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Journal of Biochemistry Advance Access originally published online on August 7, 2008
Journal of Biochemistry 2008 144(4):539-546; doi:10.1093/jb/mvn098
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© 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 200032, People's Republic of China

*To whom correspondence should be addressed. 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 tumour metastasis and is regulated by a number of signalling 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-dependent 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: apoptosis, DNA damage, E1AF, E2F1, H1299 cells

Abbreviations: EMSA, electrophoretic mobility shift assay; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; SDS–PAGE, SDS–poly-acrylamide gel; oligo, oligonucleotide


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