Anti-CD148 Monoclonal Antibody (Clone:MEM-CD148/05)

CD148 (also known as HPTP-eta or DEP-1) is a transmembrane protein tyrosin phosphatase containing eight fibronectin type III extracellular domains. This protein is known to inhibit transduction of mitogenic signals in non-hematopoietic cells (fibroblasts, epithelial cells), and signal transduction downstream of T cell receptor, however, it also augments immunoreceptor signaling in B cells and macrophages via dephosphorylating C-terminal tyrosine of Src-family tyrosine kinases. CD148 expression increases after in vitro activation of peripheral blood leucocytes. It can be also used as marker of the most mature human thymocytes, and leukemic cells corresponding to this stadium of thymocyte differentiation. In contrast, in mice the CD148 expression sharply drops through the double positive stage to the single positive thymocytes. Protein function: Tyrosine phosphatase which dephosphorylates or contributes to the dephosphorylation of CTNND1, FLT3, PDGFRB, MET, RET (variant MEN2A), KDR, LYN, SRC, MAPK1, MAPK3, EGFR, TJP1, OCLN, PIK3R1 and PIK3R2. Plays a role in cell adhesion, migration, proliferation and differentiation. Involved in vascular development. Regulator of macrophage adhesion and spreading. Positively affects cell-matrix adhesion. Positive regulator of platelet activation and thrombosis. Negative regulator of cell proliferation. Negative regulator of PDGF-stimulated cell migration, through dephosphorylation of PDGFR. Positive regulator of endothelial cell survival, as well as of VEGF-induced SRC and AKT activation, through KDR dephosphorylation. Negative regulator of EGFR signaling pathway, through EGFR dephosphorylation. Enhances the barrier function of epithelial junctions during reassembly. Negatively regulates T-cell receptor (TCR) signaling. Upon T-cell TCR activation, it is up-regulated and excluded from the immunological synapses, while upon T-cell-antigen presenting cells (APC) disengagement, it is no longer excluded and can dephosphorylate PLCG1 and LAT to down-regulate prolongation of signaling. [The UniProt Consortium]