Evidence map›Paper›PMID 20943952›Full record

ArticleMolecular biology of the cell2010

Cell death or survival promoted by alternative isoforms of ErbB4.

Maria Sundvall, Ville Veikkolainen, Kari Kurppa, Zaidoun Salah, Denis Tvorogov, E Joop van Zoelen, Rami Aqeilan, Klaus Elenius

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  5. Review
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  8. Article
  9. Article
  10. Altered immunoreactivity of ErbB4, a causative gene product for ALS19, in the spinal cord of patients with sporadic ALS.Neuropathology : official journal of the Japanese Society of Neuropathology · 2019
    Article
  11. Article
  12. Review
  13. Article
  14. Toward the Language Oscillogenome.Frontiers in psychology · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Developmental pruning of excitatory synaptic inputs to parvalbumin interneurons in monkey prefrontal cortex.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  19. ERBB4 Expression in Ovarian Serous Carcinoma Resistant to Platinum-Based Therapy.Cancer control : journal of the Moffitt Cancer Center · 2017
    Article
  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

8 authors at 3 institutions in 3 countries.

Maria SundvallDepartment of Medical Biochemistry and Genetics, and Medicity Research Laboratory, University of Turku, Turku, Finland; Department of Oncology, Turku University Hospital, FIN-20520 Turku, Finland.
Ville Veikkolainen
Kari Kurppa
Zaidoun Salah
Denis Tvorogov
E Joop van Zoelen
Rami Aqeilan
Klaus Elenius
University of Turku · FIHebrew University of Jerusalem · ILRadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The significance of ErbB4 in tumor biology is poorly understood. The ERBB4 gene is alternatively spliced producing juxtamembrane (JM-a and JM-b) and cytoplasmic (CYT-1 and CYT-2) isoforms. Here, signaling via the two alternative ErbB4 JM isoforms (JM-a CYT-2 and JM-b CYT-2) was compared. Fibroblasts expressing ErbB4 JM-a demonstrated enhanced ErbB4 autophosphorylation, growth, and survival. In contrast, cells overexpressing ErbB4 JM-b underwent starvation-induced death. Both pro- and antisurvival responses to the two ErbB4 isoforms were sensitive to an ErbB kinase inhibitor. Platelet-derived growth factor receptor-alpha (PDGFRA) was identified as an ErbB4 target gene that was differentially regulated by the two ErbB4 isoforms. The soluble intracellular domain of ErbB4, released from the JM-a but not from the JM-b isoform, associated with the transcription factor AP-2 and promoted its potential to enhance PDGFRA transcription. Survival of cells expressing JM-a was suppressed by targeting either PDGFR-α or AP-2, whereas cells expressing JM-b were rescued from cell death by the PDGFR-α agonist, PDGF-BB. These findings indicate that two alternative ErbB4 isoforms may promote antagonistic cellular responses and suggest that pharmacological inhibition of ErbB4 kinase activity may lead to either suppression or promotion of cellular growth.

Indexed as

Cell DeathCell SurvivalSignal TransductionAlternative SplicingAnimalsCell LineCell ProliferationCytoplasmErbB ReceptorsGene Expression RegulationIn Situ Nick-End LabelingMembranesMiceMicroarray AnalysisPhosphorylationProtein IsoformsErbb4 protein, mouseErbB ReceptorsProtein IsoformsReceptor, ErbB-4Receptors, Platelet-Derived Growth FactorTranscription Factor AP-2

Identifiers

PMID20943952
PMCPMC2993754
OpenAlexW2107863839

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.