ArticleMolecular biology of the cell2006
Phosphoprotein enriched in astrocytes-15 kDa expression inhibits astrocyte migration by a protein kinase C delta-dependent mechanism.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 51 citations in OpenAlex.
- Glioblastoma cell motility depends on enhanced oxidative stress coupled with mobilization of a sulfurtransferase.Cell death & disease · 2022Article
- Proteomics analysis identifies PEA-15 as an endosomal phosphoprotein that regulates α5β1 integrin endocytosis.Scientific reports · 2021Article
- S100B Protein Stimulates Proliferation and Angiogenic Mediators Release through RAGE/pAkt/mTOR Pathway in Human Colon Adenocarcinoma Caco-2 Cells.International journal of molecular sciences · 2019Article
- Chaperone-mediated autophagy substrate proteins in cancer.Oncotarget · 2017Review
- S100B-p53 disengagement by pentamidine promotes apoptosis and inhibits cellular migration via aquaporin-4 and metalloproteinase-2 inhibition in C6 glioma cells.Oncology letters · 2015Article
- RhoGDI2 expression in astrocytes after an excitotoxic lesion in the mouse hippocampus.Cellular and molecular neurobiology · 2015Article
- Phosphoprotein enriched in astrocytes (PEA)-15: a potential therapeutic target in multiple disease states.Pharmacology & therapeutics · 2014Review
- RSK2 protein suppresses integrin activation and fibronectin matrix assembly and promotes cell migration.The Journal of biological chemistry · 2012Article
- PEA15 impairs cell migration and correlates with clinical features predicting good prognosis in neuroblastoma.International journal of cancer · 2012Article
- PED/PEA-15 induces autophagy and mediates TGF-beta1 effect on muscle cell differentiation.Cell death and differentiation · 2012Article
- PED/PEA-15 interacts with the 67 kD laminin receptor and regulates cell adhesion, migration, proliferation and apoptosis.Journal of cellular and molecular medicine · 2012Article
- PED/PEA-15 controls fibroblast motility and wound closure by ERK1/2-dependent mechanisms.Journal of cellular physiology · 2012Article
- Characterization of a MAPK scaffolding protein logic gate in gonadotropes.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Expression of phosphoprotein enriched in astrocytes 15 kDa (PEA-15) in astrocytic tumors: a novel approach of correlating malignancy grade and prognosis.Journal of neuro-oncology · 2010Article
- The PEA-15 protein regulates autophagy via activation of JNK.The Journal of biological chemistry · 2010Article
- PTPmu suppresses glioma cell migration and dispersal.Neuro-oncology · 2009Article
- PEA-15 induces autophagy in human ovarian cancer cells and is associated with prolonged overall survival.Cancer research · 2008Article
- The PEA-15/PED protein protects glioblastoma cells from glucose deprivation-induced apoptosis via the ERK/MAP kinase pathway.Oncogene · 2008Article
- Transient down-regulation of beta1 integrin subtypes on kidney carcinoma cells is induced by mechanical contact with endothelial cell membranes.Journal of cellular and molecular medicineArticle
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Phosphoprotein enriched in astrocytes-15 kDa (PEA-15), a phosphoprotein enriched in astrocytes, inhibits both apoptosis and proliferation in normal and cancerous cells. Here, analysis of PEA-15 expression in glioblastoma organotypic cultures revealed low levels of PEA-15 in tumor cells migrating away from the explants, regardless of the expression levels in the originating explants. Because glioblastomas are highly invasive primary brain tumors that can originate from astrocytes, we explored the involvement of PEA-15 in the control of astrocyte migration. PEA-15-/- astrocytes presented an enhanced motility in vitro compared with their wild-type counterparts. Accordingly, NIH-3T3 cells transfected by green fluorescent protein-PEA-15 displayed a reduced migration. Reexpression of PEA-15 restored PEA-15-/- astrocyte motility to wild-type levels. Pharmacological manipulations excluded a participation of extracellular signal-regulated kinase/mitogen-activated protein kinase, phosphatidylinositol 3-kinase/Akt, and calcium/calmodulin-dependent protein kinase II in this effect of PEA-15. In contrast, treatment by bisindolylmaleimide, Gö6976, and rottlerin, and chronic application of phorbol 12-myristate 13-acetate and/or bryostatin-1 indicated that PKC delta mediated PEA-15 inhibition of astrocyte migration. PEA-15-/- astrocytes constitutively expressed a 40-kDa form of PKC delta that was down-regulated upon PEA-15 reexpression. Together, these data reveal a new function for PEA-15 in the inhibitory control of astrocyte motility through a PKC delta-dependent pathway involving the constitutive expression of a catalytic fragment of PKC delta.
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