Evidence map›Paper›PMID 11314031›Full record

ArticleOncogene2001

RB regulates transcription of the p21/WAF1/CIP1 gene.

J T Decesse, S Medjkane, M B Datto, C E Crémisi

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. The Emerging Role of p21 in Diabetes and Related Metabolic Disorders.International journal of molecular sciences · 2024
    Review
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  14. Review
  15. Article
  16. p21(Cip1) restrains pituitary tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  17. Review
  18. Article
  19. Article
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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

4 authors at 3 institutions in 2 countries.

J T DecesseLaboratoire Oncogénèse, Différenciation et Transduction du Signal, CNRS UPR 9079, Institut André Lwoff, 7 rue Guy Moquet, 94801 Villejuif, France.
S Medjkane
M B Datto
C E Crémisi
Immunology from Concept and Experiments to Translation · FRCentre National de la Recherche Scientifique · FRDuke Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously shown that RB plays an important role in the maintenance of the epithelial phenotype. p21 is also involved in several terminal differentiation systems including keratinocytes. We report here that p21 is an RB target gene in epithelial cells, but not in fibroblasts where RB is unable to transactivate p21 transcriptional expression. In epithelial cells, when RB family factors were inactivated by SV40 T antigen (LT), p21 expression was strongly repressed, whereas its expression was not affected when the cells were transformed by a mutated LT leaving RB active but inactivating p53. Moreover, retransformation by RB of LT transformed epithelial cells totally restored p21 expression. By cotransfection experiments and using deletions and point mutations of the p21 promoter, we show that the minimal region required for the RB-mediated transcriptional activation maps to a GC-rich region located between -83 and -74. This region is shown to interact specifically with the transcription factor Sp1 and Sp3. Thus for the first time, we show a positive transcriptional relationship between RB and p21 in epithelial cells. Since p21 keeps RB in a hypophosphorylated state important for its transcriptional activity during differentiation, our results imply an auto-loop of regulation between RB and p21 that may be essential for the maintenance of the differentiation state. We propose that this transcriptional relationship might be necessary of their roles in cell cycle arrest and in several differentiation pathways.

Indexed as

Transcriptional ActivationAnimalsCell CycleCell DifferentiationCells, CulturedCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsDogsEpithelial CellsFeedbackFibroblastsMiceModels, GeneticPhenotypePoint MutationCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsRetinoblastoma ProteinSp1 Transcription FactorSp3 protein, mouseSp3 Transcription FactorTranscription Factors

Identifiers

PMID11314031
OpenAlexW2314951690

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.