ArticleThe Journal of biological chemistry2012
The phosphatase PTP-PEST/PTPN12 regulates endothelial cell migration and adhesion, but not permeability, and controls vascular development and embryonic viability.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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
23 citing papers in PubMed, 41 citations in OpenAlex.
- Effect of electromagnetic field radiation on transcriptomic profile and DNA methylation level in pig conceptuses during the peri-implantation period.Scientific reports · 2025Article
- Circ_0003764 Regulates the Osteogenic Differentiation of Periodontal Ligament Stem Cells.International dental journal · 2024Article
- Identification of PTPN12 Phosphatase as a Novel Negative Regulator of Hippo Pathway Effectors YAP/TAZ in Breast Cancer.International journal of molecular sciences · 2024Article
- Protein Tyrosine Phosphatase PRL-3: A Key Player in Cancer Signaling.Biomolecules · 2024Review
- Impact of Protein Phosphatase Expressions on the Prognosis of Hepatocellular Carcinoma Patients.ACS omega · 2024Article
- Extracellular Matrix- and Integrin Adhesion Complexes-Related Genes in the Prognosis of Prostate Cancer Patients' Progression-Free Survival.Biomedicines · 2023Article
- Syntenin-1-mediated small extracellular vesicles promotes cell growth, migration, and angiogenesis by increasing onco-miRNAs secretion in lung cancer cells.Cell death & disease · 2022Article
- A fluorescent probe for monitoring PTP-PEST enzymatic activity.The Analyst · 2020Article
- Review
- Paxillin: a crossroad in pathological cell migration.Journal of hematology & oncology · 2017Review
- Transposon mutagenesis identifies genes and cellular processes driving epithelial-mesenchymal transition in hepatocellular carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- PTP1B inhibitor promotes endothelial cell motility by activating the DOCK180/Rac1 pathway.Scientific reports · 2016Article
- Loss of PTPN12 Stimulates Progression of ErbB2-Dependent Breast Cancer by Enhancing Cell Survival, Migration, and Epithelial-to-Mesenchymal Transition.Molecular and cellular biology · 2015Article
- MVP-Associated Filamin A Mutations Affect FlnA-PTPN12 (PTP-PEST) Interactions.Journal of cardiovascular development and disease · 2015Article
- Correlation between cell migration and reactive oxygen species under electric field stimulation.Biomicrofluidics · 2015Article
- Protein tyrosine phosphatase-PEST and β8 integrin regulate spatiotemporal patterns of RhoGDI1 activation in migrating cells.Molecular and cellular biology · 2015Article
- Conformational remodeling of the fibronectin matrix selectively regulates VEGF signaling.Journal of cell science · 2014Article
- Control of dendritic cell migration, T cell-dependent immunity, and autoimmunity by protein tyrosine phosphatase PTPN12 expressed in dendritic cells.Molecular and cellular biology · 2014Article
- ROS, Notch, and Wnt signaling pathways: crosstalk between three major regulators of cardiovascular biology.BioMed research international · 2014Review
- Phosphatase regulation of intercellular junctions.Tissue barriers · 2013Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Protein-tyrosine phosphatase (PTP)-PEST (PTPN12) is ubiquitously expressed. It is essential for normal embryonic development and embryonic viability in mice. Herein we addressed the involvement of PTP-PEST in endothelial cell functions using a combination of genetic and biochemical approaches. By generating primary endothelial cells from an inducible PTP-PEST-deficient mouse, we found that PTP-PEST is not needed for endothelial cell differentiation and proliferation or for the control of endothelial cell permeability. Nevertheless, it is required for integrin-mediated adhesion and migration of endothelial cells. PTP-PEST-deficient endothelial cells displayed increased tyrosine phosphorylation of Cas, paxillin, and Pyk2, which were previously also implicated in integrin functions. By eliminating PTP-PEST in endothelial cells in vivo, we obtained evidence that expression of PTP-PEST in endothelial cells is required for normal vascular development and embryonic viability. Therefore, PTP-PEST is a key regulator of integrin-mediated functions in endothelial cells seemingly through its capacity to control Cas, paxillin, and Pyk2. This function explains at least in part the essential role of PTP-PEST in embryonic development and viability.
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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.