Evidence map›Paper›PMID 19874812›Full record

ArticleDevelopmental biology2010

Dhrs3a regulates retinoic acid biosynthesis through a feedback inhibition mechanism.

L Feng, R E Hernandez, J S Waxman, D Yelon, C B Moens

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing 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

82 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
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  5. Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025
    Review
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  15. Review
  16. Retinoic acid, RARs and early development.Journal of molecular endocrinology · 2022
    Article
  17. Article
  18. Retinoid metabolism: new insights.Journal of molecular endocrinology · 2022
    Review
  19. Review
  20. Article

22 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

5 authors at 2 institutions in 1 country.

L FengDivision of Basic Science and HHMI, Fred Hutchinson Cancer Research Center, B2-152, 1100 Fairview Ave. N, Seattle, WA 98109, USA.
R E Hernandez
J S Waxman
D Yelon
C B Moens
University of Washington · USNew York University · US

Funding

INTERDISCIPLINARY TRAINING IN DEVELOPMENTAL BIOLOGYT32HD007183 · NICHD · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2015
$5.7M
Genetic Regulation of Cardiac Patterning in ZebrafishR01HL069594 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI YELON, DEBORAH · 2002 to 2015
$4.0M
GENETIC MECHANISMS OF HINDBRAIN SEGMENTATIONR01HD037909 · NICHD · FRED HUTCHINSON CANCER RESEARCH CENTER · PI MOENS, CECILIA B · 1999 to 2009
$2.4M
Elucidation of molecular networks required to limit cardiac cell numberR00HL091126 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WAXMAN, JOSHUA · 2010 to 2012
$747k
Elucidation of molecular networks required to limit cardiac cell numberK99HL091126 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WAXMAN, JOSHUA · 2008 to 2009
$173k
Retinoic Acid Signaling and Cardiac Cell DifferentiationF32HL083591 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WAXMAN, JOSHUA · 2006 to 2007
$95k
Howard Hughes Medical InstituteNHLBI NIH HHS F32 HL083591NHLBI NIH HHS F32HL083591NHLBI NIH HHS K99 HL091126NHLBI NIH HHS K99HL091126NHLBI NIH HHS R00 HL091126NHLBI NIH HHS R01 HL069594NICHD NIH HHS HD37909NICHD NIH HHS R01 HD037909NICHD NIH HHS T32 HD007183
6 · The paper itself

Abstract

Retinoic acid (RA) is an important developmental signaling molecule responsible for the patterning of multiple vertebrate tissues. RA is also a potent teratogen, causing multi-organ birth defects in humans. Endogenous RA levels must therefore be tightly controlled in the developing embryo. We used a microarray approach to identify genes that function as negative feedback regulators of retinoic acid signaling. We screened for genes expressed in early somite-stage embryos that respond oppositely to treatment with RA versus RA antagonists and validated them by RNA in situ hybridization. Focusing on genes known to be involved in RA metabolism, we determined that dhrs3a, which encodes a member of the short-chain dehydrogenase/reductase protein family, is both RA dependent and strongly RA inducible. Dhrs3a is known to catalyze the reduction of the RA precursor all-trans retinaldehyde to vitamin A; however, a developmental function has not been demonstrated. Using morpholino knockdown and mRNA over-expression, we demonstrate that Dhrs3a is required to limit RA levels in the embryo, primarily within the central nervous system. Dhrs3a is thus an RA-induced feedback inhibitor of RA biosynthesis. We conclude that retinaldehyde availability is an important level at which RA biosynthesis is regulated in vertebrate embryos.

Indexed as

Feedback, PhysiologicalAlcohol OxidoreductasesAnimalsBody PatterningEmbryo, NonmammalianGene Expression Regulation, DevelopmentalGene Knockdown TechniquesNervous SystemNeuronsOligonucleotide Array Sequence AnalysisReproducibility of ResultsRetinal DehydrogenaseRNASignal TransductionTretinoinZebrafish ProteinsAlcohol OxidoreductasesDhrs3a protein, zebrafishRetinal DehydrogenaseRNATretinoinZebrafish Proteins

Identifiers

PMID19874812
PMCPMC2858591
OpenAlexW2021584737

What OpenQuestion holds

Textmetadata
LicenceTDM
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.