wide range of human malignancies. Previously we found that the cell cycle S-phase promoting factors c-Myc and E2F1 inhibit CBP/p300 mediated transactivation in EBV-infected nasopharyngeal carcinoma cells. Since CBP/p300 mediated transactivation is associated with their localization to promyelocytic leukemia (PML) bodies, we thus postulated that PML bodies may be served as a potential target of c-Myc/E2F1 to regulate CBP/p300 function. To test this hypothesis, we have analyzed the cellular distribution of several PML proteins in E2F1 transfected cells and control cells by confocal laser scanning microscopy. Our preliminary data have shown that Sp100, one of the PML proteins, may be involved in the regulation of CBP/p300 transactivation by E2F1. Data is currently being analyzed and a manuscript in in preparation.
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EBV reactivation causes widespread host de novo promoter transcription and transcriptional interference
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EBV reactivation causes widespread host de novo promoter transcription and transcriptional interference
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Programmed splicing derangement as new EBV host cell shut-off mechanism
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  • 项目类别:
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