Evidence map›Paper›PMID 12773577›Full record

ArticleMolecular and cellular biology2003

Heart and liver defects and reduced transforming growth factor beta2 sensitivity in transforming growth factor beta type III receptor-deficient embryos.

Kaye L Stenvers, Melinda L Tursky, Kenneth W Harder, Nicole Kountouri, Supavadee Amatayakul-Chantler, Dianne Grail, Clayton Small, Robert A Weinberg, Andrew M Sizeland, Hong-Jian Zhu

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 248 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Structural insights into regulation of CCN protein activities and functions.Journal of cell communication and signaling · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Coreceptor functions of cell surface heparan sulfate proteoglycans.American journal of physiology. Cell physiology · 2022
    Review
  19. Article
  20. TGF-β superfamily co-receptors in cancer.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Review

42 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Kaye L StenversLudwig Institute for Cancer Research, Royal Melbourne Hospital, Victoria 3050, Australia. Kaye.Stenvers@ludwig.edu.au
Melinda L Tursky
Kenneth W Harder
Nicole Kountouri
Supavadee Amatayakul-Chantler
Dianne Grail
Clayton Small
Robert A Weinberg
Andrew M Sizeland
Hong-Jian Zhu
Ludwig Cancer Research · AUThe Royal Melbourne Hospital · AUMassachusetts Institute of Technology · USWhitehead Institute for Biomedical Research · US

Funding

TGFBRIII IN NORMAL AND MALIGNANT LIVER GROWTHF32CA090034 · NCI · LUDWIG INSTITUTE FOR CANCER RESEARCH · PI STENVERS, KAYE L · 2001 to 2003
$154k
NCI NIH HHS F32 CA090034NCI NIH HHS F32 CA90034
6 · The paper itself

Abstract

The type III transforming growth factor beta (TGFbeta) receptor (TbetaRIII) binds both TGFbeta and inhibin with high affinity and modulates the association of these ligands with their signaling receptors. However, the significance of TbetaRIII signaling in vivo is not known. In this study, we have sought to determine the role of TbetaRIII during development. We identified the predominant expression sites of TbetaRIII mRNA as liver and heart during midgestation and have disrupted the murine TbetaRIII gene by homologous recombination. Beginning at embryonic day 13.5, mice with mutations in TbetaRIII developed lethal proliferative defects in heart and apoptosis in liver, indicating that TbetaRIII is required during murine somatic development. To assess the effects of the absence of TbetaRIII on the function of its ligands, primary fibroblasts were generated from TbetaRIII-null and wild-type embryos. Our results indicate that TbetaRIII deficiency differentially affects the activities of TGFbeta ligands. Notably, TbetaRIII-null cells exhibited significantly reduced sensitivity to TGFbeta2 in terms of growth inhibition, reporter gene activation, and Smad2 nuclear localization, effects not observed with other ligands. These data indicate that TbetaRIII is an important modulator of TGFbeta2 function in embryonic fibroblasts and that reduced sensitivity to TGFbeta2 may underlie aspects of the TbetaRIII mutant phenotype.

Indexed as

AnimalsBlotting, NorthernBlotting, SouthernCell NucleusDose-Response Relationship, DrugFibroblastsFlow CytometryGenes, ReporterHeartImmunoblottingImmunohistochemistryInhibitory Concentration 50LigandsLiverMiceMice, KnockoutbetaglycanLigandsProteoglycansReceptors, Transforming Growth Factor betaRNA, MessengerTransforming Growth Factor beta

Identifiers

PMID12773577
PMCPMC156130
OpenAlexW2148734937

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.