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• W1977992886 abstract "Endoglin is an endothelial-specific transforming growth factor beta (TGF-β) co-receptor essential for angiogenesis and vascular remodeling. Endoglin regulates a wide range of cellular processes, including cell adhesion, migration, and proliferation, through TGF-β signaling to canonical Smad and Smad-independent pathways. Despite its overall pro-angiogenic role in the vasculature, the underlying mechanism of endoglin action is poorly characterized. We previously identified β-arrestin2 as a binding partner that causes endoglin internalization from the plasma membrane and inhibits ERK signaling towards endothelial migration. In the present study, we examined the mechanistic role of endoglin and β-arrestin2 in endothelial cell proliferation. We show that endoglin impedes cell growth through sustained inhibition of ERK-induced c-Myc and cyclin D1 expression in a TGF-β-independent manner. The down-regulation of c-Myc and cyclin D1, along with growth-inhibition, are reversed when the endoglin/β-arrestin2 interaction is disrupted. Given that TGF-β-induced Smad signaling potently represses c-Myc in most cell types, our findings here show a novel mechanism by which endoglin augments growth-inhibition by targeting ERK and key downstream mitogenic substrates." @default.
• W1977992886 created "2016-06-24" @default.
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• W1977992886 date "2012-08-01" @default.
• W1977992886 modified "2023-10-18" @default.
• W1977992886 title "Endoglin inhibits ERK-induced c-Myc and cyclin D1 expression to impede endothelial cell proliferation" @default.
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• W1977992886 doi "https://doi.org/10.1016/j.bbrc.2012.06.163" @default.
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