Evidence map›Paper›PMID 31913463›Full record

ArticleEndocrinology2020

PROP1-Dependent Retinoic Acid Signaling Regulates Developmental Pituitary Morphogenesis and Hormone Expression.

Leonard Y M Cheung, Sally A Camper

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Glis3 as a critical regulator of Pit1-lineages and renal functions.Journal of molecular medicine (Berlin, Germany) · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Gene Misexpression in aJournal of the Endocrine Society · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. ImprintedeLife · 2023
    Article
  17. Article
  18. Review
  19. Cellular interactions in the pituitary stem cell niche.Cellular and molecular life sciences : CMLS · 2022
    Review
  20. 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

2 authors at 1 institution in 1 country.

Leonard Y M CheungDepartment of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan.
Sally A CamperDepartment of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan.
University of Michigan · US

Funding

CELL-SPECIFIC EXPRESSION IN THE PITUITARY GLANDR01HD034283 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CAMPER, SALLY A. · 1996 to 2021
$7.7M
A Panhypopituitary Mouse Mutation - Diversity SupplementR01HD030428 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CAMPER, SALLY A. · 1993 to 2016
$2.6M
Hypopituitarism: role of PROP1 and retinoic acid signaling in regulation of pituitary stem cell differentiationR01HD097096 · NICHD · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CAMPER, SALLY A. · 2019 to 2023
$2.2M
Rdh10 and retinoic acid effects on differentiationR01DK112754 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI NAPOLI, JOSEPH L · 2017 to 2021
$1.9M
NICHD NIH HHS R01 HD030428NICHD NIH HHS R01 HD034283NICHD NIH HHS R01 HD097096NIDDK NIH HHS R01 DK112754
6 · The paper itself

Abstract

Dietary vitamin A is metabolized into bioactive retinoic acid (RA) in vivo and regulates the development of many embryonic tissues. RA signaling is active in the oral ectoderm-derived tissues of the neuroendocrine system, but its role there has not yet been fully explored. We show here that RA signaling is active during pituitary organogenesis and dependent on the pituitary transcription factor Prop1. Prop1-mutant mice show reduced expression of the aldehyde dehydrogenase gene Aldh1a2, which metabolizes the vitamin A-intermediate retinaldehyde into RA. To elucidate the specific function of RA signaling during neuroendocrine development, we studied a conditional deletion of Aldh1a2 and a dominant-negative mouse model of inhibited RA signaling during pituitary organogenesis. These models partially phenocopy Prop1-mutant mice by exhibiting embryonic pituitary dysmorphology and reduced hormone expression, especially thyrotropin. These findings establish the role of RA in embryonic pituitary stem cell progression to differentiated hormone cells and raise the question of gene-by-environment interactions as contributors to pituitary development and disease.

Indexed as

Aldehyde Dehydrogenase 1 FamilyAnimalsHomeodomain ProteinsMice, Inbred C57BLOrganogenesisPituitary GlandRetinal DehydrogenaseSignal TransductionStem CellsThyrotropinTretinoinAldehyde Dehydrogenase 1 FamilyAldh1a2 protein, mouseHomeodomain ProteinsProphet of Pit-1 proteinRetinal DehydrogenaseThyrotropinTretinoinALDH1A2developmentpituitaryPROP1retinoic acid

Identifiers

PMID31913463
PMCPMC7029777
OpenAlexW3000044727

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.