Evidence map›Paper›PMID 21829386›Full record

ArticlePLoS genetics2011

MK2-dependent p38b signalling protects Drosophila hindgut enterocytes against JNK-induced apoptosis under chronic stress.

Gerhard Seisenbacher, Ernst Hafen, Hugo Stocker

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

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  13. ADisease models & mechanisms · 2017
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  15. Regulation of Hippo signalling by p38 signalling.Journal of molecular cell biology · 2016
    Article
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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

3 authors at 2 institutions in 1 country.

Gerhard SeisenbacherInstitute of Molecular Systems Biology, Swiss Federal Institute of Technology Zurich (ETH Zurich), Zurich, Switzerland.
Ernst Hafen
Hugo Stocker
ETH Zurich · CHCenter for Pediatric Endocrinology Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The integrity of the intestinal epithelium is crucial for the barrier function of the gut. Replenishment of the gut epithelium by intestinal stem cells contributes to gut homeostasis, but how the differentiated enterocytes are protected against stressors is less well understood. Here we use the Drosophila larval hindgut as a model system in which damaged enterocytes are not replaced by stem cell descendants. By performing a thorough genetic analysis, we demonstrate that a signalling complex consisting of p38b and MK2 forms a branch of SAPK signalling that is required in the larval hindgut to prevent stress-dependent damage to the enterocytes. Impaired p38b/MK2 signalling leads to apoptosis of the enterocytes and a subsequent loss of hindgut epithelial integrity, as manifested by the deterioration of the overlaying muscle layer. Damaged hindguts show increased JNK activity, and removing upstream activators of JNK suppresses the loss of hindgut homeostasis. Thus, the p38/MK2 complex ensures homeostasis of the hindgut epithelium by counteracting JNK-mediated apoptosis of the enterocytes upon chronic stress.

Indexed as

ApoptosisMAP Kinase Signaling SystemStress, PhysiologicalAnimalsDrosophilaEnterocytesFemaleIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMAP-Kinase-Activated Kinase 2Mitogen-Activated Protein Kinase 11MutationPhosphorylationProtein BindingProtein Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMAP-Kinase-Activated Kinase 2Mitogen-Activated Protein Kinase 11Protein Serine-Threonine Kinases

Identifiers

PMID21829386
PMCPMC3150449
OpenAlexW2072894391

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.