Evidence map›Paper›PMID 21445266›Full record

ArticlePloS one2011

Proteomic identification of protein targets for 15-deoxy-Δ(12,14)-prostaglandin J2 in neuronal plasma membrane.

Yasuhiro Yamamoto, Kenkichi Takase, Junji Kishino, Megumi Fujita, Noboru Okamura, Toshiyuki Sakaeda, Masafumi Fujimoto, Tatsurou Yagami

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 38 citations in OpenAlex.

  1. Impact ofCells · 2024
    Article
  2. Article
  3. Article
  4. Article
  5. Cyclooxygenase-2 Induced the β-Amyloid Protein Deposition and Neuronal Apoptosis Via Upregulating the Synthesis of Prostaglandin ENeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Treatment of etoposide combined with 15-deoxy-ΔMolecular and clinical oncology · 2014
    Article
  14. Review
  15. Article
  16. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Yasuhiro YamamotoDivision of Physiology, Department of Pharmaceutical Health Care, Faculty of Pharmaceutical Sciences, Himeji Dokkyo University, Himeji, Japan.
Kenkichi Takase
Junji Kishino
Megumi Fujita
Noboru Okamura
Toshiyuki Sakaeda
Masafumi Fujimoto
Tatsurou Yagami
Himeji Dokkyo University · JPShionogi (Japan) · JPChiba Institute of Science · JPKyoto University · JPMukogawa Women's University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

15-deoxy-Δ(12,14)-prostaglandin J(2) (15d-PGJ(2)) is one of factors contributed to the neurotoxicity of amyloid β (Aβ), a causative protein of Alzheimer's disease. Type 2 receptor for prostaglandin D(2) (DP2) and peroxysome-proliferator activated receptorγ (PPARγ) are identified as the membrane receptor and the nuclear receptor for 15d-PGJ(2), respectively. Previously, we reported that the cytotoxicity of 15d-PGJ(2) was independent of DP2 and PPARγ, and suggested that 15d-PGJ(2) induced apoptosis through the novel specific binding sites of 15d-PGJ(2) different from DP2 and PPARγ. To relate the cytotoxicity of 15d-PGJ(2) to amyloidoses, we performed binding assay [(3)H]15d-PGJ(2) and specified targets for 15d-PGJ(2) associated with cytotoxicity. In the various cell lines, there was a close correlation between the susceptibilities to 15d-PGJ(2) and fibrillar Aβ. Specific binding sites of [(3)H]15d-PGJ(2) were detected in rat cortical neurons and human bronchial smooth muscle cells. When the binding assay was performed in subcellular fractions of neurons, the specific binding sites of [(3)H]15d-PGJ(2) were detected in plasma membrane, nuclear and cytosol, but not in microsome. A proteomic approach was used to identify protein targets for 15d-PGJ(2) in the plasma membrane. By using biotinylated 15d-PGJ(2), eleven proteins were identified as biotin-positive spots and classified into three different functional proteins: glycolytic enzymes (Enolase2, pyruvate kinase M1 (PKM1) and glyceraldehyde 3-phosphate dehydrogenase (GAPDH)), molecular chaperones (heat shock protein 8 and T-complex protein 1 subunit α), cytoskeletal proteins (Actin β, F-actin-capping protein, Tubulin β and Internexin α). GAPDH, PKM1 and Tubulin β are Aβ-interacting proteins. Thus, the present study suggested that 15d-PGJ(2) plays an important role in amyloidoses not only in the central nervous system but also in the peripheral tissues.

Indexed as

ProteomicsAmino Acid SequenceAnimalsBinding SitesBlotting, WesternCell MembraneCells, CulturedElectrophoresis, Gel, Two-DimensionalHumansInhibitory Concentration 50Lethal Dose 50Molecular Sequence DataNeuronsProstaglandin D2ProteinsRats15-deoxy-delta(12,14)-prostaglandin J2Prostaglandin D2Proteins

Identifiers

PMID21445266
PMCPMC3060826
OpenAlexW2025405611

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.