Evidence map›Paper›PMID 23264745›Full record

ArticleJournal of cell science2013

RARγ is essential for retinoic acid induced chromatin remodeling and transcriptional activation in embryonic stem cells.

Vasundhra Kashyap, Kristian B Laursen, Fabienne Brenet, Agnes J Viale, Joseph M Scandura, Lorraine J Gudas

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed, 65 citations in OpenAlex.

  1. Triorganotin compounds as emerging nuclear retinoid X receptor ligands and their implications in cancer.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  2. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Review
  5. The Influences of RARγ on the Behavior of Normal and Cancer Stem Cells.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Deregulation of All-International journal of molecular sciences · 2023
    Review
  15. Review
  16. Targeting the Retinoic Acid Pathway to Eradicate Cancer Stem Cells.International journal of molecular sciences · 2023
    Review
  17. Review
  18. Antagonizing RARγ Drives Necroptosis of Cancer Stem Cells.International journal of molecular sciences · 2022
    Review
  19. Review
  20. The RARγ Oncogene: An Achilles Heel for Some Cancers.International journal of molecular sciences · 2021
    Review
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

6 authors at 2 institutions in 1 country.

Vasundhra KashyapDepartment of Pharmacology, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10065, USA.
Kristian B Laursen
Fabienne Brenet
Agnes J Viale
Joseph M Scandura
Lorraine J Gudas
Cornell University · USMemorial Sloan Kettering Cancer Center · US

Funding

Retinoic Acid Binding Proteins: Functional StudiesR01CA043796 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GUDAS, LORRAINE J · 1987 to 2013
$5.0M
NCI NIH HHS R01 CA043796
6 · The paper itself

Abstract

We have utilized retinoic acid receptor γ (gamma) knockout (RARγ(-/-)) embryonic stem (ES) cells as a model system to analyze RARγ mediated transcriptional regulation of stem cell differentiation. Most of the transcripts regulated by all-trans retinoic acid (RA) in ES cells are dependent upon functional RARγ signaling. Notably, many of these RA-RARγ target genes are implicated in retinoid uptake and metabolism. For instance, Lrat (lecithin:retinol acyltransferase), Stra6 (stimulated by retinoic acid 6), Crabp2 (cellular retinoic acid binding protein 2), and Cyp26a1 (cytochrome p450 26a1) transcripts are induced in wild type (WT), but not in RARγ(-/-) cells. Transcripts for the transcription factors Pbx1 (pre-B cell leukemia homeobox-1), Wt1 (Wilm's tumor gene-1), and Meis1 (myeloid ecotropic viral integration site-1) increase upon RA treatment of WT, but not RARγ(-/-) cells. In contrast, Stra8, Dleu7, Leftb, Pitx2, and Cdx1 mRNAs are induced by RA even in the absence of RARγ. Mapping of the epigenetic signature of Meis1 revealed that RA induces a rapid increase in the H3K9/K14ac epigenetic mark at the proximal promoter and at two sites downstream of the transcription start site in WT, but not in RARγ(-/-) cells. Thus, RA-associated increases in H3K9/K14ac epigenetic marks require RARγ and are associated with increased Meis1 transcript levels, whereas H3K4me3 is present at the Meis1 proximal promoter even in the absence of RARγ. In contrast, at the Lrat proximal promoter primarily the H3K4me3 mark, and not the H3K9/K14ac mark, increases in response to RA, independently of the presence of RARγ. Our data show major epigenetic changes associated with addition of the RARγ agonist RA in ES cells.

Indexed as

Cells, CulturedChromatin Assembly and DisassemblyEmbryonic Stem CellsHumansReceptors, Retinoic AcidRetinoic Acid Receptor gammaTranscriptional ActivationTretinoinReceptors, Retinoic AcidRetinoic Acid Receptor gammaTretinoin

Identifiers

PMID23264745
PMCPMC3625813
OpenAlexW2128451913

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.