Evidence map›Paper›PMID 21459846›Full record

ArticleNucleic acids research2011

Crosstalk between c-Jun and TAp73alpha/beta contributes to the apoptosis-survival balance.

Max Koeppel, Simon J van Heeringen, Daniela Kramer, Leonie Smeenk, Eva Janssen-Megens, Marianne Hartmann, Hendrik G Stunnenberg, Marion Lohrum

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2011. 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
1.8field-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

40 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. p73 as a Tissue Architect.Frontiers in cell and developmental biology · 2021
    Review
  11. Mechanisms of Functional Pleiotropy of p73 in Cancer and Beyond.Frontiers in cell and developmental biology · 2021
    Review
  12. Review
  13. Article
  14. The C terminus of p73 is essential for hippocampal development.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Review
  16. Article
  17. The multiple mechanisms that regulate p53 activity and cell fate.Nature reviews. Molecular cell biology · 2019
    Review
  18. TheFrontiers in genetics · 2019
    Review
  19. Article
  20. Revealing a human p53 universe.Nucleic acids research · 2018
    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 1 institution in 1 country.

Max KoeppelDepartment of Molecular Biology, Faculty of Science, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen, Nijmegen, The Netherlands.
Simon J van Heeringen
Daniela Kramer
Leonie Smeenk
Eva Janssen-Megens
Marianne Hartmann
Hendrik G Stunnenberg
Marion Lohrum
Radboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53-family member p73 plays a role in various cellular signaling pathways during development and growth control and it can have tumor suppressor properties. Several isoforms of p73 exist with considerable differences in their function. Whereas the functions of the N-terminal isoforms (TA and ΔNp73) and their opposing pro- and antiapoptotic roles have become evident, the functional differences of the distinct C-terminal splice forms of TAp73 have remained unclear. Here, we characterized the global genomic binding sites for TAp73α and TAp73β by chromatin immunoprecipitation sequencing as well as the transcriptional responses by performing RNA sequencing. We identified a specific p73 consensus binding motif and found a strong enrichment of AP1 motifs in close proximity to binding sites for TAp73α. These AP1 motif-containing target genes are selectively upregulated by TAp73α, while their mRNA expression is repressed upon TAp73β induction. We show that their expression is dependent on endogenous c-Jun and that recruitment of c-Jun to the respective AP1 sites was impaired upon TAp73β expression, in part due to downregulation of c-Jun. Several of these AP1-site containing TAp73α-induced genes impinge on apoptosis induction, suggesting an underlying molecular mechanism for the observed functional differences between TAp73α and TAp73β.

Indexed as

Transcriptional ActivationApoptosisBinding SitesCell LineCell SurvivalDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportHumansInterleukin-1 Receptor Accessory ProteinNedd4 Ubiquitin Protein LigasesNuclear ProteinsProtein IsoformsProtein Structure, TertiaryProto-Oncogene Proteins c-junRegulatory Elements, TranscriptionalTranscription Factor AP-1delta Np73 protein, humanDNA-Binding ProteinsEndosomal Sorting Complexes Required for TransportIL1RAP protein, humanInterleukin-1 Receptor Accessory ProteinNedd4 Ubiquitin Protein LigasesNuclear ProteinsProtein IsoformsProto-Oncogene Proteins c-junTP73 protein, humanTranscription Factor AP-1Tumor Protein p73Tumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID21459846
PMCPMC3152320
OpenAlexW2118118849

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.