Metastasis is a complex process mediated by both adhesion molecules and chemokine secretion . One important event during cancer metastasis is tumor cell extravasation through the endothelium . In melanoma cancer, tumor cell extravasation is mediated by very late antigen (VLA)-4 molecule adhesion to vascular cell adhesion molecules (VCAM)-1 on endothelial cells . High expression levels of VLA-4 integrin are associated with a marked increase in melanoma extravasation through endothelial layers . The binding of VLA-4 to VCAM -1 induces the activation of downstream mitogen activated protein kinase (MAPK) signaling cascades, which regulate the vascular endothelial (VE)-cadherin junctions that hold together endothelial cells .
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Model Simulations Reveal VCAM-1 Augment PAK Activation Rates to Amplify p38 MAPK and VE-Cadherin Phosphorylation
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Weidert, E, Khanna, P, Vital-Lopez, F, & Dong, C. "Model Simulations Reveal VCAM-1 Augment PAK Activation Rates to Amplify p38 MAPK and VE-Cadherin Phosphorylation." Proceedings of the ASME 2012 Summer Bioengineering Conference. ASME 2012 Summer Bioengineering Conference, Parts A and B. Fajardo, Puerto Rico, USA. June 20–23, 2012. pp. 1207-1208. ASME. https://doi.org/10.1115/SBC2012-80364
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