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ERK5 is required for VEGF-mediated survival and tubular morphogenesis of primary human microvascular endothelial cells
Extracellular signal-regulated kinase 5 (ERK5) is activated in response to environmental stress and growth factors. Gene ablation of Erk5 in mice is embryonically lethal as a result of disruption ofExpand
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cAMP signalling in the vasculature: the role of Epac (exchange protein directly activated by cAMP).
The second messenger cAMP plays a central role in mediating vascular smooth muscle relaxation in response to vasoactive transmitters and in strengthening endothelial cell-cell junctions that regulateExpand
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Exchange protein activated by cAMP (Epac) induces vascular relaxation by activating Ca2+‐sensitive K+ channels in rat mesenteric artery
•  Relaxation of vascular smooth muscle, which increases blood vessel diameter, is often mediated through vasodilator‐induced elevations of intracellular 3′‐5′‐cyclic adenosine monophosphate (cAMP),Expand
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ERK5 and the regulation of endothelial cell function.
ERK5 (extracellular-signal-regulated kinase 5), also termed BMK1 [big MAPK1 (mitogen-activated protein kinase 1)], is the most recently discovered member of the MAPK family. It is expressed in aExpand
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Selective Activation of Epac Increases the Frequency of Submembrane Calcium Sparks in Mesenteric Smooth Muscle Cells
The relaxation of vascular smooth muscle, which increases blood vessel diameter, is often mediated through vasodilator-induced elevations of intracellular cyclic AMP (cAMP) [1]. The vasculatureExpand