Evidence map›Paper›PMID 25246545›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Insulin and insulin-like growth factor 1 receptors are required for normal expression of imprinted genes.

Jeremie Boucher, Marika Charalambous, Kim Zarse, Marcelo A Mori, Andre Kleinridders, Michael Ristow, Anne C Ferguson-Smith, C Ronald Kahn

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-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

36 citing papers in PubMed, 57 citations in OpenAlex.

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  10. Reciprocal communication between FAPs and muscle cells via distinct extracellular vesicle miRNAs in muscle regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  17. Distinct signaling by insulin and IGF-1 receptors and their extra- and intracellular domains.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Review
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  20. Insulin-Like Growth Factor Pathway and the Thyroid.Frontiers in endocrinology · 2021
    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

8 authors at 4 institutions in 2 countries.

Jeremie BoucherSection on Integrative Physiology and Metabolism, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02215;
Marika CharalambousDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 1TN, United Kingdom; and.
Kim ZarseSection on Integrative Physiology and Metabolism, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02215; Energy Metabolism Laboratory, Department of Health Sciences and Technology, Swiss Federal Institute of Technology, 8092 Zurich, Switzerland.
Marcelo A MoriSection on Integrative Physiology and Metabolism, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02215;
Andre KleinriddersSection on Integrative Physiology and Metabolism, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02215;
Michael RistowEnergy Metabolism Laboratory, Department of Health Sciences and Technology, Swiss Federal Institute of Technology, 8092 Zurich, Switzerland.
Anne C Ferguson-SmithDepartment of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 1TN, United Kingdom; and.
C Ronald KahnSection on Integrative Physiology and Metabolism, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02215; c.ronald.kahn@joslin.harvard.edu.
Brigham and Women's Hospital · USHarvard University · USUniversity of Cambridge · GBJoslin Diabetes Center · US

Funding

INSULIN RECEPTOR STRUCTURE AND TURNOVERR37DK031036 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 2000 to 2019
$12.9M
Developmental genes, miRNAs and adipose tissueR01DK082659 · NIDDK · JOSLIN DIABETES CENTER · PI C RONALD KAHN · 2009 to 2026
$10.7M
The Insulin Receptor and Its Signaling MechanismsR01DK031036 · NIDDK · JOSLIN DIABETES CENTER · PI C RONALD KAHN · 1986 to 2026
$4.2M
Medical Research Council MR/J001597/1NIDDK NIH HHS DK31036NIDDK NIH HHS DK34834NIDDK NIH HHS DK82659NIDDK NIH HHS R01 DK031036NIDDK NIH HHS R01 DK082659NIDDK NIH HHS R37 DK031036Wellcome Trust 095606
6 · The paper itself

Abstract

In addition to signaling through the classical tyrosine kinase pathway, recent studies indicate that insulin receptors (IRs) and insulin-like growth factor 1 (IGF1) receptors (IGF1Rs) can emit signals in the unoccupied state through some yet-to-be-defined noncanonical pathways. Here we show that cells lacking both IRs and IGF1Rs exhibit a major decrease in expression of multiple imprinted genes and microRNAs, which is partially mimicked by inactivation of IR alone in mouse embryonic fibroblasts or in vivo in brown fat in mice. This down-regulation is accompanied by changes in DNA methylation of differentially methylated regions related to these loci. Different from a loss of imprinting pattern, loss of IR and IGF1R causes down-regulated expression of both maternally and paternally expressed imprinted genes and microRNAs, including neighboring reciprocally imprinted genes. Thus, the unoccupied IR and IGF1R generate previously unidentified signals that control expression of imprinted genes and miRNAs through transcriptional mechanisms that are distinct from classical imprinting control.

Indexed as

Adipose Tissue, BrownAnimalsAzacitidineCell Line, TransformedCells, CulturedDNA MethylationEmbryo, MammalianEnzyme InhibitorsFibroblastsGene ExpressionGene Expression ProfilingGenomic ImprintingHistone Deacetylase InhibitorsHydroxamic AcidsInsulinInsulin-Like Growth Factor IAzacitidineEnzyme InhibitorsHistone Deacetylase InhibitorsHydroxamic AcidsInsulinInsulin-Like Growth Factor IMicroRNAsReceptor, IGF Type 1Receptor, Insulintrichostatin Adevelopmental controldiabetestranscriptional control

Identifiers

PMID25246545
PMCPMC4209990
OpenAlexW1972632173

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.