KLF2 Is a Novel Transcriptional Regulator of Endothelial Proinflammatory Activation (original) (raw)
KLF2 provokes a gene expression pattern that establishes functional quiescent differentiation of the endothelium
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Fluid shear stress induces endothelial KLF2 gene expression through a defined promoter region
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Kruppel-Like Factor 2 (KLF2) Regulates Endothelial Thrombotic Function
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KLF2 Primes the Antioxidant Transcription Factor Nrf2 for Activation in Endothelial Cells
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Endothelial KLF2 Links Local Arterial Shear Stress Levels to the Expression of Vascular Tone-Regulating Genes
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Prolonged shear stress and KLF2 suppress constitutive proinflammatory transcription through inhibition of ATF2
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Laminar shear stress acts as a switch to regulate divergent functions of NF-kappaB in endothelial cells
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Prolonged fluid shear stress induces a distinct set of endothelial cell genes, most specifically lung Kruppel-like factor(KLF2
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Thioredoxin Interacting Protein Promotes Endothelial Cell Inflammation in Response to Disturbed Flow by Increasing Leukocyte Adhesion and Repressing Kruppel-Like Factor 2
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Kruppel-Like Factor 2 Inhibits Protease Activated Receptor-1 Expression and Thrombin-Mediated Endothelial Activation
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The Anti-Inflammatory Actions of Platelet Endothelial Cell Adhesion Molecule-1 Do Not Involve Regulation of Endothelial Cell NF- B
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Divergent and convergent effects on gene expression and function in acute versus chronic endothelial activation
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Laminar shear stress elicit distinct endothelial cell e‐selectin expression pattern via TNFα and IL‐1β activation
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Differential regulation of genes and transcription factors in vascular endothelial cells exposed to uniform and disturbed laminar shear stress
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“Go With the Flow”: How Krüppel-Like Factor 2 Regulates the Vasoprotective Effects of Shear Stress
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Shear stress sustains atheroprotective endothelial KLF2 expression more potently than statins through mRNA stabilization
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Endothelial Kruppel-like factor 4 protects against atherothrombosis in mice
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