Evidence map›Paper›PMID 25545884›Full record

ReviewCancers2014

Regulation of the Tumor-Suppressor Function of the Class III Phosphatidylinositol 3-Kinase Complex by Ubiquitin and SUMO.

Christina Reidick, Fouzi El Magraoui, Helmut E Meyer, Harald Stenmark, Harald W Platta

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Autophagy regulator Atg9 is degraded by the proteasome.Biochemical and biophysical research communications · 2020
    Article
  9. Review
  10. Article
  11. Ubiquitin signaling and autophagy.The Journal of biological chemistry · 2018
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. 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

5 authors at 3 institutions in 2 countries.

Christina ReidickBiochemie Intrazellulärer Transportprozesse, Ruhr-Universität Bochum, Bochum 44801, Germany. christina.reidick@rub.de.
Fouzi El MagraouiBiomedical Research, Human Brain Proteomics II, Leibniz-Institut für Analytische Wissenschaften-ISAS, Dortmund 44139, Germany. fouzi.elmagraoui@isas.de.
Helmut E MeyerBiomedical Research, Human Brain Proteomics II, Leibniz-Institut für Analytische Wissenschaften-ISAS, Dortmund 44139, Germany. helmut.e.meyer@isas.de.
Harald StenmarkDepartment of Biochemistry, Institute for Cancer Research, Oslo University Hospital, Montebello, Oslo 0310, Norway. stenmark@ulrik.uio.no.
Harald W PlattaBiochemie Intrazellulärer Transportprozesse, Ruhr-Universität Bochum, Bochum 44801, Germany. harald.platta@rub.de.
Leibniz Institute for Analytical Sciences - ISAS · DERuhr University Bochum · DEOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The occurrence of cancer is often associated with a dysfunction in one of the three central membrane-involution processes-autophagy, endocytosis or cytokinesis. Interestingly, all three pathways are controlled by the same central signaling module: the class III phosphatidylinositol 3-kinase (PI3K-III) complex and its catalytic product, the phosphorylated lipid phosphatidylinositol 3-phosphate (PtdIns3P). The activity of the catalytic subunit of the PI3K-III complex, the lipid-kinase VPS34, requires the presence of the membrane-targeting factor VPS15 as well as the adaptor protein Beclin 1. Furthermore, a growing list of regulatory proteins associates with VPS34 via Beclin 1. These accessory factors define distinct subunit compositions and thereby guide the PI3K-III complex to its different cellular and physiological roles. Here we discuss the regulation of the PI3K-III complex components by ubiquitination and SUMOylation. Especially Beclin 1 has emerged as a highly regulated protein, which can be modified with Lys11-, Lys48- or Lys63-linked polyubiquitin chains catalyzed by distinct E3 ligases from the RING-, HECT-, RBR- or Cullin-type. We also point out other cross-links of these ligases with autophagy in order to discuss how these data might be merged into a general concept.

Identifiers

PMID25545884
PMCPMC4381249
OpenAlexW2065095569

What Socratic 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 Socratic graph.