Evidence map›Paper›PMID 26021298›Full record

ArticleCell death and differentiation2015

The Hippo pathway promotes cell survival in response to chemical stress.

F Di Cara, T M Maile, B D Parsons, A Magico, S Basu, N Tapon, K King-Jones

Open access · bronzeAbstract 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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  6. Review
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  9. Article
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  11. Article
  12. Review
  13. p53 shades of Hippo.Cell death and differentiation · 2018
    Review
  14. Article
  15. 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

7 authors at 3 institutions in 2 countries.

F Di CaraDepartment of Cell Biology, Medical Sciences Building, Faculty of Medicine & Dentistry, University of Alberta, Edmonton T6G 2H7, Alberta, Canada.
T M MaileGenentech Inc., 1 DNA Way, South San Francisco, CA, USA.
B D ParsonsDepartment of Medical Microbiology and Immunology, 6-020 Katz Group Centre, University of Alberta, Edmonton AB T6G 2E1, Alberta, Canada.
A MagicoDepartment of Pediatrics, Faculty of Medicine & Dentistry, Katz Group Centre, University of Alberta, Edmonton T6G 2H7, Alberta, Canada.
S BasuCentre for Molecular Oncology, Institute of Cancer, Barts and The London School of Medicine and Dentistry, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK.
N TaponApoptosis and Proliferation Control Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK.
K King-JonesDepartment of Biological Sciences, University of Alberta, G-504 Biological Sciences Bldg, Edmonton T6G 2E9, Alberta, Canada.
University of Alberta · CACancer Research UK · GBQueen Mary University of London · GB

Funding

Cancer Research UK 17064CIHR
6 · The paper itself

Abstract

Cellular stress defense mechanisms have evolved to maintain homeostasis in response to a broad variety of environmental challenges. Stress signaling pathways activate multiple cellular programs that range from the activation of survival pathways to the initiation of cell death when cells are damaged beyond repair. To identify novel players acting in stress response pathways, we conducted a cell culture RNA interference (RNAi) screen using caffeine as a xenobiotic stress-inducing agent, as this compound is a well-established inducer of detoxification response pathways. Specifically, we examined how caffeine affects cell survival when Drosophila kinases and phosphatases were depleted via RNAi. Using this approach, we identified and validated 10 kinases and 4 phosphatases that are essential for cell survival under caffeine-induced stress both in cell culture and living flies. Remarkably, our screen yielded an enrichment of Hippo pathway components, indicating that this pathway regulates cellular stress responses. Indeed, we show that the Hippo pathway acts as a potent repressor of stress-induced cell death. Further, we demonstrate that Hippo activation is necessary to inhibit a pro-apoptotic program triggered by the interaction of the transcriptional co-activator Yki with the transcription factor p53 in response to a range of stress stimuli. Our in vitro and in vivo loss-of-function data therefore implicate Hippo signaling in the transduction of cellular survival signals in response to chemical stress.

Indexed as

AnimalsApoptosisCaffeineCell LineCell SurvivalDrosophila melanogasterDrosophila ProteinsHippo KinasesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesSignal TransductionStress, PhysiologicalCaffeineDrosophila ProteinsHippo Kinaseshpo protein, DrosophilaIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID26021298
PMCPMC4532776
OpenAlexW2064941103

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.