Evidence map›Paper›PMID 25670073›Full record

ArticleCancer cell2015

14-3-3ζ turns TGF-β to the dark side.

Peter ten Dijke, Hans van Dam

Abstract readComment
PubMed Publisher
In one paragraph

Article in Cancer cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. TGF-β1-p53 cooperativity regulates a profibrotic genomic program in the kidney: molecular mechanisms and clinical implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Review
  6. Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Peter ten DijkeDepartment of Molecular Cell Biology, Cancer Genomics Centre Netherlands, Leiden University Medical Center, Postbus 9600, 2300 RC Leiden, the Netherlands; Ludwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Box 595, 75124 Uppsala, Sweden. Electronic address: p.ten_dijke@lumc.nl.
Hans van DamDepartment of Molecular Cell Biology, Cancer Genomics Centre Netherlands, Leiden University Medical Center, Postbus 9600, 2300 RC Leiden, the Netherlands; Ludwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Box 595, 75124 Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TGF-β/SMAD signaling has long been known to exhibit a dual role in cancer, questioning what determines its context-dependent functions. In this issue of Cancer Cell, Xu and colleagues describe a critical role of the adaptor protein 14-3-3ζ in modulating SMAD activities by changing its interaction partners during breast cancer progression.

Indexed as

14-3-3 ProteinsBone NeoplasmsBreast NeoplasmsFemaleHumansKruppel-Like Transcription FactorsNuclear ProteinsTransforming Growth Factor betaTumor Suppressor Protein p53Zinc Finger Protein Gli214-3-3 ProteinsGLI2 protein, humanKruppel-Like Transcription FactorsNuclear ProteinsTP53 protein, humanTransforming Growth Factor betaTumor Suppressor Protein p53YWHAZ protein, humanZinc Finger Protein Gli2

Identifiers

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.