Peptide-Mediated Disruption of Calmodulin-Cyclin E Interactions Inhibits Proliferation of Vascular Smooth Muscle Cells and Neointima Formation

[摘要]：Rationale: Cell cycle progression in vascular smooth muscle cells (VSMCs) is a therapeutic target for restenosis. Objective: Having discovered that calmodulin (CaM)-dependent cyclin E/CDK2 activity underlies Ca2+ -sensitive G(1)-to-S phase transitions in

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