Evidence map›Paper›PMID 24554762›Full record

ArticleMolecular biology of the cell2014

Transcription of the Geminin gene is regulated by a negative-feedback loop.

Yoshinori Ohno, Keita Saeki, Shin'ichiro Yasunaga, Toshiaki Kurogi, Kyoko Suzuki-Takedachi, Manabu Shirai, Keichiro Mihara, Kenichi Yoshida, J Willem Voncken, Motoaki Ohtsubo and 1 more

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.1field-weighted citation impact, top 45% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Changes inAnimals : an open access journal from MDPI · 2021
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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

11 authors at 4 institutions in 2 countries.

Yoshinori OhnoDepartment of Stem Cell Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3, Kasumi, Minami-ku, Hiroshima 734-8553, Japan Department of Hematology and Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3, Kasumi, Minami-ku, Hiroshima 734-8553, Japan Department of Bioscience and Genetics, National Cerebral and Cardiovascular Center Research Institute, Suita 562-0025, Japan Department of Life Sciences, Meiji University School of Agriculture, Kawasaki 214-8571, Japan Department of Molecular Genetics, Maastricht University Medical Centre, 6229ER Maastricht, Netherlands Department of Food and Fermentation Science, Faculty of Food Science and Nutrition, Beppu University, Beppu 874-0915, Japan.
Keita Saeki
Shin'ichiro Yasunaga
Toshiaki Kurogi
Kyoko Suzuki-Takedachi
Manabu Shirai
Keichiro Mihara
Kenichi Yoshida
J Willem Voncken
Motoaki Ohtsubo
Yoshihiro Takihara
Hiroshima University · JPMaastricht University Medical Centre · NLMeiji University · JPNational Cerebral and Cardiovascular Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Geminin performs a central function in regulating cellular proliferation and differentiation in development and also in stem cells. Of interest, down-regulation of Geminin induces gene transcription regulated by E2F, indicating that Geminin is involved in regulation of E2F-mediated transcriptional activity. Because transcription of the Geminin gene is reportedly regulated via an E2F-responsive region (E2F-R) located in the first intron, we first used a reporter vector to examine the effect of Geminin on E2F-mediated transcriptional regulation. We found that Geminin transfection suppressed E2F1- and E2F2-mediated transcriptional activation and also mildly suppressed such activity in synergy with E2F5, 6, and 7, suggesting that Geminin constitutes a negative-feedback loop for the Geminin promoter. Of interest, Geminin also suppressed nuclease accessibility, acetylation of histone H3, and trimethylation of histone H3 at lysine 4, which were induced by E2F1 overexpression, and enhanced tri-methylation of histone H3 at lysine 27 and monoubiquitination of histone H2A at lysine 119 in E2F-R. However, Geminin5EQ, which does not interact with Brahma or Brg1, did not suppress accessibility to nuclease digestion or transcription but had an overall dominant-negative effect. These findings suggest that E2F-mediated activation of Geminin transcription is negatively regulated by Geminin through the inhibition of chromatin remodeling.

Indexed as

Feedback, Physiological3T3 CellsAcetylationAnimalsAntibodiesCell CycleCell DifferentiationCell LineCell ProliferationChromatin Assembly and DisassemblyDNA-Binding ProteinsDNA HelicasesE2F Transcription FactorsGemininGene Expression RegulationHEK293 CellsAntibodiesDNA-Binding ProteinsDNA HelicasesE2F Transcription FactorsGemininHistonesNuclear ProteinsRNA, Small InterferingSMARCA4 protein, humanTranscription Factors

Identifiers

PMID24554762
PMCPMC3983001
OpenAlexW2142960225

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.