Evidence map›Paper›PMID 16918502›Full record

ArticleThe Biochemical journal2007

Differential regulation of human YY1 and caspase 7 promoters by prohibitin through E2F1 and p53 binding sites.

B Joshi, S Rastogi, M Morris, L M Carastro, C DeCook, E Seto, S P Chellappan

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Transcription factors that interact with p53 and Mdm2.International journal of cancer · 2016
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Use of biotinylated plasmid DNA as a surrogate for HSV DNA to identify proteins that repress or activate viral gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  15. Article
  16. Article
  17. Article
  18. The oncogenic role of Yin Yang 1.Critical reviews in oncogenesis · 2011
    Review
  19. Article
  20. HIC1 regulates tumor cell responses to endocrine therapies.Molecular endocrinology (Baltimore, Md.) · 2009
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

B JoshiDepartment of Interdisciplinary Oncology, H. Lee Moffitt Cancer Center and Research Institute, University of South Florida, 12902 Magnolia Dr., Tampa, FL 33612, USA.
S Rastogi
M Morris
L M Carastro
C DeCook
E Seto
S P Chellappan
Moffitt Cancer Center · US

Funding

PROHIBITION GENE IN GROWTH CONTROL AND TUMOR SUPPRESSIONR01CA077301 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI CHELLAPPAN, SRIKUMAR P. · 1999 to 2009
$2.0M
NCI NIH HHS CA77301NCI NIH HHS R01 CA077301
6 · The paper itself

Abstract

Prohibitin is a 30 kDa growth suppressive protein that has pleiotropic functions in the cell. Although prohibitin has been demonstrated to have potent transcriptional regulatory functions, it has also been proposed to facilitate protein folding in the mitochondria and promote cell migration in association with Raf-1. Our previous studies have shown that prohibitin physically interacts with the marked-box domain of E2F family members and represses their transcriptional activity; in contrast, prohibitin could bind to and enhance the transcriptional activity of p53. Here, we show that promoters of human YY1 (Yin and Yang 1) as well as caspase 7 genes are modulated by prohibitin. YY1 promoter activity was reduced upon overexpression of prohibitin, while it was enhanced when prohibitin was depleted by small interfering RNA techniques. The repressive effects of prohibitin on the YY1 promoter were mediated through E2F binding sites, as seen by mutational analysis and chromatin immunoprecipitation assays. Further, depletion of E2F1 prevented prohibitin from repressing the YY1 promoter. In contrast with YY1, prohibitin overexpression led to enhanced levels of caspase 7, whereas depletion of prohibitin reduced it. Interestingly, the caspase 7 promoter was found to have p53-binding sites and prohibitin activated this promoter through p53. These studies show that prohibitin can have diverse effects on the expression of different genes and the activity of various cellular promoters is affected by prohibitin. Further, it appears very likely that prohibitin carries out many of its cellular functions by affecting the transcription of different genes.

Indexed as

Gene Expression RegulationPromoter Regions, GeneticCaspase 7Cell Line, TumorDNA PrimersE2F1 Transcription FactorGene Expression Regulation, EnzymologicHumansMutagenesisPlasmidsProhibitinsRepressor ProteinsRNA, NeoplasmRNA, Small InterferingTransfectionTumor Suppressor Protein p53Caspase 7DNA PrimersE2F1 protein, humanE2F1 Transcription FactorProhibitinsRepressor ProteinsRNA, NeoplasmRNA, Small InterferingTumor Suppressor Protein p53YY1 protein, humanYY1 Transcription Factor

Identifiers

PMID16918502
PMCPMC1698671
OpenAlexW2030028099

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.