Evidence map›Paper›PMID 20452983›Full record

ArticleThe Journal of biological chemistry2010

The PEA-15 protein regulates autophagy via activation of JNK.

Barbara C Böck, Katrin E Tagscherer, Anne Fassl, Anika Krämer, Ina Oehme, Hans-Walter Zentgraf, Martina Keith, Wilfried Roth

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Article
  4. Article
  5. Article
  6. Role of the MAPK/cJun NHAutophagy · 2018
    Article
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  8. Unbiased phosphoproteomic method identifies the initial effects of a methacrylic acid copolymer on macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. The inhibitory effect of ellagic Acid on cell growth of ovarian carcinoma cells.Evidence-based complementary and alternative medicine : eCAM · 2013
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

8 authors at 3 institutions in 2 countries.

Barbara C BöckDepartments of Molecular Neuro-Oncology, German Cancer Research Center DKFZ, 69120 Heidelberg, Germany.
Katrin E Tagscherer
Anne Fassl
Anika Krämer
Ina Oehme
Hans-Walter Zentgraf
Martina Keith
Wilfried Roth
German Cancer Research Center · DEHeidelberg University · DEPediatric Oncology Group · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PEA-15/PED (phosphoprotein enriched in astrocytes 15 kDa/phosphoprotein enriched in diabetes) is a death effector domain-containing protein which is known to modulate apoptotic cell death. The mechanism by which PEA-15 inhibits caspase activation and increases ERK (extracellular-regulated kinase) activity is well characterized. Here, we demonstrate that PEA-15 is not only pivotal in the activation of the ERK pathway but also modulates JNK (c-Jun N-terminal kinase) signaling. Upon overexpression of PEA-15 in malignant glioma cells, JNK is potently activated. The PEA-15-induced JNK activation depends on the phosphorylation of PEA-15 at both phosphorylation sites (serine 104 and serine 116). The activation of JNK is substantially inhibited by siRNA-mediated down-regulation of endogenous PEA-15. Moreover, we demonstrate that glioma cells overexpressing PEA-15 show increased signs of autophagy in response to classical autophagic stimuli such as ionizing irradiation, serum deprivation, or rapamycin treatment. In contrast, the non-phosphorylatable mutants of PEA-15 are not capable of promoting autophagy. The inhibition of JNK abrogates the PEA-15-mediated increase in autophagy. In conclusion, our data show that PEA-15 promotes autophagy in glioma cells in a JNK-dependent manner. This might render glioma cells more resistant to adverse stimuli such as starvation or ionizing irradiation.

Indexed as

AutophagyGene Expression Regulation, NeoplasticApoptosisApoptosis Regulatory ProteinsBrain NeoplasmsCell Line, TumorExtracellular Signal-Regulated MAP KinasesFlow CytometryGliomaHumansIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesModels, BiologicalPhosphoproteinsPhosphorylationRNA, Small InterferingApoptosis Regulatory ProteinsExtracellular Signal-Regulated MAP KinasesIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesPEA15 protein, humanPhosphoproteinsRNA, Small Interfering

Identifiers

PMID20452983
PMCPMC2898427
OpenAlexW2072522514

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.