The transcriptional activity of HERV-I LTR is negatively regulated by its cis-elements and wild type p53 tumor suppressor protein

Nien Tzu Chang, Wen K. Yang*, Huey Chung Huang, Kai Wun Yeh, Cheng-Wen Wu Lee

*此作品的通信作者

研究成果: Article同行評審

12 引文 斯高帕斯(Scopus)

摘要

Human endogenous retroviruses (HERVs), abundantly inter-dispersed in the genome, carry long terminal repeats (LTRs) that may potentially retro-transpose to new genomic sites and deregulate the neighboring cellular genes. However, normally HERVs are either structurally defective or inactive due possibly to stringent negative control mechanisms. To study the possible negative regulation of HERV, we isolated the LTR of RTVL-Ia and constructed site-specific mutations for analysis of the promoter and enhancer functions by using chloramphenicol acetyl transferase (CAT) reporter assay. Our results showed that in most transfected human cells the LTR-mediated CAT expression was negligible unless a sequence segment at the AGTAAA polyadenylation site was deleted. In addition, we have found that the wild type p53 may inhibit whereas a p53 mutant (V143A) stimulate the transcriptional activity of HERV-I LTR. Our results imply that HERV-I LTR, while under negative control by its LTR cis-elements and by wild type p53, may become active upon p53 mutation.

原文English
頁(從 - 到)211-222
頁數12
期刊Journal of Biomedical Science
14
發行號2
DOIs
出版狀態Published - 1 三月 2007

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