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Stimuli such as shear stress, vascular endothelial growth factor (VEGF), and insulin activate kinases including protein kinase B (Akt), AMP-activated protein kinase (AMPK), calcium/calmodulin-dependent protein kinase II (CaMKII), protein kinase A (PKA), and protein kinase G (PKG), which phosphorylate Ser1177 (Fulton et al., 1999
These endotoxins activate KCs through the TLR4 signaling pathway, further increasing TNF- production [127, 128]
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