REGULATION OF CBP/P300 TRANSACTIVATION BY E2FI

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。爱泼斯坦-巴尔病毒（EBV）是一种人类DNA肿瘤病毒，它与多种人类恶性肿瘤的发展有关。先前我们发现细胞周期s期促进因子c-Myc和E2F1抑制ebv感染鼻咽癌细胞中CBP/p300介导的转激活。由于CBP/p300介导的交易激活与其定位于早幼粒细胞白血病（PML）小体相关，因此我们假设PML小体可能是c-Myc/E2F1调节CBP/p300功能的潜在靶点。为了验证这一假设，我们通过共聚焦激光扫描显微镜分析了转染E2F1细胞和对照细胞中几种PML蛋白的细胞分布。我们的初步数据表明，PML蛋白之一Sp100可能参与了E2F1对CBP/p300转激活的调控。

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.