about
The major astrocytic phosphoprotein PEA-15 is encoded by two mRNAs conserved on their full length in mouse and humanSIRT2, a multi-talented deacetylaseRegulation of expression of phospholipase D1 and D2 by PEA-15, a novel protein that interacts with themPEA-15 mediates cytoplasmic sequestration of ERK MAP kinaseEndothelin induces a calcium-dependent phosphorylation of PEA-15 in intact astrocytes: identification of Ser104 and Ser116 phosphorylated, respectively, by protein kinase C and calcium/calmodulin kinase II in vitroComparative expression study of the endo-G protein coupled receptor (GPCR) repertoire in human glioblastoma cancer stem-like cells, U87-MG cells and non malignant cells of neural origin unveils new potential therapeutic targetsChemical Library Screening and Structure-Function Relationship Studies Identify Bisacodyl as a Potent and Selective Cytotoxic Agent Towards Quiescent Human Glioblastoma Tumor Stem-Like CellsFunctional analysis of HOXD9 in human gliomas and glioma cancer stem cellsA cell-penetrating peptide based on the interaction between c-Src and connexin43 reverses glioma stem cell phenotype.The multifunctional protein PEA-15 is involved in the control of apoptosis and cell cycle in astrocytes.Data in support of metabolic reprogramming in transformed mouse cortical astrocytes: A proteomic studyClinical relevance of tumor cells with stem-like properties in pediatric brain tumors.CD133, CD15/SSEA-1, CD34 or side populations do not resume tumor-initiating properties of long-term cultured cancer stem cells from human malignant glio-neuronal tumors.The anti-hypertensive drug prazosin inhibits glioblastoma growth via the PKCδ-dependent inhibition of the AKT pathway.An ANOCEF genomic and transcriptomic microarray study of the response to radiotherapy or to alkylating first-line chemotherapy in glioblastoma patients.Keeping TNF-induced apoptosis under control in astrocytes: PEA-15 as a 'double key' on caspase-dependent and MAP-kinase-dependent pathways.Death effector domain protein PEA-15 potentiates Ras activation of extracellular signal receptor-activated kinase by an adhesion-independent mechanismA preclinical mouse model of glioma with an alternative mechanism of telomere maintenance (ALT).Akt down-regulates ERK1/2 nuclear localization and angiotensin II-induced cell proliferation through PEA-15.Endothelial secreted factors suppress mitogen deprivation-induced autophagy and apoptosis in glioblastoma stem-like cells.Phosphoprotein enriched in astrocytes-15 kDa expression inhibits astrocyte migration by a protein kinase C delta-dependent mechanismAstrocytes reverted to a neural progenitor-like state with transforming growth factor alpha are sensitized to cancerous transformation.Connective-Tissue Growth Factor (CTGF/CCN2) Induces Astrogenesis and Fibronectin Expression of Embryonic Neural Cells In Vitro.Absence of the Adaptor Protein PEA-15 Is Associated with Altered Pattern of Th Cytokines Production by Activated CD4+ T Lymphocytes In Vitro, and Defective Red Blood Cell Alloimmune Response In Vivo.Development of a DIPG Orthotopic Model in Mice Using an Implantable Guide-Screw System.Bisacodyl and its cytotoxic activity on human glioblastoma stem-like cells. Implication of inositol 1,4,5-triphosphate receptor dependent calcium signaling.Retinoblastoma protein regulates the crosstalk between autophagy and apoptosis, and favors glioblastoma resistance to etoposide.CHD7 promotes proliferation of neural stem cells mediated by MIF.A driver role for GABA metabolism in controlling stem and proliferative cell state through GHB production in gliomaCritical multiple angiogenic factors secreted by glioblastoma stem-like cells underline the need for combinatorial anti-angiogenic therapeutic strategies.Calcium signaling orchestrates glioblastoma development: Facts and conjunctures.Flavonoids suppress human glioblastoma cell growth by inhibiting cell metabolism, migration, and by regulating extracellular matrix proteins and metalloproteinases expression.Tumorigenic potential of miR-18A* in glioma initiating cells requires NOTCH-1 signaling.The miR 302-367 cluster drastically affects self-renewal and infiltration properties of glioma-initiating cells through CXCR4 repression and consequent disruption of the SHH-GLI-NANOG networkCalcium fingerprints induced by calmodulin interactors in eukaryotic cells.DLG1/SAP97 modulates transforming growth factor alpha bioavailability.The PEA-15/PED protein protects glioblastoma cells from glucose deprivation-induced apoptosis via the ERK/MAP kinase pathway.Cell-based therapy using miR-302-367 expressing cells represses glioblastoma growth.Opposite effects of GCN5 and PCAF knockdowns on the alternative mechanism of telomere maintenance.Fostering responsible research with genome editing technologies: a European perspective.
P50
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P50
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hulumtues
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onderzoeker
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հետազոտող
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name
Hervé Chneiweiss
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Hervé Chneiweiss
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Hervé Chneiweiss
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Hervé Chneiweiss
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Hervé Chneiweiss
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type
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Hervé Chneiweiss
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Hervé Chneiweiss
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Hervé Chneiweiss
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Hervé Chneiweiss
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Hervé Chneiweiss
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prefLabel
Hervé Chneiweiss
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Hervé Chneiweiss
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Hervé Chneiweiss
@es
Hervé Chneiweiss
@nl
Hervé Chneiweiss
@sl
P214
P106
P1153
7005840012
P21
P214
P2798
P31
P496
0000-0001-7675-5061
P569
2000-01-01T00:00:00Z
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P7859
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