ArticleThe Journal of biological chemistry2010
Critical role of the platelet-derived growth factor receptor (PDGFR) beta transmembrane domain in the TEL-PDGFRbeta cytosolic oncoprotein.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Case of crypticLeukemia research reports · 2023Article
- Activation of the PDGF β Receptor by a Persistent Artificial Signal Peptide.Journal of molecular biology · 2021Article
- Molecular Pathogenesis and Treatment Perspectives for Hypereosinophilia and Hypereosinophilic Syndromes.International journal of molecular sciences · 2021Review
- Deregulation of kinase signaling and lymphoid development in EBF1-PDGFRB ALL leukemogenesis.Leukemia · 2018Article
- PDGF-induced fibroblast growth requires monounsaturated fatty acid production by stearoyl-CoA desaturase.FEBS open bio · 2017Article
- Article
- Idiopathic basal ganglia calcification-associated PDGFRB mutations impair the receptor signalling.Journal of cellular and molecular medicine · 2015Article
- Article
- The tyrosine phosphatase SHP2 is required for cell transformation by the receptor tyrosine kinase mutants FIP1L1-PDGFRα and PDGFRα D842V.Molecular oncology · 2014Article
- Targeting the PDGF signaling pathway in tumor treatment.Cell communication and signaling : CCS · 2013Review
- Structural and functional properties of platelet-derived growth factor and stem cell factor receptors.Cold Spring Harbor perspectives in biology · 2013Review
- Review of current classification, molecular alterations, and tyrosine kinase inhibitor therapies in myeloproliferative disorders with hypereosinophilia.Journal of blood medicine · 2013Article
- ETV6-PDGFRB and FIP1L1-PDGFRA stimulate human hematopoietic progenitor cell proliferation and differentiation into eosinophils: the role of nuclear factor-κB.Haematologica · 2012Article
- Macropinocytosis of the PDGF β-receptor promotes fibroblast transformation by H-RasG12V.Molecular biology of the cell · 2012Article
- Autocrine PDGF stimulation in malignancies.Upsala journal of medical sciences · 2012Review
- Tyrosine kinase gene fusions in cancer: translating mechanisms into targeted therapies.Journal of cellular and molecular medicine · 2012Review
- Platelet-derived growth factors and their receptors in normal and malignant hematopoiesis.American journal of blood research · 2012Article
- Multiple oligomerization domains of KANK1-PDGFRβ are required for JAK2-independent hematopoietic cell proliferation and signaling via STAT5 and ERK.Haematologica · 2011Article
- Stimulation of platelet-derived growth factor receptor beta (PDGFRbeta) activates ADAM17 and promotes metalloproteinase-dependent cross-talk between the PDGFRbeta and epidermal growth factor receptor (EGFR) signaling pathways.The Journal of biological chemistry · 2010Article
- Complex Genetic Evolution and Treatment Challenges in Myeloid Neoplasms: A Case of Persistent t(2;3)(p15~23;q26)/Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fusion of TEL with platelet-derived growth factor receptor (PDGFR) beta (TPbeta) is found in a subset of patients with atypical myeloid neoplasms associated with eosinophilia and is the archetype of a larger group of hybrid receptors that are produced by rearrangements of PDGFR genes. TPbeta is activated by oligomerization mediated by the pointed domain of TEL/ETV6, leading to constitutive activation of the PDGFRbeta kinase domain. The receptor transmembrane (TM) domain is retained in TPbeta and in most of the described PDGFRbeta hybrids. Deletion of the TM domain (DeltaTM-TPbeta) strongly impaired the ability of TPbeta to sustain growth factor-independent cell proliferation. We confirmed that TPbeta resides in the cytosol, indicating that the PDGFRbeta TM domain does not act as a transmembrane domain in the context of the hybrid receptor but has a completely different function. The DeltaTM-TPbeta protein was expressed at a lower level because of increased degradation. It could form oligomers, was phosphorylated at a slightly higher level, co-immunoprecipitated with the p85 adaptor protein, but showed a much reduced capacity to activate STAT5 and ERK1/2 in Ba/F3 cells, compared with TPbeta. In an in vitro kinase assay, DeltaTM-TPbeta was more active than TPbeta and less sensitive to imatinib, a PDGFR inhibitor. In conclusion, we show that the TM domain is required for TPbeta-mediated signaling and proliferation, suggesting that the activation of the PDGFRbeta kinase domain is not enough for cell transformation.
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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 Socratic graph.