ArticleProceedings of the National Academy of Sciences of the United States of America2009
Multiple myeloma phosphotyrosine proteomic profile associated with FGFR3 expression, ligand activation, and drug inhibition.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. 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, 48 citations in OpenAlex.
- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- Article
- Ex vivo drug response heterogeneity reveals personalized therapeutic strategies for patients with multiple myeloma.Nature cancer · 2023Article
- Simultaneous multiple myeloma and non-small cell lung carcinoma: A case report and review of the literature.Oncology letters · 2022Article
- Responses of Epibranchial Placodes to Disruptions of the FGF and BMP Signaling Pathways in Embryonic Mice.Frontiers in cell and developmental biology · 2021Article
- Proteomics-inspired precision medicine for treating and understanding multiple myeloma.Expert review of precision medicine and drug development · 2020Article
- Clinical prognostic implications of EPB41L4A expression in multiple myeloma.Journal of Cancer · 2020Article
- Review
- Overcoming multiple myeloma drug resistance in the era of cancer 'omics'.Leukemia & lymphoma · 2018Review
- Peripherally derived FGF21 promotes remyelination in the central nervous system.The Journal of clinical investigation · 2017Article
- LMP1 signaling pathway activates IRF4 in latent EBV infection and a positive circuit between PI3K and Src is required.Oncogene · 2017Article
- Review
- Article
- Tyrosine phosphorylation of the Lyn Src homology 2 (SH2) domain modulates its binding affinity and specificity.Molecular & cellular proteomics : MCP · 2015Article
- Differential regulation of FGFR3 by PTPN1 and PTPN2.Proteomics · 2015Article
- Retroviral retention activates a Syk-dependent HemITAM in human tetherin.Cell host & microbe · 2014Article
- Interferon regulatory factor 4 is activated through c-Src-mediated tyrosine phosphorylation in virus-transformed cells.Journal of virology · 2013Article
- Identification of alternatively translated Tetherin isoforms with differing antiviral and signaling activities.PLoS pathogens · 2012Article
- FGF and ERK signaling coordinately regulate mineralization-related genes and play essential roles in osteocyte differentiation.Journal of bone and mineral metabolism · 2012Article
- Comparison of three quantitative phosphoproteomic strategies to study receptor tyrosine kinase signaling.Journal of proteome research · 2011Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Signaling by growth factor receptor tyrosine kinases is manifest through networks of proteins that are substrates and/or bind to the activated receptors. FGF receptor-3 (FGFR3) is a drug target in a subset of human multiple myelomas (MM) and is mutationally activated in some cervical and colon and many bladder cancers and in certain skeletal dysplasias. To define the FGFR3 network in multiple myeloma, mass spectrometry was used to identify and quantify phosphotyrosine (pY) sites modulated by FGFR3 activation and inhibition in myeloma-derived KMS11 cells. Label-free quantification of peptide ion currents indicated the activation of FGFR3 by phosphorylation of tandem tyrosines in the kinase domain activation loop when cellular pY phosphatases were inhibited by pervanadate. Among the 175 proteins that accumulated pY in response to pervanadate was a subset of 52 including FGFR3 that contained a total of 61 pY sites that were sensitive to inhibition by the FGFR3 inhibitor PD173074. The FGFR3 isoform containing the tandem pY motif in its activation loop was targeted by PD173074. Forty of the drug-sensitive pY sites, including two located within the 35-residue cytoplasmic domain of the transmembrane growth factor binding proteoglycan (and multiple myeloma biomarker) Syndecan-1/CD138, were also stimulated in cells treated with the ligand FGF1, providing additional validation of their link to FGFR3. The identification of these overlapping sets of co-modulated tyrosine phosphorylations presents an outline of an FGFR3 network in the MM model and demonstrates the potential for pharmacodynamic monitoring by label-free quantitative phospho-proteomics.
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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.