Evidence map›Paper›PMID 23874519›Full record

ArticlePloS one2013

In vivo function and evolution of the eutherian-specific pluripotency marker UTF1.

Masazumi Nishimoto, Miyuki Katano, Toshiyuki Yamagishi, Tomoaki Hishida, Masayoshi Kamon, Ayumu Suzuki, Masataka Hirasaki, Yoko Nabeshima, Yo-ichi Nabeshima, Yukako Katsura and 10 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.7field-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

12 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. HNF1α controls glucagon secretion in pancreatic α-cells through modulation of SGLT1.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. From blastocyst to gastrula: gene regulatory networks of embryonic stem cells and early mouse embryogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  11. Review
  12. 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

20 authors at 9 institutions in 2 countries.

Masazumi NishimotoRadioisotope Experimental Laboratory, Research Center for Genomic Medicine, Saitama Medical University, Yamane Hidaka, Saitama, Japan. masamasa@saitama-med.ac.jp
Miyuki Katano
Toshiyuki Yamagishi
Tomoaki Hishida
Masayoshi Kamon
Ayumu Suzuki
Masataka Hirasaki
Yoko Nabeshima
Yo-ichi Nabeshima
Yukako Katsura
Yoko Satta
Janine E Deakin
Jennifer A Marshall Graves
Yoko Kuroki
Ryuichi Ono
Fumitoshi Ishino
Masatsugu Ema
Satoru Takahashi
Hidemasa Kato
Akihiko Okuda
Saitama Medical University · JPAustralian National University · AUFoundation for Biomedical Research and Innovation · JPThe Graduate University for Advanced Studies, SOKENDAI · JPTokyo Medical and Dental University · JPUniversity of Tsukuba · JPJapan Science and Technology Agency · JPOsaka City University · JPRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Embryogenesis in placental mammals is sustained by exquisite interplay between the embryo proper and placenta. UTF1 is a developmentally regulated gene expressed in both cell lineages. Here, we analyzed the consequence of loss of the UTF1 gene during mouse development. We found that homozygous UTF1 mutant newborn mice were significantly smaller than wild-type or heterozygous mutant mice, suggesting that placental insufficiency caused by the loss of UTF1 expression in extra-embryonic ectodermal cells at least in part contributed to this phenotype. We also found that the effects of loss of UTF1 expression in embryonic stem cells on their pluripotency were very subtle. Genome structure and sequence comparisons revealed that the UTF1 gene exists only in placental mammals. Our analyses of a family of genes with homology to UTF1 revealed a possible mechanism by which placental mammals have evolved the UTF1 genes.

Indexed as

Amino Acid SequenceAnimalsChromosomal Proteins, Non-HistoneEmbryonic DevelopmentEmbryonic Stem CellsEvolution, MolecularFemaleGene Knockout TechniquesGene TargetingGenotypeMiceMolecular Sequence DataMutationPhenotypePhylogenyPlacentaChromosomal Proteins, Non-HistoneTrans-ActivatorsUtf1 protein, mouse

Identifiers

PMID23874519
PMCPMC3706607
OpenAlexW2041621429

What OpenQuestion holds

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LicenceCC BY
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.