Evidence map›Paper›PMID 12165850›Full record

ArticleOncogene2002

Differential contributions of ERK and PI3-kinase to the regulation of cyclin D1 expression and to the control of the G1/S transition in mouse embryonic stem cells.

Ludmila Jirmanova, Marielle Afanassieff, Stéphanie Gobert-Gosse, Suzy Markossian, Pierre Savatier

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 207 citations in OpenAlex.

  1. Article
  2. Article
  3. Chicken Primordial Germ Cells Do Not Proliferate in Insulin-Lacking Media.International journal of molecular sciences · 2025
    Article
  4. Review
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  6. Article
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  8. Article
  9. Article
  10. Frontiers in molecular neuroscience · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Mechanisms of pluripotency maintenance in mouse embryonic stem cells.Cellular and molecular life sciences : CMLS · 2017
    Review
  18. Article
  19. Erk signaling is indispensable for genomic stability and self-renewal of mouse embryonic stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  20. Article

15 more citing papers are in PubMed but not listed here.

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.

Ludmila JirmanovaLaboratoire de Biologie Moléculaire et Cellulaire, CNRS UMR 5665, INRA LA913, Ecole Normale Supérieure de Lyon, 46 allée d'Italie, 69364 Lyon Cedex 07, France.
Marielle Afanassieff
Stéphanie Gobert-Gosse
Suzy Markossian
Pierre Savatier
Centre National de la Recherche Scientifique · FRÉcole Normale Supérieure de Lyon · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mouse embryonic stem (ES) cells are known to express D-type cyclins at very low levels and these levels increase dramatically during in vitro and in vivo differentiation. Here, we investigate some of the signalling pathways regulating expression of cyclin D1 and progression to S phase, the Ras/Extracellular signal-regulated protein kinase (ERK) pathway and the phosphatidylinositol 3-kinase (PI3-kinase) pathway. We demonstrate that ERK phosphorylation is fully dispensable for the regulation of cyclin D1 level and for the progression from G1 to S phase in ES cells. By contrast, PI3-kinase activity is required for both. Differentiation induced by retinoic acid results in the gain of ERK-dependent control of cyclin D1 expression and of S phase progression. Differentiation is also paralleled by an increase in PI3-kinase activity. This leads (a) to an increase in the p70 S6 kinase-dependent regulation of the steady-state level of cyclin D1, and (b) to a concomitant decrease in the GSK3beta-dependent rate of cyclin D1 degradation. Altogether, these multiple pathways account for the dramatic increase in the level of cyclin D1 protein which parallels ES cell differentiation. Our studies suggest that PI3-kinase is an important regulator of the ES cell cycle and that its activity is not regulated by mitogen stimulation.

Indexed as

AnimalsAntineoplastic AgentsBlotting, NorthernBlotting, WesternCalcium-Calmodulin-Dependent Protein KinasesCell DifferentiationCyclin D1Embryo, MammalianEnzyme InhibitorsG1 PhaseGene Expression RegulationGlycogen Synthase Kinase 3Immunosuppressive AgentsMiceMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesAntineoplastic AgentsCalcium-Calmodulin-Dependent Protein KinasesCyclin D1Enzyme InhibitorsGlycogen Synthase Kinase 3Immunosuppressive AgentsMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesRNA, MessengerSirolimusTretinoin

Identifiers

PMID12165850
OpenAlexW2099724117

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.