Evidence map›Paper›PMID 22031548›Full record

ArticleDevelopment (Cambridge, England)2011

FGF/EGF signaling regulates the renewal of early nephron progenitors during embryonic development.

Aaron C Brown, Derek Adams, Mark de Caestecker, Xuehui Yang, Robert Friesel, Leif Oxburgh

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing 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

54 citing papers in PubMed, 98 citations in OpenAlex.

  1. A knock inbioRxiv : the preprint server for biology · 2026
    Article
  2. Article
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  5. Article
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  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. MAPK/ERK Signaling in Regulation of Renal Differentiation.International journal of molecular sciences · 2019
    Review
  20. 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

6 authors at 3 institutions in 1 country.

Aaron C BrownCenter for Molecular Medicine, Maine Medical Center Research Institute, 81 Research Drive, Scarborough, ME 04074, USA.
Derek Adams
Mark de Caestecker
Xuehui Yang
Robert Friesel
Leif Oxburgh
Maine Medical Center · USMaine Medical Center Research Institute · USVanderbilt University Medical Center · US

Funding

Transcriptional Decisions in Endothelial Cell DifferentiationP20RR015555 · NCRR · MAINE MEDICAL CENTER · PI PRUDOVSKY, IGOR · 2000 to 2009
$21.4M
WNT SIGNALING IN PREIMPLANTATION EMBRYOP20RR018789 · NCRR · MAINE MEDICAL CENTER · PI WANG, ZACK Z. · 2003 to 2011
$18.9M
Defining the progenitor cell niche of the developing kidneyR01DK078161 · NIDDK · MAINEHEALTH · PI OXBURGH, LEIF · 2008 to 2016
$3.4M
NCRR NIH HHS 2P20RR15555NCRR NIH HHS 2P20RR18789NCRR NIH HHS P20 RR015555NCRR NIH HHS P20 RR018789NIDDK NIH HHS R01DK073781NIDDK NIH HHS R01DK07816NIDDK NIH HHS R01 DK078161
6 · The paper itself

Abstract

Recent studies indicate that nephron progenitor cells of the embryonic kidney are arranged in a series of compartments of an increasing state of differentiation. The earliest progenitor compartment, distinguished by expression of CITED1, possesses greater capacity for renewal and differentiation than later compartments. Signaling events governing progression of nephron progenitor cells through stages of increasing differentiation are poorly understood, and their elucidation will provide key insights into normal and dysregulated nephrogenesis, as well as into regenerative processes that follow kidney injury. In this study, we found that the mouse CITED1(+) progenitor compartment is maintained in response to receptor tyrosine kinase (RTK) ligands that activate both FGF and EGF receptors. This RTK signaling function is dependent on RAS and PI3K signaling but not ERK. In vivo, RAS inactivation by expression of sprouty 1 (Spry1) in CITED1(+) nephron progenitors results in loss of characteristic molecular marker expression and in increased death of progenitor cells. Lineage tracing shows that surviving Spry1-expressing progenitor cells are impaired in their subsequent epithelial differentiation, infrequently contributing to epithelial structures. These findings demonstrate that the survival and developmental potential of cells in the earliest embryonic nephron progenitor cell compartment are dependent on FGF/EGF signaling through RAS.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosis Regulatory ProteinsCell DifferentiationCell LineageCells, CulturedEpidermal Growth FactorFibroblast Growth FactorsGalactosidesIndolesIn Situ Nick-End LabelingMembrane ProteinsMiceMicroscopy, FluorescenceNephronsNuclear Proteins5-bromo-4-chloro-3-indolyl beta-galactosideAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCited1 protein, mouseEpidermal Growth FactorFibroblast Growth FactorsGalactosidesIndolesMembrane ProteinsNuclear ProteinsPhosphatidylinositol 3-KinasesPhosphoproteinsras ProteinsReceptor Protein-Tyrosine KinasesSpry1 protein, mouseTrans-Activators

Identifiers

PMID22031548
PMCPMC3210493
OpenAlexW2098604249

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.