ArticleSmall GTPases
Phosphorylation is the switch that turns PEA-15 from tumor suppressor to tumor promoter.
Article in Small GTPases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Article
- The Complex Role of Chaperone-Mediated Autophagy in Cancer Diseases.Biomedicines · 2023Review
- Discovery of pathway-independent protein signatures associated with clinical outcome in human cancer cohorts.Scientific reports · 2022Article
- PEA-15 engages in allosteric interactions using a common scaffold in a phosphorylation-dependent manner.Scientific reports · 2022Article
- Ago-RIP Sequencing Identifies New MicroRNA-449a-5p Target Genes Increasing Sorafenib Efficacy in Hepatocellular Carcinoma.Journal of Cancer · 2022Article
- Article
- The microRNA212 regulated PEA15 promotes ovarian cancer progression by inhibiting of apoptosis.Journal of Cancer · 2020Article
- PEA-15 C-Terminal Tail Allosterically Modulates Death-Effector Domain Conformation and Facilitates Protein-Protein Interactions.International journal of molecular sciences · 2019Article
- PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway.Oncology reports · 2019Article
- Astroglial role in the pathophysiology of statusOncotarget · 2018Review
- Circadian expression and functional characterization of PEA-15 within the mouse suprachiasmatic nucleus.The European journal of neuroscience · 2018Article
- Phosphoprotein enriched in diabetes (PED/PEA15) promotes migration in hepatocellular carcinoma and confers resistance to sorafenib.Cell death & disease · 2017Article
- PEA-15 (Phosphoprotein Enriched in Astrocytes 15) Is a Protective Mediator in the Vasculature and Is Regulated During Neointimal Hyperplasia.Journal of the American Heart Association · 2017Article
- Next-Generation CDK2/9 Inhibitors and Anaphase Catastrophe in Lung Cancer.Journal of the National Cancer Institute · 2017Article
- Effects of anti-depressant treatments on FADD and p-FADD protein in rat brain cortex: enhanced anti-apoptotic p-FADD/FADD ratio after chronic desipramine and fluoxetine administration.Psychopharmacology · 2016Article
- Integrin α5β1 and p53 convergent pathways in the control of anti-apoptotic proteins PEA-15 and survivin in high-grade glioma.Cell death and differentiation · 2016Article
- On the Quest of Cellular Functions of PEA-15 and the Therapeutic Opportunities.Pharmaceuticals (Basel, Switzerland) · 2015Review
- Development of PEA-15 using a potent non-viral vector for therapeutic application in breast cancer.Cancer letters · 2015Article
- Phosphorylation-regulated degradation of the tumor-suppressor form of PED by chaperone-mediated autophagy in lung cancer cells.Journal of cellular physiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Abnormal ERK signaling is implicated in many human diseases including cancer. This signaling cascade is a good target for the therapy of certain malignancies because of its important role in regulating cell proliferation and survival. The small phosphoprotein PEA-15 is a potent regulator of the ERK signaling cascade, and, by acting on this pathway, has been described to have both tumor-suppressor and tumor-promoter functions. However, the exact mechanism by which PEA-15 drives the outcome one way or the other remains unclear. We propose that the cellular environment is crucial in determining PEA-15 protein function by affecting the protein's phosphorylation state. We hypothesize that only unphosphorylated PEA-15 can act as a tumor-suppressor and that phosphorylation alters the interaction with binding partners to promote tumor development. In order to use PEA-15 as a prognostic marker or therapeutic target it is therefore important to evaluate its phosphorylation status.
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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.