Evidence map›Paper›PMID 10362258›Full record

ArticleOncogene1999

Cooperation of Sp1 and p300 in the induction of the CDK inhibitor p21WAF1/CIP1 during NGF-mediated neuronal differentiation.

N Billon, D Carlisi, M B Datto, L A van Grunsven, A Watt, X F Wang, B B Rudkin

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 150 citations in OpenAlex.

  1. Article
  2. Function ofOncology letters · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Beyond HAT Adaptor: TRRAP Liaisons with Sp1-Mediated Transcription.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Overexpression of histone deacetylases in cancer cells is controlled by interplay of transcription factors and epigenetic modulators.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  19. Article
  20. Sumoylation differentially regulates Sp1 to control cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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 3 institutions in 3 countries.

N BillonDifferentiation & Cell Cycle Group, Laboratoire de Biologie Moleculaire et Cellulaire, UMR 49 CNRS/Ecole Normale Supérieure de Lyon, France.
D Carlisi
M B Datto
L A van Grunsven
A Watt
X F Wang
B B Rudkin
École Normale Supérieure de Lyon · FRDuke University Hospital · USBrandeis University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Addition of nerve growth factor (NGF) to PC12 cells promotes neuronal differentiation while inhibiting cell proliferation. In order to understand how NGF exerts its antimitogenic effect during differentiation, we have studied the mechanism by which this factor activates the promoter of the CDK inhibitor p21W4F1/CIP1. The minimal region of the p21 promoter required for the NGF-induction was mapped to a contiguous stretch of 10 bp located 83 bases upstream of the transcription initiation site. This GC-rich region was shown to interact specifically with the transcription factor Sp1 and the related protein Sp3, in either exponentially-growing or NGF-treated PC12 cells. The addition of NGF resulted in an accumulation of the transcriptional co-activator p300 in complexes associated with the NGF-responsive region. Transcriptional activity of Sp1, Sp3 and p300 was specifically induced by NGF in a Gal4-fusion assay, indicating that induction of p21 during neuronal differentiation may involve regulation of the activity of these factors by NGF. Furthermore, p300 was able to act as a co-activator for Sp1-mediated transcriptional activation in PC12 cells, suggesting that p300 and Sp1 may cooperate in activating p21 transcription during the withdrawal of neuronal precursors from the cell cycle. This hypothesis is supported by experiments showing that p300 and Sp1 form complexes in PC12 cells.

Indexed as

AnimalsBinding SitesCell DifferentiationCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsDNA Mutational AnalysisE1A-Associated p300 ProteinGalactosidasesHumansNerve Growth FactorsNeuronsNuclear ProteinsPC12 CellsPromoter Regions, GeneticRatsCDKN1A protein, humanCdkn1a protein, ratCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsE1A-Associated p300 ProteinEp300 protein, ratGalactosidasesNerve Growth FactorsNuclear ProteinsRecombinant Fusion ProteinsSp1 Transcription FactorSP3 protein, humanSp3 protein, ratSp3 Transcription FactorTrans-ActivatorsTranscription Factors

Identifiers

PMID10362258
OpenAlexW1989142029

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.