Evidence map›Paper›PMID 25053427›Full record

ArticleDevelopment (Cambridge, England)2014

Insm1 promotes endocrine cell differentiation by modulating the expression of a network of genes that includes Neurog3 and Ripply3.

Anna B Osipovich, Qiaoming Long, Elisabetta Manduchi, Rama Gangula, Susan B Hipkens, Judsen Schneider, Tadashi Okubo, Christian J Stoeckert, Shinji Takada, Mark A Magnuson

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
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  8. Fgf8Neuroscience bulletin · 2023
    Article
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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

10 authors at 5 institutions in 2 countries.

Anna B OsipovichCenter for Stem Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Qiaoming LongDepartment of Animal Science, Cornell University, Ithaca, NY 14850, USA.
Elisabetta ManduchiPenn Center for Bioinformatics, Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Rama GangulaCenter for Stem Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Susan B HipkensCenter for Stem Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Judsen SchneiderCenter for Stem Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
Tadashi OkuboDepartment of Laboratory Animal Science, Kitasato University School of Medicine, Sagamihara, 252-0374, Japan.
Christian J StoeckertPenn Center for Bioinformatics, Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Shinji TakadaOkazaki Institute for Integrative Bioscience, National Institutes of Natural Sciences, Okazaki, Aichi, 444-8787, Japan.
Mark A MagnusonCenter for Stem Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA mark.magnuson@vanderbilt.edu.
Vanderbilt University · USUniversity of Pennsylvania · USCornell University · USKitasato University · JPOkazaki Institute for Integrative Bioscience · JP

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Coordinating Center for Beta Cell Biology ConsortiumU01DK072473 · NIDDK · VANDERBILT UNIVERSITY · PI MAGNUSON, MARK A · 2005 to 2014
$61.0M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
Training Program in Stem Cell and Regenerative Developmental BiologyT32HD007502 · NICHD · VANDERBILT UNIVERSITY · PI WRIGHT, CHRISTOPHER V · 1997 to 2022
$5.4M
Genetic control of pancreatic endocrine cell developmentU01DK089523 · NIDDK · VANDERBILT UNIVERSITY · PI MAGNUSON, MARK A · 2010 to 2014
$5.3M
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NICHD NIH HHS T32 HD007502NIDDK NIH HHS DK20593NIDDK NIH HHS DK58404NIDDK NIH HHS DK72473NIDDK NIH HHS DK89523NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P30 DK058404NIDDK NIH HHS U01 DK072473NIDDK NIH HHS U01 DK089523
6 · The paper itself

Abstract

Insulinoma associated 1 (Insm1) plays an important role in regulating the development of cells in the central and peripheral nervous systems, olfactory epithelium and endocrine pancreas. To better define the role of Insm1 in pancreatic endocrine cell development we generated mice with an Insm1(GFPCre) reporter allele and used them to study Insm1-expressing and null populations. Endocrine progenitor cells lacking Insm1 were less differentiated and exhibited broad defects in hormone production, cell proliferation and cell migration. Embryos lacking Insm1 contained greater amounts of a non-coding Neurog3 mRNA splice variant and had fewer Neurog3/Insm1 co-expressing progenitor cells, suggesting that Insm1 positively regulates Neurog3. Moreover, endocrine progenitor cells that express either high or low levels of Pdx1, and thus may be biased towards the formation of specific cell lineages, exhibited cell type-specific differences in the genes regulated by Insm1. Analysis of the function of Ripply3, an Insm1-regulated gene enriched in the Pdx1-high cell population, revealed that it negatively regulates the proliferation of early endocrine cells. Taken together, these findings indicate that in developing pancreatic endocrine cells Insm1 promotes the transition from a ductal progenitor to a committed endocrine cell by repressing a progenitor cell program and activating genes essential for RNA splicing, cell migration, controlled cellular proliferation, vasculogenesis, extracellular matrix and hormone secretion.

Indexed as

Gene Expression Regulation, DevelopmentalAllelesAlternative SplicingAnimalsBasic Helix-Loop-Helix ProteinsCell DifferentiationCell LineageCell MovementCell ProliferationCell SeparationDNA-Binding ProteinsEndocrine CellsExtracellular MatrixFlow CytometryGene Regulatory NetworksGenes, ReporterBasic Helix-Loop-Helix ProteinsDNA-Binding ProteinsGreen Fluorescent ProteinsInsm1 protein, mouseNerve Tissue ProteinsNeurog3 protein, mouseRepressor ProteinsRipply3 protein, mouseRNATranscription FactorsEndocrine progenitor cellsGene expressionMousePancreas developmentTranscription factors

Identifiers

PMID25053427
PMCPMC4197673
OpenAlexW2145856823

What OpenQuestion holds

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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.