Evidence map›Paper›PMID 25165462›Full record

ArticleFrontiers in endocrinology2014

Gene Expression Profiling in Mouse Embryonic Stem Cells Reveals Glycogen Synthase Kinase-3-Dependent Targets of Phosphatidylinositol 3-Kinase and Wnt/β-Catenin Signaling Pathways.

Colleen M Bartman, Jennifer Egelston, Sravya Kattula, Leigh C Zeidner, Anthony D'Ippolito, Bradley W Doble, Christopher J Phiel

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. High-Throughput Screening Data Interpretation in the Context of In Vivo Transcriptomic Responses to Oral Cr(VI) Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    Article
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  5. Combination of 5-fluorouracil and 2-morphilino-8-phenyl-4H-chromen-4-one may inhibit liver cancer stem cell activity.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  6. Article
  7. 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

7 authors at 3 institutions in 2 countries.

Colleen M BartmanDepartment of Integrative Biology, University of Colorado Denver , Denver, CO , USA.
Jennifer EgelstonDepartment of Integrative Biology, University of Colorado Denver , Denver, CO , USA.
Sravya KattulaDepartment of Integrative Biology, University of Colorado Denver , Denver, CO , USA.
Leigh C ZeidnerCenter for Human and Molecular Genetics, Research Institute at Nationwide Children's Hospital , Columbus, OH , USA.
Anthony D'IppolitoCenter for Human and Molecular Genetics, Research Institute at Nationwide Children's Hospital , Columbus, OH , USA.
Bradley W DobleStem Cell and Cancer Research Institute, Department of Biochemistry and Biomedical Sciences, McMaster University , Hamilton, ON , Canada.
Christopher J PhielDepartment of Integrative Biology, University of Colorado Denver , Denver, CO , USA.
University of Denver · USNationwide Children's Hospital · USMcMaster University · CA

Funding

Effects of Conditional GSK3 Knockout on the Pathogenesis of Alzheimers DiseaseR01AG031883 · NIA · UNIVERSITY OF COLORADO DENVER · PI PHIEL, CHRISTOPHER J · 2008 to 2012
$1.4M
NIA NIH HHS R01 AG031883
6 · The paper itself

Abstract

Glycogen synthase kinase-3 (Gsk-3) activity is an important regulator of numerous signal transduction pathways. Gsk-3 activity is the sum of two largely redundant proteins, Gsk-3α and Gsk-3β, and in general, Gsk-3 is a negative regulator of cellular signaling. Genetic deletion of both Gsk-3α and Gsk-3β in mouse embryonic stem cells (ESCs) has previously been shown to lead to the constitutive activation of the Wnt/β-catenin signaling pathway. However, in addition to Wnt signaling, all Gsk-3-regulated pathways, such as insulin signaling, are also affected simultaneously in Gsk-3α(-) (/) (-); Gsk-3β(-) (/) (-)ESCs. In an effort to better understand how specific signaling pathways contribute to the global pattern of gene expression in Gsk-3α(-) (/) (-); Gsk-3β(-) (/) (-)ESCs, we compared the gene expression profiles in Gsk-3α(-) (/) (-); Gsk-3β(-) (/) (-) ESCs to mouse ESCs in which either Wnt/β-catenin signaling or phosphatidylinositol 3-kinase (PI3K)-dependent insulin signaling are constitutively active. Our results show that Wnt signaling has a greater effect on up-regulated genes in the Gsk-3α(-) (/) (-); Gsk-3β(-) (/) (-)ESCs, whereas PI3K-dependent insulin signaling is more responsible for the down-regulation of genes in the same cells. These data show the importance of Gsk-3 activity on gene expression in mouse ESCs, and that these effects are due to the combined effects of multiple signaling pathways.

Indexed as

embryonic stem cellsgene expressionglycogen synthase kinase-3microarrayphosphatidylinositol 3-kinasequantitative PCRsignal transductionWnt

Identifiers

PMID25165462
PMCPMC4131280
OpenAlexW2025493780

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.