BR-1 is a cell-permeable PRL-3 inhibitor with IC50 value of 900nM. It dephosphorylates Tyr783 onintegrin β1 and modulates VEGF-mediated endothelial cell migration.
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HazMat fee for 500 gram (Estimated)
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USD 15-60
Inaccessible (Haz class 6.1), Domestic
USD 80+
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Accessible (Haz class 3, 4, 5 or 8), International
PRL-3 is a member of phosphatases of regenerating liver family, characterized by phosphatase active domain and C-terminal prenylation motif. Overexpression of PRL-3 has been implicated in multiple cancers[3]. In gastric cancer cells, PRL-3 upregulated miR-210 expression in a HIF-1α-dependent fashion under normoxia and hypoxia. In addition, PRL-3 activated NF-κB signaling and promoted HIF-1α expression through modulating phosphorylation of p65. NF-κB signaling, HIF-1α, and miR-210 partially contributed to PRL-3-induced migration and invasion[4]. Knockdown of PRL-3 in MCF-7 cells resulted in decreased proliferation, wound healing and invasion. PRL-3 knockdown in MCF-7 cells resulted in a significant reduction of heparanase, MMP-9, actin gamma-2 and Myosin 9 expression, and significant elevation of E-cadherin[5]. BR-1 is a phosphatase of regenerating liver 3 (PRL-3) inhibitor which blocks the migration and invasion of metastatic cancer cells. PRL-3 inhibitor, in a dose-dependent fashion, blocked the dephosphorylation of DiFMUP by PRL-3 and strongly suppressed the activity of PRL-3 phosphatase in PRL-3 overexpressing DLD-1 colon tumor cells [DLD-1 (PRL-3)]. Also, PRL-3 inhibitor dose-dependently blocked the migration of DLD-1 (PRL-3) cells, however, it did not inhibit the proliferation of DLD-1(PRL-3) cells, suggesting that PRL-3 inhibitor significantly blocked cell immigration and invasion without cytotoxicity[6].
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