Evidence map›Paper›PMID 25857265›Full record

ArticleCell death and differentiation2015

The tumor-modulatory effects of Caspase-2 and Pidd1 do not require the scaffold protein Raidd.

L Peintner, L Dorstyn, S Kumar, T Aneichyk, A Villunger, C Manzl

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Cell-Cycle Cross Talk with Caspases and Their Substrates.Cold Spring Harbor perspectives in biology · 2020
    Review
  8. Article
  9. Caspase-2 Substrates: To Apoptosis, Cell Cycle Control, and Beyond.Frontiers in cell and developmental biology · 2020
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. The DNA damage-induced cell death response: a roadmap to kill cancer cells.Cellular and molecular life sciences : CMLS · 2016
    Review
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 3 institutions in 2 countries.

L PeintnerDivision of Developmental Immunology, Medical University of Innsbruck, 6020 Innsbruck, Austria.
L DorstynCentre for Cancer Biology - An Alliance between SA Pathology and the University of South Australia, Adelaide, SA 5001, Australia.
S KumarCentre for Cancer Biology - An Alliance between SA Pathology and the University of South Australia, Adelaide, SA 5001, Australia.
T AneichykDivision of Molecular Pathophysiology, Biocenter, Medical University of Innsbruck, Innsbruck 6020, Austria.
A VillungerDivision of Developmental Immunology, Medical University of Innsbruck, 6020 Innsbruck, Austria.
C ManzlDivision of Developmental Immunology, Medical University of Innsbruck, 6020 Innsbruck, Austria.
Innsbruck Medical University · ATUniversity of South Australia · AUUniversität Innsbruck · AT

Funding

Austrian Science Fund FWF W 1101
6 · The paper itself

Abstract

The receptor-interacting protein-associated ICH-1/CED-3 homologous protein with a death domain (RAIDD/CRADD) functions as a dual adaptor and is a constituent of different multi-protein complexes implicated in the regulation of inflammation and cell death. Within the PIDDosome complex, RAIDD connects the cell death-related protease, Caspase-2, with the p53-induced protein with a death domain 1 (PIDD1). As such, RAIDD has been implicated in DNA-damage-induced apoptosis as well as in tumorigenesis. As loss of Caspase-2 leads to an acceleration of tumor onset in the Eμ-Myc mouse lymphoma model, whereas loss of Pidd1 actually delays onset of this disease, we set out to interrogate the role of Raidd in cancer in more detail. Our data obtained analyzing Eμ-Myc/Raidd(-/-) mice indicate that Raidd is unable to protect from c-Myc-driven lymphomagenesis. Similarly, we failed to observe a modulatory effect of Raidd deficiency on DNA-damage-driven cancer. The role of Caspase-2 as a tumor suppressor and that of Pidd1 as a tumor promoter can therefore be uncoupled from their ability to interact with the Raidd scaffold, pointing toward the existence of alternative signaling modules engaging these two proteins in this context.

Indexed as

AnimalsCaspase 2Cell CycleCells, CulturedCell SurvivalCRADD Signaling Adaptor ProteinDeath Domain Receptor Signaling Adaptor ProteinsDNA DamageFibrosarcomaMiceProto-Oncogene Proteins c-mycCaspase 2Cradd protein, mouseCRADD Signaling Adaptor ProteinDeath Domain Receptor Signaling Adaptor ProteinsPidd1 protein, mouseProto-Oncogene Proteins c-myc

Identifiers

PMID25857265
PMCPMC4648327
OpenAlexW2048749222

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.