Evidence map›Paper›PMID 20231276›Full record

ArticleThe Journal of biological chemistry2010

Epigenetic regulatory mechanisms distinguish retinoic acid-mediated transcriptional responses in stem cells and fibroblasts.

Vasundhra Kashyap, Lorraine J Gudas

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2010. 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
2.8field-weighted citation impact, top 9% 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, 82 citations in OpenAlex.

  1. Review
  2. Article
  3. Retinoic acid receptor assembly dynamics governs dual functions in cochlear organogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  19. Corepressor SMRT is required to maintain Hox transcriptional memory during somitogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  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

2 authors at 1 institution in 1 country.

Vasundhra KashyapDepartment of Pharmacology, Weill Cornell Medical College of Cornell University, New York, New York 10065, USA.
Lorraine J Gudas
Cornell University · 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 CA043796NCI NIH HHS R01CA043796
6 · The paper itself

Abstract

Retinoic acid (RA), a vitamin A metabolite, regulates transcription by binding to RA receptor (RAR) and retinoid X receptor (RXR) heterodimers. This transcriptional response is determined by receptor interactions with transcriptional regulators and chromatin modifying proteins. We compared transcriptional responses of three RA target genes (Hoxa1, Cyp26a1, RARbeta(2)) in primary embryo fibroblasts (mouse embryonic fibroblasts), immortalized fibroblasts (Balb/c3T3), and F9 teratocarcinoma stem cells. Hoxa1 and Cyp26a1 transcripts are not expressed, but RARbeta(2) transcripts are induced by RA in mouse embryonic fibroblasts and Balb/c3T3 cells. Retinoid receptors (RARgamma, RXRalpha), coactivators (pCIP (NCOA3, SRC3)), and p300 and RNA polymerase II are recruited only to the RARbeta(2) RA response element (RARE) in Balb/c3T3, whereas these proteins are recruited to RAREs of all three genes by RA in F9 cells. In F9, RA reduces polycomb (PcG) protein Suz12 and the associated H3K27me3 repressive epigenetic modification at the RAREs of all three genes. In contrast, in Balb/c3T3 cells cultured in the +/-RA, Suz12 is not associated with the Hoxa1, RARbeta(2), and Cyp26a1 RAREs, whereas slow levels of the H3K27me3 mark are seen at these RAREs. Thus, Suz12 is not required for gene repression in the absence of RA. Even though the Hoxa1 RARE and proximal promoter show high levels of H3K9,K14 acetylation in Balb/c3T3, the Hoxa1 gene is not transcriptionally activated by RA. In Balb/c3T3, CpG islands are methylated in the Cyp26a1 promoter region but not in the Hoxa1 promoter or in these promoters in F9 cells. We have delineated the complex mechanisms that control RA-mediated transcription in fibroblasts versus stem cells.

Indexed as

Epigenesis, GeneticGene Expression RegulationAnimalsBALB 3T3 CellsBlotting, WesternCells, CulturedChromatin ImmunoprecipitationCytochrome P-450 Enzyme SystemDNA MethylationE1A-Associated p300 ProteinElectrophoretic Mobility Shift AssayEmbryo, MammalianEmbryonal Carcinoma Stem CellsFibroblastsHistonesHomeobox A1 ProteinCyp26a1 protein, mouseCytochrome P-450 Enzyme SystemE1A-Associated p300 ProteinEp300 protein, mouseHistonesHomeobox A1 ProteinHomeodomain ProteinsReceptors, Retinoic AcidRetinoic Acid 4-Hydroxylaseretinoic acid receptor betaRNA, MessengerRNA Polymerase IITranscription FactorsTretinoin

Identifiers

PMID20231276
PMCPMC2863236
OpenAlexW1993296289

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.