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• W2069454329 abstract "Erk-5, a member of the MAPK superfamily, has a catalytic domain similar to Erk1/2 and a unique C-terminal domain enabling binding with transcription factors. Aberrant vascularization in the Erk5-null mice suggested a link to angiogenesis. Ectopic expression of constitutively active Erk5 blocks endothelial cell morphogenesis and causes HIF1-alpha destabilization/degradation. However the mechanisms by which endogenous Erk5 regulates angiogenesis remain unknown. We show that Erk5 and its activating kinase MEK5 are the upstream mediators of the anti-angiogenic signal by the natural angiogenesis inhibitor, pigment epithelial-derived factor (PEDF). We demonstrate that Erk5 phosphorylation allows activation of PPARgamma transcription factor by displacement of SMRT co-repressor. PPARgamma, in turn is critical for NFkappaB activation, PEDF-dependent apoptosis, and anti-angiogenesis. The dominant negative MEK5 mutant and Erk5 shRNA diminished PEDF-dependent apoptosis, inhibition of the endothelial cell chemotaxis, and angiogenesis. This is the first evidence of Erk5-dependent transduction of signals by endogenous angiogenesis inhibitors." @default.
• W2069454329 created "2016-06-24" @default.
• W2069454329 creator A5015018175 @default.
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• W2069454329 date "2010-04-01" @default.
• W2069454329 modified "2023-09-26" @default.
• W2069454329 title "Natural Angiogenesis Inhibitor Signals through Erk5 Activation of Peroxisome Proliferator-activated Receptor γ (PPARγ)" @default.
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• W2069454329 doi "https://doi.org/10.1074/jbc.m110.117374" @default.
• W2069454329 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2859512" @default.
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