Skip Navigation



Journal of Biochemistry Advance Access published online on August 7, 2008
Journal of Biochemistry, doi:10.1093/jb/mvn098
This Article
Right arrow Advance Access manuscript (PDF)
Right arrow All Versions of this Article:
144/4/539    most recent
mvn098v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Wei, Y.
Right arrow Articles by Jiang, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wei, Y.
Right arrow Articles by Jiang, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2008 The Japanese Biochemical Society

Identification of E1AF as a target gene of E2F1-induced apoptosis in response to DNA damage

Yuanyan Wei1, Dan Liu1, Yuqing Ge1, Fengbiao Zhou1, Jiejie Xu1, Hong Chen1, Jianxin Gu1 and Jianhai Jiang1,2,*

1Key Laboratory of Glycoconjuates Research & Gene Research Center, Shanghai Medical College of Fudan University, and 2Institutes of Brain Science of Fudan University, Shanghai, People's Republic of China, 200032

*Corresponding Author: Dr. Jianhai Jiang, PhD. Shanghai Medical College and Institutes of Brain Science of Fudan University. Tel: 86-21-54237660, Fax: 86-21-54237660, E-mail: jianhaijiang{at}fudan.edu.cn

Received June 30, 2008; Accepted July 26, 2008


  Abstract

Transcription factor E1AF plays critical roles in neuronal development and tumor metastasis and is regulated by a number of signaling cascades, including the mitogen-activated protein kinase pathways. Accumulated evidence indicted that E1AF might contribute to cell survival in response to environment factors. Here, we provided evidence the cell-cycle and apoptosis regulator E2F1 induces E1AF expression at the transcriptional level. DNA damage by etoposide causes E2F1-dependnet induction of E1AF expression at transcriptional level. Furthermore, disruption of E1AF expression by E1AF RNAi decreased E2F1-induced apoptosis in response to etoposide. Thus, we conclude that activation of E1AF provides a means for E2F1 to induce cell apoptosis in response to DNA damage.

Key Words: E1AF, E2F1, apoptosis, DNA damage, H1299 cells


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol. Cell. Biol.Home page
B. Guo and A. D. Sharrocks
Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase Signaling Initiates a Dynamic Interplay between Sumoylation and Ubiquitination To Regulate the Activity of the Transcriptional Activator PEA3
Mol. Cell. Biol., June 1, 2009; 29(11): 3204 - 3218.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.