Evidence map›Paper›PMID 11593402›Full record

ArticleOncogene2001

Common and reversible regulation of wild-type p53 function and of ribosomal biogenesis by protein kinases in human cells.

T David-Pfeuty, Y Nouvian-Dooghe, V Sirri, P Roussel, D Hernandez-Verdun

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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
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  8. Article
  9. Review
  10. Article
  11. Article
  12. Nucleolus: the fascinating nuclear body.Histochemistry and cell biology · 2008
    Review
  13. Review
  14. Review
  15. Article
  16. Nucleolus: from structure to dynamics.Histochemistry and cell biology · 2006
    Review
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 3 institutions in 1 country.

T David-PfeutyUMR 146 du CNRS, Institut Curie-Recherche, Bâtiment 110, Centre Universitaire, 91405 Orsay Cédex, France. Thérèse.Pfeuty@curie.u-psud.fr
Y Nouvian-Dooghe
V Sirri
P Roussel
D Hernandez-Verdun
Institut Jacques Monod · FRCentre National de la Recherche Scientifique · FRInstitut Curie · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Two specific inhibitors of cyclin-dependent kinase 2 (Cdk2), roscovitine and olomoucine, have been shown recently to induce nuclear accumulation of wt p53 and nucleolar unravelling in interphase human untransformed IMR-90 and breast tumor-derived MCF-7 cells. Here, we show that the early response of MCF-7 cells to roscovitine is fully reversible since a rapid restoration of nucleolar organization followed by an induction of p21(WAF1/CIP1), a downregulation of nuclear wt p53 and normal cell cycle resumption occurs if the compound is removed after 4 h. Interestingly, similar reversible effects are also induced by the casein kinase II (CKII) inhibitor, 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole. Upon short-term treatment also, both compounds significantly, but reversibly, reduce the level of 45S precursor ribosomal RNA. Cells exposed to the two types of protein kinase inhibitors for longer times keep exhibiting altered nucleolar and wt p53 features, yet they strikingly differentiate in that most roscovitine-treated cells fail to ever accumulate high levels of p21(WAF1/CIP1) in contrast with DRB-treated ones. In both cases, however, the cells eventually fall into an irreversible state and die. Moreover, we found that constitutive overexpression of p21(WAF1/CIP1) alters the nucleolar unravelling process in the presence of DRB, but not of roscovitine, suggesting a role for this physiological Cdk inhibitor in the regulation of nucleolar function. Our data also support the notion that both roscovitine- and DRB-sensitive protein kinases, probably including Cdk2 and CKII, via their dual implication in the p53-Rb pathway and in ribosomal biogenesis, would participate in coupling cell growth with cell division.

Indexed as

CDC2-CDC28 KinasesCasein Kinase IICell CycleCell LineCell NucleolusCell NucleusCyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesCyclinsDichlororibofuranosylbenzimidazoleEnzyme InhibitorsGene Expression RegulationHumansMitomycinModels, BiologicalCasein Kinase IICDC2-CDC28 KinasesCDK2 protein, humanCDKN1A protein, humanCyclin-Dependent Kinase 2Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesCyclinsDichlororibofuranosylbenzimidazoleEnzyme InhibitorsMitomycinProtein Serine-Threonine KinasesPurinesRNA, RibosomalRNA, ribosomal, 45SRoscovitineTumor Suppressor Protein p53

Identifiers

PMID11593402
OpenAlexW2312795792

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.