Evidence map›Paper›PMID 29870719›Full record

ArticleDevelopmental cell2018

A Drosophila Tumor Suppressor Gene Prevents Tonic TNF Signaling through Receptor N-Glycosylation.

Geert de Vreede, Holly A Morrison, Alexandra M Houser, Ryan M Boileau, Ditte Andersen, Julien Colombani, David Bilder

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 77 citations in OpenAlex.

  1. iScience · 2026
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  5. Journal of proteome research · 2024
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  8. An Efficient and EconomicalMetabolites · 2022
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  14. Review
  15. Article
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  17. Article
  18. Separation of PermethylatedMetabolites · 2020
    Article
  19. Article
  20. 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

7 authors at 2 institutions in 2 countries.

Geert de VreedeDepartment of Molecular and Cell Biology, University of California-Berkeley, Berkeley, CA 94720, USA.
Holly A MorrisonDepartment of Molecular and Cell Biology, University of California-Berkeley, Berkeley, CA 94720, USA.
Alexandra M HouserDepartment of Molecular and Cell Biology, University of California-Berkeley, Berkeley, CA 94720, USA.
Ryan M BoileauDepartment of Molecular and Cell Biology, University of California-Berkeley, Berkeley, CA 94720, USA.
Ditte AndersenUniversity Nice Sophia Antipolis, CNRS, Inserm, iBV, Nice 06108, France.
Julien ColombaniUniversity Nice Sophia Antipolis, CNRS, Inserm, iBV, Nice 06108, France.
David BilderDepartment of Molecular and Cell Biology, University of California-Berkeley, Berkeley, CA 94720, USA. Electronic address: bilder@berkeley.edu.
University of California, Berkeley · USInserm · FR

Funding

Mechanisms of Drosophila Tumor SuppressionR01GM090150 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI BILDER, DAVID · 2010 to 2018
$2.0M
NIGMS NIH HHS R01 GM090150
6 · The paper itself

Abstract

Drosophila tumor suppressor genes have revealed molecular pathways that control tissue growth, but mechanisms that regulate mitogenic signaling are far from understood. Here we report that the Drosophila TSG tumorous imaginal discs (tid), whose phenotypes were previously attributed to mutations in a DnaJ-like chaperone, are in fact driven by the loss of the N-linked glycosylation pathway component ALG3. tid/alg3 imaginal discs display tissue growth and architecture defects that share characteristics of both neoplastic and hyperplastic mutants. Tumorous growth is driven by inhibited Hippo signaling, induced by excess Jun N-terminal kinase (JNK) activity. We show that ectopic JNK activation is caused by aberrant glycosylation of a single protein, the fly tumor necrosis factor (TNF) receptor homolog, which results in increased binding to the continually circulating TNF. Our results suggest that N-linked glycosylation sets the threshold of TNF receptor signaling by modifying ligand-receptor interactions and that cells may alter this modification to respond appropriately to physiological cues.

Indexed as

Genes, Tumor SuppressorAnimalsCell ProliferationDrosophila melanogasterDrosophila ProteinsFemaleGlycosylationHippo KinasesImaginal DiscsIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMaleMutationPhenotypeProtein Serine-Threonine KinasesReceptors, Tumor Necrosis FactorDrosophila ProteinsHippo Kinaseshpo protein, DrosophilaIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesReceptors, Tumor Necrosis FactorDrosophilaEigerGrindelwaldHippoJNK signalingN-linked glycosylationTNFTNFRTNF-αtumor suppressor

Identifiers

PMID29870719
PMCPMC5995582
OpenAlexW2805722079

What OpenQuestion holds

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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.