REGULATION OF CBP/P300 TRANSACTIVATION BY E2FI

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。EB病毒（Epstein-Barr virus，EBV）是一种人类DNA肿瘤病毒，它与多种人类恶性肿瘤的发生有关。我们以前发现细胞周期S期促进因子c-Myc和E2 F1抑制CBP/p300介导的EBV感染的鼻咽癌细胞的反式激活。由于CBP/p300介导的反式激活与其定位于早幼粒细胞白血病（PML）小体有关，因此我们推测PML小体可能是c-Myc/E2 F1调节CBP/p300功能的潜在靶点。为了验证这一假设，我们分析了几个PML蛋白在E2 F1转染细胞和对照细胞的共聚焦激光扫描显微镜的细胞分布。我们的初步数据表明，PML蛋白之一的Sp100可能参与E2 F1对CBP/p300反式激活的调节。

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.