ArticleMolecular bioSystems2010
Phosphotyrosine signaling analysis of site-specific mutations on EGFRvIII identifies determinants governing glioblastoma cell growth.
Article in Molecular bioSystems, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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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.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Identifying and exploiting combinatorial synthetic lethality by characterizing adaptive kinome rewiring of EGFRvIII-driven glioblastoma.Acta neuropathologica communications · 2025Article
- Current Research Trends in Glioblastoma: Focus on Receptor Tyrosine Kinases.International journal of molecular sciences · 2025Review
- Hypoxia Induced Lnc191 Upregulation Dictates the Progression of Esophageal Squamous Cell Carcinoma by Activating GRP78/ERK Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Characterization of Phosphorylated Peptides by Electron-Activated and Ultraviolet Dissociation Mass Spectrometry: A Comparative Study with Collision-Induced Dissociation.Journal of the American Society for Mass Spectrometry · 2024Article
- Article
- Phosphoproteomics: a valuable tool for uncovering molecular signaling in cancer cells.Expert review of proteomics · 2021Review
- Quantitative phosphoproteomics uncovers dysregulated kinase networks in Alzheimer's disease.Nature aging · 2021Article
- EGFRJournal of oncology · 2019Review
- Review
- Cell line with endogenous EGFRvIII expression is a suitable model for research and drug development purposes.Oncotarget · 2016Article
- Emerging Proteomic Technologies Provide Enormous and Underutilized Potential for Brain Cancer Research.Molecular & cellular proteomics : MCP · 2016Review
- Inhibition of oncogenic epidermal growth factor receptor kinase triggers release of exosome-like extracellular vesicles and impacts their phosphoprotein and DNA content.The Journal of biological chemistry · 2015Article
- Significance of filamin A in mTORC2 function in glioblastoma.Molecular cancer · 2015Article
- Phosphotyrosine signaling analysis in human tumors is confounded by systemic ischemia-driven artifacts and intra-specimen heterogeneity.Cancer research · 2015Article
- Evaluation of phosphopeptide enrichment strategies for quantitative TMT analysis of complex network dynamics in cancer-associated cell signalling.EuPA open proteomics · 2015Article
- Quantitative proteomic analysis reveals effects of epidermal growth factor receptor (EGFR) on invasion-promoting proteins secreted by glioblastoma cells.Molecular & cellular proteomics : MCP · 2014Article
- System level dynamics of post-translational modifications.Current opinion in biotechnology · 2014Review
- Suppression of microRNA-9 by mutant EGFR signaling upregulates FOXP1 to enhance glioblastoma tumorigenicity.Cancer research · 2014Article
- Epithelial wounds induce differential phosphorylation changes in response to purinergic and EGF receptor activation.The American journal of pathology · 2013Article
- Molecular network analysis of phosphotyrosine and lipid metabolism in hepatic PTP1b deletion mice.Integrative biology : quantitative biosciences from nano to macro · 2013Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
To evaluate the role of individual EGFR phosphorylation sites in activating components of the cellular signaling network we have performed a mass spectrometry-based analysis of the phosphotyrosine network downstream of site-specific EGFRvIII mutants, enabling quantification of network-level effects of site-specific point mutations. Mutation at Y845, Y1068 or Y1148 resulted in diminished receptor phosphorylation, while mutation at Y1173 led to increased phosphorylation on multiple EGFRvIII residues. Altered phosphorylation at the receptor was recapitulated in downstream signaling network activation levels, with Y1173F mutation leading to increased phosphorylation throughout the network. Computational modeling of GBM cell growth as a function of network phosphorylation levels highlights the Erk pathway as crucial for regulating EGFRvIII-driven U87MG GBM cell behavior, with the unexpected finding that Erk1/2 is negatively correlated to GBM cell growth. Genetic manipulation of this pathway supports the model, demonstrating that EGFRvIII-expressing U87MG GBM cells are sensitive to Erk activation levels. Additionally, we developed a model describing glioblastoma cell growth based on a reduced set of phosphoproteins, which represent potential candidates for future development as therapeutic targets for EGFRvIII-positive glioblastoma patients.
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What OpenQuestion holds
Registered trials
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.