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- W2076548587 abstract "Endothelial cell–cell junctions control efflux of small molecules and leukocyte transendothelial migration (TEM) between blood and tissues. Inhibitors of phosphoinositide 3-kinases (PI3Ks) increase endothelial barrier function, but the roles of different PI3K isoforms have not been addressed. In this study, we determine the contribution of each of the four class I PI3K isoforms (p110α, -β, -γ, and -δ) to endothelial permeability and leukocyte TEM. We find that depletion of p110α but not other p110 isoforms decreases TNF-induced endothelial permeability, Tyr phosphorylation of the adherens junction protein vascular endothelial cadherin (VE-cadherin), and leukocyte TEM. p110α selectively mediates activation of the Tyr kinase Pyk2 and GTPase Rac1 to regulate barrier function. Additionally, p110α mediates the association of VE-cadherin with Pyk2, the Rac guanine nucleotide exchange factor Tiam-1 and the p85 regulatory subunit of PI3K. We propose that p110α regulates endothelial barrier function by inducing the formation of a VE-cadherin–associated protein complex that coordinates changes to adherens junctions with the actin cytoskeleton." @default.
- W2076548587 created "2016-06-24" @default.
- W2076548587 creator A5051010078 @default.
- W2076548587 creator A5052293314 @default.
- W2076548587 creator A5066743266 @default.
- W2076548587 date "2010-03-22" @default.
- W2076548587 modified "2023-10-18" @default.
- W2076548587 title "The PI3K p110α isoform regulates endothelial adherens junctions via Pyk2 and Rac1" @default.
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- W2076548587 doi "https://doi.org/10.1083/jcb.200907135" @default.
- W2076548587 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2845076" @default.
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- W2076548587 hasPublicationYear "2010" @default.
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