Evidence map›Paper›PMID 11463824›Full record

ArticleMolecular and cellular biology2001

Histone H1 phosphorylation by Cdk2 selectively modulates mouse mammary tumor virus transcription through chromatin remodeling.

R N Bhattacharjee, G C Banks, K W Trotter, H L Lee, T K Archer

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

51 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Phenotypical microRNA screen reveals a noncanonical role of CDK2 in regulating neutrophil migration.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  8. Article
  9. Article
  10. Hierarchical looping of zigzag nucleosome chains in metaphase chromosomes.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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 2 institutions in 2 countries.

R N BhattacharjeeDepartment of Obstetrics and Gynaecology, The University of Western Ontario, London, Ontario N6A 4L6, Canada.
G C Banks
K W Trotter
H L Lee
T K Archer
National Institute of Environmental Health Sciences · USWestern University · CA

Funding

Transcriptional Functions of Nuclear Receptors in Cancer CellsZIAES071006 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ARCHER, TREVOR KEITH · 2009 to 2025
$58.0M
Transcriptional Functions of Nuclear Receptors in Cancer CellsZ01ES071006 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ARCHER, TREVOR KEITH · 1999 to 2008
$6.9M
6 · The paper itself

Abstract

Transcriptional activation of the mouse mammary tumor virus (MMTV) promoter by ligand-bound glucocorticoid receptor (GR) is transient. Previously, we demonstrated that prolonged hormone exposure results in displacement of the transcription factor nuclear factor 1 (NF1) and the basal transcription complex from the promoter, the dephosphorylation of histone H1, and the establishment of a repressive chromatin structure. We have explored the mechanistic link between histone H1 dephosphorylation and silencing of the MMTV promoter by describing the putative kinase responsible for H1 phosphorylation. Both in vitro kinase assays and in vivo protein expression studies suggest that in hormone-treated cells the ability of cdk2 to phosphorylate histone H1 is decreased and the cdk2 inhibitory p21 protein level is increased. To address the role of cdk2 and histone H1 dephosphorylation in the silencing of the MMTV promoter, we used potent cdk2 inhibitors, Roscovitine and CVT-313, to generate an MMTV promoter which is associated predominantly with the dephosphorylated form of histone H1. Both Roscovitine and CVT-313 block phosphorylation of histone H1 and, under these conditions, the GR is unable to remodel chromatin, recruit transcription factors to the promoter, or stimulate MMTV mRNA accumulation. These results suggest a model where cdk2-directed histone H1 phosphorylation is a necessary condition to permit GR-mediated chromatin remodeling and activation of the MMTV promoter in vivo.

Indexed as

CDC2-CDC28 KinasesAnimalsChromatinCyclin-Dependent Kinase 2Cyclin-Dependent KinasesHistonesMammary Tumor Virus, MouseMicePhosphorylationPromoter Regions, GeneticProtein Serine-Threonine KinasesTranscription, GeneticVirus ReplicationCDC2-CDC28 KinasesCdk2 protein, mouseChromatinCyclin-Dependent Kinase 2Cyclin-Dependent KinasesHistonesProtein Serine-Threonine Kinases

Identifiers

PMID11463824
PMCPMC87264
OpenAlexW2129782312

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.