ArticleMolecular and cellular biology1998
Epidermal growth factor receptor and the adaptor protein p52Shc are specific substrates of T-cell protein tyrosine phosphatase.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
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Who cites it
88 citing papers in PubMed, 223 citations in OpenAlex.
- PTPN1/PTPN2 inhibition improves NK cancer therapy by enhancing IL-2 and mitigating TGFβ1 responses.EMBO reports · 2026Article
- Protein tyrosine phosphatase receptor type kappa (PTPRK) revisited: evolving insights into structure, function, and pathology.Journal of translational medicine · 2025Review
- EGFR targeting PhosTACs as a dual inhibitory approach reveals differential downstream signaling.Science advances · 2024Article
- Immunotherapeutic implications of negative regulation by protein tyrosine phosphatases in T cells: the emerging cases of PTP1B and TCPTP.Frontiers in medicine · 2024Review
- Protein Tyrosine Phosphatases: Mighty oaks from little acorns grow.IUBMB life · 2023Article
- Protein tyrosine phosphatase non-receptor type 2 as the therapeutic target of atherosclerotic diseases: past, present and future.Frontiers in pharmacology · 2023Review
- The catalytic activity of TCPTP is auto-regulated by its intrinsically disordered tail and activated by Integrin alpha-1.Nature communications · 2022Article
- Protein tyrosine phosphatase PTPN2 regulates TGF-β signaling through Smad4 dephosphorylation.American journal of cancer research · 2022Article
- Protein Tyrosine Phosphatases: Mechanisms in Cancer.International journal of molecular sciences · 2021Review
- T Cell Protein Tyrosine Phosphatase in Glucose Metabolism.Frontiers in cell and developmental biology · 2021Review
- T Cell Protein Tyrosine Phosphatase in Osteoimmunology.Frontiers in immunology · 2021Review
- Nonphagocytic Activation of NOX2 Is Implicated in Progressive Nonalcoholic Steatohepatitis During Aging.Hepatology (Baltimore, Md.) · 2020Article
- Platelet-derived growth factor receptor β activation and regulation in murine myelofibrosis.Haematologica · 2020Article
- Growth Factor Deregulation and Emerging Role of Phosphatases in Diabetic Peripheral Artery Disease.Frontiers in cardiovascular medicine · 2020Review
- Advances in Knowledge of Candidate Genes Acting at the Beta-Cell Level in the Pathogenesis of T1DM.Frontiers in endocrinology · 2020Review
- The role of T-cell protein tyrosine phosphatase in epithelial carcinogenesis.Molecular carcinogenesis · 2019Review
- The effects of PTPN2 loss on cell signalling and clinical outcome in relation to breast cancer subtype.Journal of cancer research and clinical oncology · 2019Article
- PTPN2 deficiency along with activation of nuclear Akt predict endocrine resistance in breast cancer.Journal of cancer research and clinical oncology · 2019Article
- Regulation of platelet-activating factor-mediated interleukin-6 promoter activation by the 48 kDa but not the 45 kDa isoform of protein tyrosine phosphatase non-receptor type 2.Cell & bioscience · 2019Article
- Interdependence between EGFR and Phosphatases Spatially Established by Vesicular Dynamics Generates a Growth Factor Sensing and Responding Network.Cell systems · 2018Article
28 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
T-cell protein tyrosine phosphatase (TCPTP) exists as two forms generated by alternative splicing: a 48-kDa endoplasmic reticulum (ER)-associated form (TC48) and a 45-kDa nuclear form (TC45). To identify TCPTP substrates, we have generated substrate-trapping mutants, in which the invariant catalytic acid of TCPTP (D182) is mutated to alanine. The TCPTP D182A substrate-trapping mutants were transiently overexpressed in COS cells, and their ability to form complexes with tyrosine-phosphorylated (pTyr) proteins was assessed. No pTyr proteins formed complexes with wild-type TCPTP. In contrast, TC48-D182A formed a complex in the ER with pTyr epidermal growth factor receptor (EGFR). In response to EGF, TC45-D182A exited the nucleus and accumulated in the cytoplasm, where it bound pTyr proteins of approximately 50, 57, 64, and 180 kDa. Complex formation was disrupted by vanadate, highlighting the importance of the PTP active site in the interaction and supporting the characterization of these proteins as substrates. Of these TC45 substrates, the approximately 57- and 180-kDa proteins were identified as p52Shc and EGFR, respectively. We examined the effects of TC45 on EGFR signaling and observed that it did not modulate EGF-induced activation of p42Erk2. However, TC45 inhibited the EGF-induced association of p52Shc with Grb2, which was attributed to the ability of the PTP to recognize specifically p52Shc phosphorylated on Y239. These results indicate that TC45 recognizes not only selected substrates in a cellular context but also specific sites within substrates and thus may regulate discrete signaling events.
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