Evidence map›Paper›PMID 19729440›Full record

ArticleJournal of the American Society of Nephrology : JASN2009

p53 regulates metanephric development.

Zubaida Saifudeen, Susana Dipp, Jana Stefkova, Xiao Yao, Sarah Lookabaugh, Samir S El-Dahr

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Metabolic requirements of the nephron.Pediatric nephrology (Berlin, Germany) · 2020
    Review
  5. Review
  6. Cell Death in the Kidney.International journal of molecular sciences · 2019
    Review
  7. Article
  8. The role of p53 in developmental syndromes.Journal of molecular cell biology · 2019
    Review
  9. Article
  10. Article
  11. Regulation of Nephron Progenitor Cell Self-Renewal by Intermediary Metabolism.Journal of the American Society of Nephrology : JASN · 2017
    Article
  12. Article
  13. Regulation of kidney development by the Mdm2/Mdm4-p53 axis.Journal of molecular cell biology · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. The MDM2-p53 pathway: multiple roles in kidney development.Pediatric nephrology (Berlin, Germany) · 2014
    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 1 institution in 1 country.

Zubaida SaifudeenSection of Pediatric Nephrology, Department of Pediatrics, and the Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, LA 70112, USA. zubisaif@tulane.edu
Susana Dipp
Jana Stefkova
Xiao Yao
Sarah Lookabaugh
Samir S El-Dahr
Tulane University · US

Funding

TULANE COBRE: TRANSGENIC &GENE-TARGETED ANIMAL COREP20RR017659 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI PRIETO, MINOLFA C · 2002 to 2011
$22.1M
Inducible Dysplastic Nephropathy in B2-Deficient MiceR01DK056264 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI EL-DAHR, SAMIR S · 2000 to 2014
$3.8M
TERMINAL DIFFERENTIATION OF THE RENAL EPITHELIUMR01DK062250 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI EL-DAHR, SAMIR S · 2003 to 2012
$2.5M
NCRR NIH HHS 1P20 RR-017659NCRR NIH HHS P20 RR017659NIDDK NIH HHS DK56264NIDDK NIH HHS DK62250NIDDK NIH HHS R01 DK056264NIDDK NIH HHS R01 DK062250
6 · The paper itself

Abstract

p53 is best known as a tumor suppressor that regulates cell-cycle, differentiation, and apoptosis pathways, but its potential role in embryonic development and organogenesis remains controversial. Here, p53(-/-) embryos bred on C57Bl6 background exhibited a spectrum of congenital abnormalities of the kidney and urinary tract, including ureteric bud (UB) ectopia, double ureters/collecting systems, delayed primary branching of the UB, and hypoplastic metanephroi. We observed ectopic UB outgrowth from the Wolffian duct (WD) in one third of p53(-/-) embryos. The prevalence of duplex was higher in embryos than in neonates, and ex vivo organ culture suggested that ectopic ureters can regress over time, leaving behind a dysplastic pole ("segmental dysgenesis"). Transgenic expression of dominant negative p53 or conditional inactivation of p53 in the UB but not in the metanephric mesenchyme lineage recapitulated the duplex phenotype. Mechanistically, p53 inactivation in the WD associated with enhanced sensitivity to glial cell line-derived neurotrophic factor (GDNF)-induced ectopic budding and potentiated phosphatidylinositol-3 kinase activation by GDNF in UB cells. Unlike several other models of UB ectopia, hypersensitivity of p53(-/-) WD to GDNF is not accompanied by reduced Sprouty-1 or anterior expansion of the GDNF domain. In summary, our data lend support for a restrictive role for p53 activity in UB outgrowth from the WD.

Indexed as

AnimalsGene ExpressionGlial Cell Line-Derived Neurotrophic FactorKidneyMiceOrganogenesisTumor Suppressor Protein p53Wolffian DuctsGlial Cell Line-Derived Neurotrophic FactorTumor Suppressor Protein p53

Identifiers

PMID19729440
PMCPMC2799183
OpenAlexW2111623323

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.