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http://purl.obolibrary.org/obo/RO_0002204
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p(HGNC:THBS1) -> bp(GO:"regulation of vascular permeability")
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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Similarly in cultured EC, VE-cadherin-blocking antibody increased permeability (124) and enhanced neutrophil transendothelial migration while producing reorganization of the actin cytoskeleton (72). The observation that VE-cadherin-blocking antibodies produce barrier disruption primarily in the alveolar capillary bed (25) suggests that differential adherens junction functioning exists within segments of the pulmonary vasculature. The MAPK pathway may be involved in regulating adherens junction/VE-cadherin function because MAPK inhibitors attenuate vascular endothelial growth factor (VEGF)-mediated VE-cadherin rearrangement and subsequent EC monolayer permeability (83). Tyrosine phosphorylation may provide an additional regulatory link between actin cytoskeletal rearrangement and adherens junction function. Pervanadate treatment of cultured cells resulted in tyrosine hyperphosphorylation of catenins, partial dissociation of the catenin-cadherin complex, and subsequent decreased cell-cell adhesion (107). Similarly, the anti-adhesive protein thrombospondin-1-induced tyrosine phosphorylation of adherens junction proteins, actin rearrangement, and increased albumin flux across EC monolayers,
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Selventa
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2014-07-03T14:29:58.267+02:00
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