Evidence map›Paper›PMID 24162658›Full record

ArticleCell death and differentiation2014

Bendless modulates JNK-mediated cell death and migration in Drosophila.

X Ma, W Li, H Yu, Y Yang, M Li, L Xue, T Xu

Abstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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

41 citing papers in PubMed.

  1. Article
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  8. International journal of molecular sciences · 2022
    Review
  9. Article
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  12. Article
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  14. Article
  15. Article
  16. Spz/Toll-6 signal guides organotropic metastasis inDisease models & mechanisms · 2019
    Article
  17. Article
  18. Article
  19. POSH regulates Hippo signaling through ubiquitin-mediated expanded degradation.Proceedings of the National Academy of Sciences of the United States of America · 2018
    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

7 authors.

X MaDepartment of Interventional Radiology, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China.
W LiDepartment of Interventional Radiology, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China.
H YuDepartment of Interventional Radiology, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China.
Y YangDepartment of Interventional Radiology, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China.
M LiDepartment of Interventional Radiology, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China.
L Xue1] Department of Interventional Radiology, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China [2] Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, New Haven, CT 06519, USA.
T Xu1] Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, New Haven, CT 06519, USA [2] Institute of Developmental Biology and Molecular Medicine, Fudan-Yale Center for Biomedical Research, School of Life Sciences, Fudan University, Shanghai, China.

Funding

TUMOR SUPPRESSORS AND CELL PROLIFERATION IN DROSOPHILAR01CA069408 · NCI · YALE UNIVERSITY · PI XU, TIAN · 1996 to 2016
$5.1M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA069408
6 · The paper itself

Abstract

The TNF-JNK pathway is a highly conserved signaling pathway that regulates a wide spectrum of biological processes including cell death and migration. To further delineate this pathway, we carried out a genetic screen for dominant modifiers of the cell death phenotype triggered by ectopic expression of Eiger (Egr), the Drosophila TNF ortholog. Here we show that Bendless (Ben), an E2 ubiquitin-conjugating enzyme, modulates Egr-induced JNK activation and cell death through dTRAF2. Furthermore, Ben physically interacts with dTRAF2 and regulates Egr-induced dTRAF2 polyubiquitination. Finally, Ben is required for JNK-dependent tumor progression, cell migration, oxidative stress resistance and longevity. Our results indicate that Ben constitutes an essential component of the evolutionarily conserved TNF-JNK pathway that modulates cell death and invasion, tumor progression, stress response and lifespan in metazoans.

Indexed as

AnimalsCell DeathCell MovementDrosophilaDrosophila ProteinsFemaleJNK Mitogen-Activated Protein KinasesMaleMAP Kinase Signaling SystemMatrix Metalloproteinase 1Oxidative StressTNF Receptor-Associated Factor 2UbiquitinationUbiquitin-Conjugating Enzymesben protein, DrosophilaDrosophila ProteinsJNK Mitogen-Activated Protein KinasesMatrix Metalloproteinase 1TNF Receptor-Associated Factor 2Ubiquitin-Conjugating Enzymes

Identifiers

PMID24162658
PMCPMC3921588

What OpenQuestion holds

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Registered trials

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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.