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Receptor-type tyrosine-protein phosphatase eta (PTPRJ), widely known as CD148 or DEP-1, is a transmembrane enzyme that regulates diverse cellular processes by dephosphorylating key signaling molecules. It is highly expressed in vascular endothelial cells, epithelial cells, and hematopoietic cells, including platelets and T lymphocytes [1, 6]. In platelets, CD148 serves as a critical positive regulator of Src family kinases (SFKs), making it essential for platelet activation and thrombus formation; consequently, it is under investigation as a novel antithrombotic target with potentially lower bleeding risks than current therapies [3, 14]. Conversely, in many epithelial tissues, CD148 acts as a tumor suppressor by dephosphorylating growth factor receptors such as EGFR and VEGFR2, thereby inhibiting cell proliferation and migration [2, 7]. However, its role can be context-dependent, as it has been shown to promote invasion and metastasis in specific aggressive breast cancer models [2, 10]. Beyond its roles in cancer and thrombosis, CD148 is involved in metabolic signaling as a negative regulator of insulin and leptin receptors, suggesting therapeutic potential in diabetes and obesity [2, 9].
Modulation of intracellular signaling pathways through the dephosphorylation of substrate tyrosine kinases including Src family kinases (SFKs), EGFR, PDGFR, VEGFR2, and JAK2.
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