title: Interactions between Epac1 and ezrin in the control of endothelial barrier function.
abstract: Loss of barrier function in the vasculature promotes inflammatory signalling which in turn contributes to the progression of cardiovascular disease. cAMP can protect against endothelial dysfunction through the effectors PKA (protein kinase A) and Epac (exchange protein directly activated by cAMP). The present review outlines the role of Epac1 signalling within the endothelium and, in particular, the role of Epac1 in cytoskeletal dynamics and the control of cell morphology. The actin/cytoskeleton linker ezrin will be described in terms of the growing body of evidence placing it downstream of cAMP signalling as a mediator of altered cellular morphology.
authors.affiliation: *Institute of Molecular, Cell and Systems Biology, University of Glasgow, Glasgow G12 8QQ, Scotland, U.K.
authors.forename: Euan
authors.initials: E
authors.lastname: Parnell
authors.affiliation: *Institute of Molecular, Cell and Systems Biology, University of Glasgow, Glasgow G12 8QQ, Scotland, U.K.
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Yarwood
mesh_terms: D003598:Cytoskeletal Proteins / Q000378:metabolism*; D003599:Cytoskeleton / Q000378:metabolism*; D004727:Endothelium / Q000378:metabolism*; D020662:Guanine Nucleotide Exchange Factors / Q000378:metabolism*; D006801:Humans; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D000099149:Ezrin
chemical_list: D003598:Cytoskeletal Proteins; D020662:Guanine Nucleotide Exchange Factors; D000099149:Ezrin; C116122:RAPGEF3 protein, human