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SNO of CFL1 serves as a novel pathway after NO biosynthesis for mediating estrogen-induced cytoskeleton remodeling in endothelial cells. Estrogen stimulates dynamic SNOCys80 of CFL1 via eNOS-derived NO. Activation of this pathway cooperates with the CFL1 pathway via dephosphorylation on Ser3, resulting in increased actin-severing activity of CFL1 for regulating actin dynamics and cytoskeleton remodeling in endothelial cells.
