IR@PKUHSC  > 北京大学基础医学院  > 病理学系
学科主题基础医学
TEIF associated centrosome activity is regulated by EGF/PI3K/Akt signaling
Zhao, Jing; Zou, Yongxin; Liu, Haijing; Wang, Huali; Zhang, Hong; Hou, Wei; Li, Xin; Jia, Xinying; Zhang, Jing; Hou, Lin; Zhang, Bo
关键词Centrosome amplification EGF Akt C-NAP1
刊名BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
2014-09-01
DOI10.1016/j.bbamcr.2014.04.021
1843期:9页:1851-1864
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]CELL-CYCLE ; CHROMOSOMAL INSTABILITY ; DNA-DAMAGE ; MITOTIC PROGRESSION ; GENOMIC INSTABILITY ; CANCER PROGRESSION ; AURORA KINASES ; AKT INHIBITOR ; AMPLIFICATION ; PATHWAY
英文摘要

Centrosome amplification, which is a characteristic of cancer cells, has been understood as a driving force of genetic instability in the development of cancer. In previous work, we demonstrated that TEIF (transcriptional element-interacting factor) distributes in the centrosomes and regulates centrosome status under both physiologic and pathologic conditions. Here we identify TEIF as a downstream effector in EGF/PI3K/Akt signaling. The addition of EGF or transfection of active Akt stimulates centrosome TEIF distribution, resulting in an increase of centrosome splitting and amplification, while inhibitors of either PI3K or Akt attenuate these changes in TEIF and the associated centrosome status. A consensus motif for Akt phosphorylation (RHRVLT) proved to be involved in centrosomal TEIF localization, and the 469-threonine of this motif may be phosphorylated by Akt both in vitro and in vivo. Elimination of this phosphorylated site on TEIF caused reduced centrosome distribution and centrosome splitting or amplification. Moreover, TEIF closely co-localized with C-NAP1 at the proximal ends of centrioles, and centriolar loading of TEIF stimulated by EGF/Akt could displace C-NAP1, resulting in centrosome splitting. These findings reveal linkage of the EGF/PI3K/Akt signaling pathway to regulation of centrosome status which may act as an oncogenic pathway and induce genetic instability in carcinogenesis. (C) 2014 Elsevier B.V. All rights reserved.

语种英语
WOS记录号WOS:000339535300007
项目编号30770830 ; 81171907 ; 200800010060
资助机构National Natural Science Foundation of China ; Research Fund for the Doctoral Program of Higher Education
引用统计
被引频次:1[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/64026
专题北京大学基础医学院_病理学系
北京大学基础医学院
北京大学精神卫生研究所_精神科
作者单位Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Pathol, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Zhao, Jing,Zou, Yongxin,Liu, Haijing,et al. TEIF associated centrosome activity is regulated by EGF/PI3K/Akt signaling[J]. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH,2014,1843(9):1851-1864.
APA Zhao, Jing.,Zou, Yongxin.,Liu, Haijing.,Wang, Huali.,Zhang, Hong.,...&Zhang, Bo.(2014).TEIF associated centrosome activity is regulated by EGF/PI3K/Akt signaling.BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH,1843(9),1851-1864.
MLA Zhao, Jing,et al."TEIF associated centrosome activity is regulated by EGF/PI3K/Akt signaling".BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH 1843.9(2014):1851-1864.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
TEIF associated cent(2412KB)期刊论文出版稿开放获取CC BY-NC-SA浏览 请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Zhao, Jing]的文章
[Zou, Yongxin]的文章
[Liu, Haijing]的文章
百度学术
百度学术中相似的文章
[Zhao, Jing]的文章
[Zou, Yongxin]的文章
[Liu, Haijing]的文章
必应学术
必应学术中相似的文章
[Zhao, Jing]的文章
[Zou, Yongxin]的文章
[Liu, Haijing]的文章
相关权益政策
暂无数据
收藏/分享
文件名: TEIF associated centrosome activity is regulated by EGF PI3K Akt signaling.pdf
格式: Adobe PDF
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。