ArticleNature communications2017
Chronic activation of JNK JAK/STAT and oxidative stress signalling causes the loser cell status.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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.
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.
Who cites it
69 citing papers in PubMed.
- NAT10 governs development through the Xrp1-mediated stress response rather than its RNA acetylation activity.Science advances · 2026Article
- Protective Effects of Leonurine on Alcoholic Liver Injury Through Modulation of Oxidative Stress and JAK2-STAT3 Signaling.Current issues in molecular biology · 2026Article
- Tumour-host interactions in Drosophila: mechanisms in the tumour micro- and macroenvironment.Molecular oncology · 2026Review
- Autocrine Motility Factor-Derived Tetradecapeptides as Dual-Action Chemosensitizers: Bridging Cell Competition Mechanisms with Clinical MDR Reversal in Hematological Malignancies.Oncology research · 2026Article
- Non-canonical EGFR signaling promotes MAPK-dependent extrusion of epithelial cells.Journal of cell science · 2025Article
- Interplay of EGFR, JNK, and ROS signaling in soma-germline communication in the Drosophila testis.Stem cell reports · 2025Article
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- Mechanisms of cellular fitness and cell competition: Towards an integrated view.Current opinion in cell biology · 2025Review
- Article
- Article
- Epithelial cell competition is promoted by signaling from immune cells.Nature communications · 2025Article
- Health position paper and redox perspectives - Bench to bedside transition for pharmacological regulation of NRF2 in noncommunicable diseases.Redox biology · 2025Review
- Corticosterone effects induced by stress and immunity and inflammation: mechanisms of communication.Frontiers in endocrinology · 2025Review
- Mechanisms of Germline Stem Cell Competition across Species.Life (Basel, Switzerland) · 2024Review
- The Drosophila tumor necrosis factor Eiger promotes Myc supercompetition independent of canonical Jun N-terminal kinase signaling.Genetics · 2024Article
- P53 and BCL-2 family proteins PUMA and NOXA define competitive fitness in pluripotent cell competition.PLoS genetics · 2024Article
- Maintenance of proteostasis by Drosophila Rer1 is essential for competitive cell survival and Myc-driven overgrowth.PLoS genetics · 2024Article
- Non-Mass Spectrometric Targeted Single-Cell Metabolomics.Trends in analytical chemistry : TRAC · 2023Article
- Article
- Ribosomal protein mutations and cell competition: autonomous and nonautonomous effects on a stress response.Genetics · 2023Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Cell competition is a form of cell interaction that causes the elimination of less fit cells, or losers, by wild-type (WT) cells, influencing overall tissue health. Several mutations can cause cells to become losers; however, it is not known how. Here we show that Drosophila wing disc cells carrying functionally unrelated loser mutations (Minute and mahjong) display the common activation of multiple stress signalling pathways before cell competition and find that these pathways collectively account for the loser status. We find that JNK signalling inhibits the growth of losers, while JAK/STAT signalling promotes competition-induced winner cell proliferation. Furthermore, we show that losers display oxidative stress response activation and, strikingly, that activation of this pathway alone, by Nrf2 overexpression, is sufficient to prime cells for their elimination by WT neighbours. Since oxidative stress and Nrf2 are linked to several diseases, cell competition may occur in a number of pathological conditions.Cell competition causes the removal of less fit cells ('losers') but why some gene mutations turn cells into losers is unclear. Here, the authors show that Drosophila wing disc cells carrying some loser mutations activate Nrf2 and JNK signalling, which contribute to the loser status.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.