Evidence map›Paper›PMID 26263999›Full record

ReviewPharmaceuticals (Basel, Switzerland)2015

On the Quest of Cellular Functions of PEA-15 and the Therapeutic Opportunities.

Yufeng Wei

Open access · goldAbstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025
    Review
  4. CAR T Cell Nanosymbionts: Revealing the Boundless Potential of a New Dyad.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Chimeric antigen receptor T cells form nonclassical and potent immune synapses driving rapid cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2018
    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

1 author at 1 institution in 1 country.

Yufeng WeiDepartment of Chemistry, New Jersery City University, 2039 Kennedy Blvd, Jersey City, NJ 07305, USA. Yufeng.Wei@shu.edu.
New Jersey City University · US

Funding

Conformations and Dynamics of PED/PEA-15 in Protein-Protein InteractionsR15CA179410 · NCI · SETON HALL UNIVERSITY · PI WEI, YUFENG · 2013 to 2013
$330k
NCI NIH HHS R15 CA179410
6 · The paper itself

Abstract

Phosphoprotein enriched in astrocytes, 15 KDa (PEA-15), a ubiquitously expressed small protein in all mammals, is known for decades for its potent interactions with various protein partners along distinct biological pathways. Most notable interacting partners of PEA-15 include extracellular signal-regulated kinase 1 and 2 (ERK1/2) in the mitogen activated protein kinase (MAPK) pathway, the Fas-associated death domain (FADD) protein involving in the formation of the death-inducing signaling complex (DISC), and the phospholipase D1 (PLD1) affecting the insulin sensitivity. However, the actual cellular functions of PEA-15 are still mysterious, and the question why this protein is expressed in almost all cell and tissue types remains unanswered. Here we synthesize the most recent structural, biological, and clinical studies on PEA-15 with emphases on its anti-apoptotic, anti-proliferative, and anti-inflammative properties, and propose a converged protective role of PEA-15 that maintains the balance of death and survival in different cell types. Under conditions that this delicate balance is unsustainable, PEA-15 may become pathological and lead to various diseases, including cancers and diabetes. Targeting PEA-15 interactions, or the use of PEA-15 protein as therapeutics, may provide a wider window of opportunities to treat these diseases.

Indexed as

apoptosisMAP kinasePEA-15phosphorylationprotein-protein interaction

Identifiers

PMID26263999
PMCPMC4588177
OpenAlexW1636180567

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.