Evidence map›Paper›PMID 24415131›Full record

ArticleStem cell reviews and reports2014

Disrupted WNT signaling in mouse embryonic stem cells in the absence of calreticulin.

Jody Groenendyk, Marek Michalak

Abstract read
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In one paragraph

Article in Stem cell reviews and reports, 2014. 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
1.9field-weighted citation impact, top 14% 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, 19 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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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.

Jody GroenendykDepartment of Biochemistry, University of Alberta, Edmonton, Alberta, Canada, T6G 2S7.
Marek Michalak
University of Alberta · CA

Funding

Canadian Institutes of Health Research MOP-15291Canadian Institutes of Health Research MOP-15415Canadian Institutes of Health Research MOP-53050
6 · The paper itself

Abstract

The role of endoplasmic reticulum (ER) homeostasis and protein quality control in the regulation of WNT signaling is not understood. Here we provide evidence for a role of calreticulin in the regulation of WNT signaling. We show that a deficiency in calreticulin disrupted WNT signaling, and prevented cell cycle progression via the miR-302 microRNA family. These effects were dependent on the Ca(2+) buffering capacity of calreticulin, as the protein is important in regulating ER Ca(2+) release and activation of Ca(2+)-dependent kinase and phosphatase cascades (including c-Src, Akt, and PTP1B). We also show that calreticulin plays a role in the secretion and ER retention of WNT3a, thereby affecting downstream WNT signaling. In calreticulin-deficient ES cells, the WNT and miR-302 dependent maintenance of the naïve ES cell state and the transition to primed pluripotency transition were lost, preventing cells from undergoing accurate differentiation. Together, these findings demonstrate unexpected roles of calreticulin and ER Ca(2+) homeostasis/signaling in the canonical WNT signaling pathway.

Indexed as

Wnt Signaling PathwayAnimalsbeta CateninBiomarkersCalciumCalreticulinCell Adhesion MoleculesCell Cycle CheckpointsCell DifferentiationCell MembraneEmbryonic Stem CellsEndoplasmic ReticulumGene ExpressionIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsMicebeta CateninBiomarkersCalciumCalreticulinCell Adhesion MoleculesCTNNB1 protein, mouseIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsMicroRNAsWnt3A ProteinWnt3a protein, mouse

Identifiers

PMID24415131
OpenAlexW2052097134

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.