ArticleMolecular bioSystems2009
An integrated comparative phosphoproteomic and bioinformatic approach reveals a novel class of MPM-2 motifs upregulated in EGFRvIII-expressing glioblastoma cells.
Article in Molecular bioSystems, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Phosphorylation regulates the chromatin remodeler SMARCAD1 in nucleosome binding, ATP hydrolysis, and histone exchange.The Journal of biological chemistry · 2024Article
- Phosphoproteomics identifies microglial Siglec-F inflammatory response during neurodegeneration.Molecular systems biology · 2020Article
- CaCold Spring Harbor perspectives in biology · 2019Review
- Substrate-based kinase activity inference identifies MK2 as driver of colitis.Integrative biology : quantitative biosciences from nano to macro · 2019Article
- Review
- CK2 in Cancer: Cellular and Biochemical Mechanisms and Potential Therapeutic Target.Pharmaceuticals (Basel, Switzerland) · 2017Review
- ProteomeScout: a repository and analysis resource for post-translational modifications and proteins.Nucleic acids research · 2015Article
- A microphysiological system model of therapy for liver micrometastases.Experimental biology and medicine (Maywood, N.J.) · 2014Review
- Casein Kinase 2: a novel player in glioblastoma therapy and cancer stem cells.Journal of molecular and genetic medicine : an international journal of biomedical research · 2013Article
- Targeting protein kinase CK2 suppresses prosurvival signaling pathways and growth of glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Quantitative phospho-proteomics to investigate the polo-like kinase 1-dependent phospho-proteome.Molecular & cellular proteomics : MCP · 2011Article
- MCAM: multiple clustering analysis methodology for deriving hypotheses and insights from high-throughput proteomic datasets.PLoS computational biology · 2011Article
- Ca2+ signaling during mammalian fertilization: requirements, players, and adaptations.Cold Spring Harbor perspectives in biology · 2011Review
- Phosphoproteomics in cancer.Molecular oncology · 2010Review
- Phosphoproteomics-based modeling defines the regulatory mechanism underlying aberrant EGFR signaling.PloS one · 2010Article
- PTMScout, a Web resource for analysis of high throughput post-translational proteomics studies.Molecular & cellular proteomics : MCP · 2010Article
- Phosphotyrosine signaling analysis of site-specific mutations on EGFRvIII identifies determinants governing glioblastoma cell growth.Molecular bioSystems · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM, WHO grade IV) is an aggressively proliferative and invasive brain tumor that carries a poor clinical prognosis with a median survival of 9 to 12 months. In a prior phosphoproteomic study performed in the U87MG glioblastoma cell line, we identified tyrosine phosphorylation events that are regulated as a result of titrating EGFRvIII, a constitutively active mutant of the epidermal growth factor receptor (EGFR) associated with poor prognosis in GBM patients. In the present study, we have used the phosphoserine/phosphothreonine-specific antibody MPM-2 (mitotic protein monoclonal #2) to quantify serine/threonine phosphorylation events in the same cell lines. By employing a bioinformatic tool to identify amino acid sequence motifs regulated in response to increasing oncogene levels, a set of previously undescribed MPM-2 epitope sequence motifs orthogonal to the canonical "pS/pT-P" motif was identified. These motifs contain acidic amino acids in combinations of the -5, -2, +1, +3, and +5 positions relative to the phosphorylated amino acid. Phosphopeptides containing these motifs are upregulated in cells expressing EGFRvIII, raising the possibility of a general role for a previously unrecognized acidophilic kinase (e.g. casein kinase II (CK2)) in cell proliferation downstream of EGFR signaling.
Indexed as
Identifiers
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.