Evidence map›Paper›PMID 24673559›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2014

Notch signaling in postnatal pituitary expansion: proliferation, progenitors, and cell specification.

Leah B Nantie, Ashley D Himes, Dan R Getz, Lori T Raetzman

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Association Study BetweenInternational journal of molecular sciences · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Cellular interactions in the pituitary stem cell niche.Cellular and molecular life sciences : CMLS · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Methylation status of hypothalamicFrontiers in endocrinology · 2022
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Leah B NantieDepartment of Molecular and Integrative Physiology (L.B.N., A.D.H., D.R.G., L.T.R.) and Neuroscience Program (L.T.R.), University of Illinois at Urbana-Champaign, Urbana, Illinois 61801.
Ashley D Himes
Dan R Getz
Lori T Raetzman
University of Illinois Urbana-Champaign · US

Funding

Cellular and Molecular Biology Training GrantT32GM007283 · NIGMS · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI MORRISSEY, JAMES H. · 1985 to 2011
$4.7M
Notch Signaling Regulates Pituitary OrganogenesisR01DK076647 · NIDDK · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI RAETZMAN, LORI T · 2007 to 2016
$2.7M
NIDDK NIH HHS R01 DK076647NIGMS NIH HHS T32 GM007283
6 · The paper itself

Abstract

Mutations in PROP1 account for up to half of the cases of combined pituitary hormone deficiency that result from known causes. Despite this, few signaling molecules and pathways that influence PROP1 expression have been identified. Notch signaling has been linked to Prop1 expression, but the developmental periods during which Notch signaling influences Prop1 and overall pituitary development remain unclear. To test the requirement for Notch signaling in establishing the normal pituitary hormone milieu, we generated mice with early embryonic conditional loss of Notch2 (conditional knockout) and examined the consequences of chemical Notch inhibition during early postnatal pituitary maturation. We show that loss of Notch2 has little influence on early embryonic pituitary proliferation but is crucial for postnatal progenitor maintenance and proliferation. In addition, we show that Notch signaling is necessary embryonically and postnatally for Prop1 expression and robust Pit1 lineage hormone cell expansion, as well as repression of the corticotrope lineage. Taken together, our studies identify temporal and cell type-specific roles for Notch signaling and highlight the importance of this pathway throughout pituitary development.

Indexed as

Cell ProliferationAnimalsCell DifferentiationCorticotrophsEmbryonic Stem CellsGene ExpressionGrowth HormoneMice, 129 StrainMice, KnockoutPituitary GlandPro-OpiomelanocortinReceptor, Notch2Signal TransductionThyrotropin, beta SubunitTissue Culture TechniquesTranscription Factor Pit-1Growth HormoneNotch2 protein, mousePou1f1 protein, mousePro-OpiomelanocortinReceptor, Notch2Thyrotropin, beta SubunitTranscription Factor Pit-1

Identifiers

PMID24673559
PMCPMC4004773
OpenAlexW2166781998

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.