Evidence map›Paper›PMID 15870295›Full record

ArticleMolecular and cellular biology2005

Hes1 directly controls cell proliferation through the transcriptional repression of p27Kip1.

Kaoru Murata, Masakazu Hattori, Norihito Hirai, Yoriko Shinozuka, Hiromi Hirata, Ryoichiro Kageyama, Toshiyuki Sakai, Nagahiro Minato

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

107 citing papers in PubMed, 201 citations in OpenAlex.

  1. Article
  2. Article
  3. HES1 oscillations are required for cell cycle reentry in oestrogen receptor-positive breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. HES1 is required for mouse fetal hematopoiesis.Stem cell research & therapy · 2024
    Article
  10. Article
  11. Dachshund Homolog 1: Unveiling Its Potential Role in Megakaryopoiesis andInternational journal of molecular sciences · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. An X-linkedTranslational pediatrics · 2022
    Article
  20. Article

47 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

8 authors at 2 institutions in 1 country.

Kaoru MurataDepartment of Immunology and Cell Biology, Graduate School of Biostudies, Kyoto University, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Masakazu Hattori
Norihito Hirai
Yoriko Shinozuka
Hiromi Hirata
Ryoichiro Kageyama
Toshiyuki Sakai
Nagahiro Minato
Kyoto University · JPKyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A transcriptional regulator, Hes1, plays crucial roles in the control of differentiation and proliferation of neuronal, endocrine, and T-lymphocyte progenitors during development. Mechanisms for the regulation of cell proliferation by Hes1, however, remain to be verified. In embryonic carcinoma cells, endogenous Hes1 expression was repressed by retinoic acid in concord with enhanced p27(Kip1) expression and cell cycle arrest. Conversely, conditional expression of a moderate but not maximal level of Hes1 in HeLa cells by a tetracycline-inducible system resulted in reduced p27(Kip1) expression, which was attributed to decreased basal transcript rather than enhanced proteasomal degradation, with concomitant increases in the growth rate and saturation density. Hes1 induction repressed the promoter activity of a 5' flanking basal enhancer region of p27(Kip1) gene in a manner dependent on Hes1 expression levels, and this was mediated by its binding to class C sites in the promoter region. Finally, hypoplastic fetal thymi, as well as livers and brains of Hes1-deficient mice, showed significantly increased p27(Kip1) transcripts compared with those of control littermates. These results have suggested that Hes1 directly contributes to the promotion of progenitor cell proliferation through transcriptional repression of a cyclin-dependent kinase inhibitor, p27(Kip1).

Indexed as

Down-Regulation5' Flanking RegionAnimalsBasic Helix-Loop-Helix ProteinsCell CountCell Cycle ProteinsCell DifferentiationCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p27Embryo, MammalianHeLa CellsHomeodomain ProteinsHumansMicePromoter Regions, GeneticBasic Helix-Loop-Helix ProteinsCdkn1b protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p27Hes1 protein, mouseHomeodomain ProteinsProteasome Endopeptidase ComplexRepressor ProteinsTranscription Factor HES-1TretinoinTumor Suppressor Proteins

Identifiers

PMID15870295
PMCPMC1087711
OpenAlexW2144458244

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.