Transcriptional Regulation of the Human Tumor Suppressor p14 ARF by E2F1, E2F2, E2F3, and Sp1-like Factors
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 291, Issue: 5, Page: 1138-1145
2002
- 47Citations
- 17Captures
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations47
- Citation Indexes47
- 47
- CrossRef26
- Captures17
- Readers17
- 17
Article Description
The human ARF/INK4a locus encodes two cell cycle inhibitors, p16 INK4a and p14 ARF, by using separate promoters. A variety of mitogenic stimuli upregulate ARF but a direct modulation at the transcriptional level has been reported only for E2F-1. We show here that the ARF promoter is strongly responsive also to E2F2 and E2F3, thus providing a strong support to their suggested role in the induction of apoptosis. Through the usage of both deletion mutants and/or site-directed mutants, we surprisingly found that none of the four putative E2F consensus sites is strictly necessary for the upregulation of ARF expression, as a minimal deletion mutant, lacking all the putative E2F binding sites, is still transactivated by E2F. Moreover, our data suggest that the ARF promoter is regulated by E2F through both direct binding to the promoter sequences and indirectly, probably by being tethered to the ARF promoter by Sp1-like factors.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X02965915; http://dx.doi.org/10.1006/bbrc.2002.6591; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0036297530&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/11883935; https://linkinghub.elsevier.com/retrieve/pii/S0006291X02965915; https://dx.doi.org/10.1006/bbrc.2002.6591
Elsevier BV
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