ArticleCurrent biology : CB2009
An unbiased screen identifies DEP-1 tumor suppressor as a phosphatase controlling EGFR endocytosis.
Article in Current biology : CB, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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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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Who cites it
67 citing papers in PubMed, 125 citations in OpenAlex.
- The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.Journal of biomedical science · 2026Review
- CD148 agonistic antibody alleviates renal injury induced by chronic angiotensin II infusion in mice.BMC nephrology · 2025Article
- The receptor protein tyrosine phosphatase PTPRK promotes intestinal repair and catalysis-independent tumour suppression.Journal of cell science · 2024Article
- System-Level Analysis of the Effects of RPTPs on Cellular Signaling Networks.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Identifying Transmembrane Interactions in Receptor Protein Tyrosine Phosphatase Homodimerization and Heterodimerization.Methods in molecular biology (Clifton, N.J.) · 2024Article
- An integrated study to decipher immunosuppressive cellular communication in the PDAC environment.NPJ systems biology and applications · 2023Article
- Promoting the activity of a receptor tyrosine phosphatase with a novel pH-responsive transmembrane agonist inhibits cancer-associated phenotypes.Protein science : a publication of the Protein Society · 2023Article
- MFN2 suppresses clear cell renal cell carcinoma progression by modulating mitochondria-dependent dephosphorylation of EGFR.Cancer communications (London, England) · 2023Article
- Review
- R-PTP-κ Inhibits Contact-Dependent Cell Growth by Suppressing E2F Activity.Biomedicines · 2022Article
- The effects of CD148 Q276P/R326Q polymorphisms in A431D epidermoid cancer cell proliferation and epidermal growth factor receptor signaling.Cancer reports (Hoboken, N.J.) · 2022Article
- Syndecan-2 selectively regulates VEGF-induced vascular permeability.Nature cardiovascular research · 2022Article
- Disrupting PTPRJ transmembrane-mediated oligomerization counteracts oncogenic receptor tyrosine kinase FLT3 ITD.Frontiers in oncology · 2022Article
- Review
- Prediction of combination therapies based on topological modeling of the immune signaling network in multiple sclerosis.Genome medicine · 2021Article
- RAC1B modulates intestinal tumourigenesis via modulation of WNT and EGFR signalling pathways.Nature communications · 2021Article
- Increase of the Intracellular Zinc Concentration Leads to an Activation and Internalisation of the Epidermal Growth Factor Receptor in A549 Cells.International journal of molecular sciences · 2020Article
- Agonistic anti-CD148 monoclonal antibody attenuates diabetic nephropathy in mice.American journal of physiology. Renal physiology · 2020Article
- Article
- CD148 Serves as a Prognostic Marker of Gastric Cancer and Hinders Tumor Progression by Dephosphorylating EGFR.Journal of Cancer · 2020Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundThe epidermal growth factor (EGF) stimulates rapid tyrosine phosphorylation of the EGF receptor (EGFR). This event precedes signaling from both the plasma membrane and from endosomes, and it is essential for recruitment of a ubiquitin ligase, CBL, that sorts activated receptors to endosomes and degradation. Because hyperphosphorylation of EGFR is involved in oncogenic pathways, we performed an unbiased screen of small interfering RNA (siRNA) oligonucleotides targeting all human tyrosine phosphatases.
resultsWe report the identification of PTPRK and PTPRJ (density-enhanced phosphatase-1 [DEP-1]) as EGFR-targeting phosphatases. DEP-1 is a tumor suppressor that dephosphorylates and thereby stabilizes EGFR by hampering its ability to associate with the CBL-GRB2 ubiquitin ligase complex. DEP-1 silencing enhanced tyrosine phosphorylation of endosomal EGFRs and, accordingly, increased cell proliferation. In line with functional interactions, EGFR and DEP-1 form physical associations, and EGFR phosphorylates a substrate-trapping mutant of DEP-1. Interestingly, the interactions of DEP-1 and EGFR are followed by physical segregation: whereas EGFR undergoes endocytosis, DEP-1 remains confined to the cell surface.
conclusionsEGFR and DEP-1 physically interact at the cell surface and maintain bidirectional enzyme-substrate interactions, which are relevant to their respective oncogenic and tumor-suppressive functions. These observations highlight the emerging roles of vesicular trafficking in malignant processes.
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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.