- 作者: Nien-Tzu Chang; Wen K. Yang; Huey-Chung Huang; Kai-Wun Yeh; Cheng-Wen Wu
- 作者服務機構: 1 Graduate Institute of Life Science, National Defense Medical Center, Taipei, Taiwan; ; 2 Institute of Biomedical Sciences, Academia S璯ica, Taipei, Taiwan; ; 3 China Medical University Hospital, 2 Yu-ter Road, Taichung, 404, Taiwan; ; 4 Department of Biochemistry, National Taiwan University, Taipei, Taiwan; ; 5 Department of Botany, National Taiwan University, Taipei, Taiwan; ; 6 National Health Research Institutes, Miaoli County, Taiwan, ROC
- 中文摘要: --
- 英文摘要: 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.
- 中文關鍵字: --
- 英文關鍵字: human endogenous retrovirus I type, long terminal repeat, negative regulatory element, wild type p53, mutant p53