BRD7, a novel bromodomain gene, inhibits G1-S progression by transcriptionally regulating some important molecules involved in ras/MEK/ERK and Rb/E2F pathways.

Zhou J; Ma J; Zhang BCLi XLShen SRZhu SGXiong WLiu HYHuang HZhou MLi GY

首页> 外文期刊>Journal of Cellular Physiology >BRD7, a novel bromodomain gene, inhibits G1-S progression by transcriptionally regulating some important molecules involved in ras/MEK/ERK and Rb/E2F pathways.

【24h】

BRD7, a novel bromodomain gene, inhibits G1-S progression by transcriptionally regulating some important molecules involved in ras/MEK/ERK and Rb/E2F pathways.

机译：BRD7,小说bromodomain基因,抑制G1-S通过转录调节一些发展重要的分子参与ras / MEK / ERK和Rb - E2F pathways。

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相似文献
相关主题

摘要

Bromodomain is a 110 amino acid domain. It is evolutionally conserved and is found in proteins strongly implicated in signal-dependent transcriptional regulation. BRD7 is a novel bromodomain gene and it is downexpressed in nasopharyngeal carcinoma (NPC) biopsies and cell lines; its function is poorly understood. In the present study, tet-on inducible expression system was used to investigate the role of BRD7 in cell growth and cell cycle progression. We found that ectopic expression of BRD7 in NPC cells inhibited cell growth and cell cycle progression from G1 to S. We further performed cell cycle cDNA array to screen potential transcriptional targets of BRD7 in cell cycle. Thirteen important signaling molecules, mainly implicated in ras/MEK/ERK and Rb/E2F pathways, were differentially expressed by induction of BRD7. Moreover, we observed that BRD7 could regulate the promoter activity of E2F3, one of its targets. Taken together, the present study indicated that BRD7 inhibited G1-S progression by transcriptionally regulating some important molecules involved in ras/MEK/ERK and Rb/E2F pathways and suggested that BRD7 may present a promising candidate of NPC trade mark associated tumor suppressor gene.

机译：Bromodomain是110氨基酸领域。散播他们保守中发现的蛋白质强烈与相互依赖转录调控。bromodomain基因和downexpressed在鼻咽癌(NPC)切片和细胞行;目前的研究中,tet-on诱导表达系统被用来调查BRD7的角色在细胞生长和细胞周期进程。异位表达BRD7的NPC细胞抑制从G1细胞生长和细胞周期进程我们进一步进行细胞周期cDNA数组筛选潜在转录BRD7的目标在细胞周期。分子,主要涉及在ras / MEK / ERK和Rb / E2F通路,差异表达BRD7的感应。BRD7可以调节的推广活动E2F3,它的一个目标。本研究表明,BRD7抑制G1-S通过转录调节一些发展重要的分子参与ras / MEK / ERK和Rb / E2F途径和建议BRD7可能目前人大商标的一个有前途的候选人相关的肿瘤抑制基因。

著录项

来源
《Journal of Cellular Physiology》 |2004年第1期|89-98|共10页
作者
Zhou J; Ma J; Zhang BCLi XLShen SRZhu SGXiong WLiu HYHuang HZhou MLi GY;
展开▼
作者单位

Cancer Research Institute, Xiang-Ya School of Medicine, Central South University, Changsha, Hunan, People's Republic of China.;

展开▼
收录信息
原文格式 PDF
正文语种英语
中图分类细胞生物学;
关键词
Cell Cycle Progression; Bromodomain; Ectopic Gene ExpressionprogressionsCell CycleE2F Transcription FactorsNovelsBRD7 gene;

机译：细胞周期进展;Bromodomain;异位基因ExpressionprogressionsCell CycleE2F转录FactorsNovelsBRD7基因;

相似文献

外文文献
中文文献

BRD7, a novel bromodomain gene, inhibits G1-S progression by transcriptionally regulating some important molecules involved in ras/MEK/ERK and Rb/E2F pathways.

摘要

著录项

相似文献

相关主题

期刊订阅