Evidence map›Paper›PMID 9811866›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

AP-2-null cells disrupt morphogenesis of the eye, face, and limbs in chimeric mice.

T Nottoli, S Hagopian-Donaldson, J Zhang, A Perkins, T Williams

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

66 citing papers in PubMed, 181 citations in OpenAlex.

  1. Ventral body wall closure: Mechanistic insights from mouse models and translation to human pathology.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
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  9. CXCL12-CXCR4 Interplay Facilitates Palatal Osteogenesis in Mice.Frontiers in cell and developmental biology · 2020
    Article
  10. Protein kinase D up-regulates transcription ofThe Journal of biological chemistry · 2019
    Article
  11. A functional indel polymorphism rs34396413 in TFAP2A intron-5 significantly increases female encephalocele risk in Han Chinese population.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2019
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  20. Molecular mechanisms of midfacial developmental defects.Developmental dynamics : an official publication of the American Association of Anatomists · 2016
    Review

6 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.

T NottoliDepartment of Molecular, Cellular, and Developmental Biology, Yale University, 266 Whitney Avenue, New Haven, CT 06511, USA.
S Hagopian-Donaldson
J Zhang
A Perkins
T Williams
Yale University · USWhitney Museum of American Art · US

Funding

MOLECULAR MECHANISMS IN EVI1-INDUCED MYELOID LEUKEMIAR29CA067013 · NCI · YALE UNIVERSITY · PI PERKINS, ARCHIBALD S · 1996 to 2000
$67k
TRANSCRIPTION FACTOR REGULATION DURING DEVELOPMENTR01GM046770 · NIGMS · YALE UNIVERSITY · PI WILLIAMS, TREVOR J · 1992 to 1996
–
NCI NIH HHS CA67013NIGMS NIH HHS GM46770
6 · The paper itself

Abstract

The homozygous disruption of the mouse AP-2 gene yields a complex and lethal phenotype that results from defective development of the neural tube, head, and body wall. The severe and pleiotropic developmental abnormalities observed in the knockout mouse suggested that AP-2 may regulate several morphogenic pathways. To uncouple the individual developmental mechanisms that are dependent on AP-2, we have now analyzed chimeric mice composed of both wild-type and AP-2-null cells. The phenotypes obtained from these chimeras indicate that there is an independent requirement for AP-2 in the formation of the neural tube, body wall, and craniofacial skeleton. In addition, these studies reveal that AP-2 exerts a major influence on eye formation, which is a critical new role for AP-2 that was masked previously in the knockout mice. Furthermore, we also have uncovered an unexpected influence of AP-2 on limb pattern formation; this influence is typified by major limb duplications. The range of phenotypes observed in the chimeras displays a significant overlap with those caused by teratogenic levels of retinoic acid, strongly suggesting that AP-2 is an important component of the mechanism of action of this morphogen.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsChimeraDNA-Binding ProteinsEmbryonic and Fetal DevelopmentExtremitiesEyeFaceMiceMice, KnockoutMorphogenesisTranscription Factor AP-2Transcription FactorsDNA-Binding ProteinsTranscription Factor AP-2Transcription Factors

Identifiers

PMID9811866
PMCPMC24885
OpenAlexW2129904436

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.