共查询到20条相似文献,搜索用时 78 毫秒
1.
2.
3.
Overlapping CRE and E box motifs in the enhancer sequences of the bovine leukemia virus 5' long terminal repeat are critical for basal and acetylation-dependent transcriptional activity of the viral promoter: implications for viral latency
下载免费PDF全文
![点击此处可从《Journal of virology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Calomme C Dekoninck A Nizet S Adam E Nguyên TL Van Den Broeke A Willems L Kettmann R Burny A Van Lint C 《Journal of virology》2004,78(24):13848-13864
4.
Suboptimal Enhancer Sequences Are Required for Efficient Bovine Leukemia Virus Propagation In Vivo: Implications for Viral Latency
下载免费PDF全文
![点击此处可从《Journal of virology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
C. Merezak C. Pierreux E. Adam F. Lemaigre G. G. Rousseau C. Calomme C. Van Lint D. Christophe P. Kerkhofs A. Burny R. Kettmann L. Willems 《Journal of virology》2001,75(15):6977-6988
5.
6.
7.
8.
van der Stoep N Quinten E van den Elsen PJ 《Journal of immunology (Baltimore, Md. : 1950)》2002,169(9):5061-5071
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
Human T-cell leukemia virus type 1 Tax transactivates the human proliferating cell nuclear antigen promoter. 总被引:10,自引:4,他引:6
下载免费PDF全文
![点击此处可从《Journal of virology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
The human T-cell leukemia virus type 1 (HTLV-1) transforming protein, Tax, is a potent transactivator of both viral and cellular gene expression. The ability of Tax to transform cells is believed to depend on its transactivation of cellular-growth-regulatory genes. Expression of proliferating cell nuclear antigen (PCNA) is intimately linked to cell growth and DNA replication and repair. By testing a series of PCNA promoter deletion constructs, we have demonstrated that the PCNA promoter can be transactivated by Tax. The smallest construct that was activated did not include the ATF/CRE binding site at nucleotide -50, and mutations in the ATF/CRE element in the context of a larger promoter were still activated by Tax. In addition, a Tax mutant that is defective for activation of the CRE pathway retained the ability to activate the -397 promoter construct. When a series of linker scanner mutations that span the region from nucleotide -45 to -7 were assayed, mutations in and around a repeat sequence were found to abolish Tax transactivation. Multimerized copies of either half of the repeat were Tax responsive. A single protein complex was shown to bind specifically to the Tax-responsive region, and the binding of this complex was enhanced in the presence of Tax. These results demonstrate that the PCNA promoter contains a Tax-responsive element located between nucleotides -45 and -7 whose sequence is different from those of other, previously identified Tax-responsive elements. The ability of Tax to activate the PCNA promoter may play an important role in cellular transformation by HTLV-1. 相似文献
19.