Evidence map›Paper›PMID 25804736›Full record

ArticleDevelopment (Cambridge, England)2015

WT1 targets Gas1 to maintain nephron progenitor cells by modulating FGF signals.

Martin Kann, Eunnyung Bae, Maximilian O Lenz, Liangji Li, BaoTran Trannguyen, Valerie A Schumacher, Mary E Taglienti, Liliana Bordeianou, Sunny Hartwig, Markus M Rinschen and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  5. Gene regulatory networks in disease and ageing.Nature reviews. Nephrology · 2024
    Review
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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

14 authors at 7 institutions in 3 countries.

Martin KannDivision of Nephrology, Department of Medicine, Boston Children's Hospital, Boston, MA 02115, USA Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA Department II of Medicine and Center for Molecular Medicine Cologne, University of Cologne, 50931 Cologne, Germany.
Eunnyung BaeDivision of Nephrology, Department of Medicine, Boston Children's Hospital, Boston, MA 02115, USA Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Maximilian O LenzDepartment II of Medicine and Center for Molecular Medicine Cologne, University of Cologne, 50931 Cologne, Germany.
Liangji LiDepartment of Embryology, Carnegie Institution of Washington, Baltimore, MD 21218, USA.
BaoTran TrannguyenDivision of Nephrology, Department of Medicine, Boston Children's Hospital, Boston, MA 02115, USA Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Valerie A SchumacherDivision of Nephrology, Department of Medicine, Boston Children's Hospital, Boston, MA 02115, USA Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Mary E TaglientiDivision of Nephrology, Department of Medicine, Boston Children's Hospital, Boston, MA 02115, USA Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Liliana BordeianouDivision of Nephrology, Department of Medicine, Boston Children's Hospital, Boston, MA 02115, USA Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
Sunny HartwigDepartment of Biomedical Sciences, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE, Canada C1A 4P3.
Markus M RinschenDepartment II of Medicine and Center for Molecular Medicine Cologne, University of Cologne, 50931 Cologne, Germany.
Bernhard SchermerDepartment II of Medicine and Center for Molecular Medicine Cologne, University of Cologne, 50931 Cologne, Germany Cluster of Excellence on Cellular Stress Responses in Ageing-Associated Diseases (CECAD) and Systems Biology of Ageing Cologne, University of Cologne, 50931 Cologne, Germany.
Thomas BenzingDepartment II of Medicine and Center for Molecular Medicine Cologne, University of Cologne, 50931 Cologne, Germany Cluster of Excellence on Cellular Stress Responses in Ageing-Associated Diseases (CECAD) and Systems Biology of Ageing Cologne, University of Cologne, 50931 Cologne, Germany.
Chen-Ming FanDepartment of Embryology, Carnegie Institution of Washington, Baltimore, MD 21218, USA.
Jordan A KreidbergDivision of Nephrology, Department of Medicine, Boston Children's Hospital, Boston, MA 02115, USA Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA Harvard Stem Cell Institute, Cambridge, MA 02138, USA jordan.kreidberg@childrens.harvard.edu.
Boston Children's Hospital · USUniversity of Cologne · DEHarvard University · USCarnegie Institution for Science · USCologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEDepartment of Embryology · USUniversity of Prince Edward Island · CA

Funding

BMP and FGF Signaling in kidney progenitor cellsR01DK087794 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI KREIDBERG, JORDAN A · 2010 to 2013
$1.5M
NIDDK NIH HHS R01 DK087794PHS HHS NIDDK R01 DK087794-A1
6 · The paper itself

Abstract

Development of the metanephric kidney depends on tightly regulated interplay between self-renewal and differentiation of a nephron progenitor cell (NPC) pool. Several key factors required for the survival of NPCs have been identified, including fibroblast growth factor (FGF) signaling and the transcription factor Wilms' tumor suppressor 1 (WT1). Here, we present evidence that WT1 modulates FGF signaling by activating the expression of growth arrest-specific 1 (Gas1), a novel WT1 target gene and novel modulator of FGF signaling. We show that WT1 directly binds to a conserved DNA binding motif within the Gas1 promoter and activates Gas1 mRNA transcription in NPCs. We confirm that WT1 is required for Gas1 expression in kidneys in vivo. Loss of function of GAS1 in vivo results in hypoplastic kidneys with reduced nephron mass due to premature depletion of NPCs. Although kidney development in Gas1 knockout mice progresses normally until E15.5, NPCs show decreased rates of proliferation at this stage and are depleted as of E17.5. Lastly, we show that Gas1 is selectively required for FGF-stimulated AKT signaling in vitro. In summary, our data suggest a model in which WT1 modulates receptor tyrosine kinase signaling in NPCs by directing the expression of Gas1.

Indexed as

Signal TransductionAnimalsCell Cycle ProteinsCell ProliferationDNAEnzyme ActivationFibroblast Growth FactorsGene Expression Regulation, DevelopmentalGene Knockdown TechniquesGPI-Linked ProteinsMice, KnockoutModels, AnimalNephronsOrgan Culture TechniquesPromoter Regions, GeneticProtein BindingCell Cycle ProteinsDNAFibroblast Growth FactorsGas1 protein, mouseGPI-Linked ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-retRNA, MessengerWT1 ProteinsFibroblast growth factor signalingKidney developmentMouseNephron progenitor cell

Identifiers

PMID25804736
PMCPMC4378252
OpenAlexW2096806980

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.