Evidence map›Paper›PMID 24821725›Full record

ArticleThe Journal of biological chemistry2014

Retinoic acid and histone deacetylases regulate epigenetic changes in embryonic stem cells.

Alison M Urvalek, Lorraine J Gudas

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 88 citations in OpenAlex.

  1. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
    Review
  2. All-trans retinoic acid suppresses CD8Signal transduction and targeted therapy · 2026
    Article
  3. Article
  4. Review
  5. Article
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  8. Review
  9. Article
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  16. Article
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  19. Retinoid metabolism: new insights.Journal of molecular endocrinology · 2022
    Review
  20. Transcriptional Repression of Aerobic Glycolysis by OVOL2 in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    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

2 authors at 1 institution in 1 country.

Alison M UrvalekFrom the Department of Pharmacology and the Meyer Cancer Center, Weill Cornell Medical College of Cornell University, New York, New York 10065.
Lorraine J GudasFrom the Department of Pharmacology and the Meyer Cancer Center, Weill Cornell Medical College of Cornell University, New York, New York 10065 ljgudas@med.cornell.edu.
Cornell University · US

Funding

CANCER PHARMACOLOGYT32CA062948 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI LORRAINE J GUDAS · 1994 to 2026
$12.1M
Retinoic Acid Binding Proteins: Functional StudiesR01CA043796 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GUDAS, LORRAINE J · 1987 to 2013
$5.0M
Diet and Alcohol Induced Epigenetic Changes in Oral Cavity Carcinogenesis ModelR01AA018332 · NIAAA · WEILL MEDICAL COLL OF CORNELL UNIV · PI GUDAS, LORRAINE J · 2010 to 2014
$2.1M
Molecular Analysis of Alcohol Effects on Human Oral Epithelium Cells' EpigenomeF32AA021045 · NIAAA · WEILL MEDICAL COLL OF CORNELL UNIV · PI URVALEK, ALISON · 2011 to 2013
$101k
NCI NIH HHS R01 CA043796NCI NIH HHS R01CA43778NCI NIH HHS T32 CA062948NCI NIH HHS T32CA062948NIAAA NIH HHS F32 AA021045NIAAA NIH HHS F32-AA021045NIAAA NIH HHS R01 AA018332
6 · The paper itself

Abstract

All-trans-retinoic acid (RA) is a vitamin A metabolite that plays major roles in regulating stem cell differentiation and development. RA is the ligand of the retinoic acid receptor (RAR) family of transcription factors, which interact with retinoic acid response elements (RAREs) within target gene proximal promoters and enhancers. Although RA-mediated gene activation is well understood, less is known about the mechanisms for repression at RA-regulated genes. Using chromatin immunoprecipitation experiments, we show that in embryonic stem cells in the absence of RA, histone deacetylases (HDACs) differentially bind to various RAREs in proximal promoters or enhancer regions of RA-regulated genes; HDAC1, HDAC2, and HDAC3 bind at RAREs in the Hoxa1 and Cyp26a1 gene regulatory regions, whereas only HDAC1 binds at the RARβ2 RARE. shRNA knockdown of HDAC1, HDAC2, or HDAC3 differentially increases the deposition of the histone 3 lysine 27 acetylation (H3K27ac) epigenetic mark associated with increases in these three transcripts. Importantly, RA treatment differentially mediates the removal of HDACs from the Hoxa1, Cyp26a1, and RARβ2 genes and promotes the deposition of the H3K27ac mark at these genes. Overall, we show that HDACs differentially bind to RA-regulated genes to control key epigenetic marks involved in stem cell differentiation.

Indexed as

AnimalsAntineoplastic AgentsCell DifferentiationCytochrome P-450 Enzyme SystemEmbryonic Stem CellsEpigenesis, GeneticHEK293 CellsHistone DeacetylasesHistonesHomeobox A1 ProteinHomeodomain ProteinsHumansMiceReceptors, Retinoic AcidResponse ElementsRetinoic Acid 4-HydroxylaseAntineoplastic AgentsCyp26a1 protein, mouseCytochrome P-450 Enzyme SystemHistone DeacetylasesHistonesHomeobox A1 ProteinHomeodomain ProteinsReceptors, Retinoic AcidRetinoic Acid 4-Hydroxylaseretinoic acid receptor betaTranscription FactorsTretinoinEpigeneticsHistone Deacetylase (HDAC)Retinoic AcidRetinoidSproutyStem CellsTranscriptionWnt3a

Identifiers

PMID24821725
PMCPMC4094062
OpenAlexW2008469210

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.