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Matches in Nanopublications for { ?s ?p "Figure 7 Model of PMN NADPH oxidaseâ�?��??derived oxidant signaling in mediating the TLR4-TLR2 cross talk in endothelial cells. LPS stimulation induces NADPH oxidase activation and production of reactive oxygen species (ROS) in PMNs as well as the initiation of MyD88-dependent NF-�?ºB signaling in endothelial cells and the consequent expression of TLR2 and ICAM-1. Adhesion of PMNs to endothelial cells is mediated by binding of constitutive ICAM-1 to CD18 integrin and provides the appropriate coupling required for PMNs to transmit oxidant signals to endothelial cells. The oxidants augment NF-�?ºB signaling and TLR2 expression (+), which results in the augmented response of the cell to PGN, thereby amplifying ICAM-1 expression (circled +) and promoting stable adhesion of PMNs to endothelial cells and increased PMN migration. Thus, the PMN NADPH oxidaseâ�?��??mediated TLR4-TLR2 cross talk activates a positive feedback signal leading to sustained and amplified endothelial activation in response to invading pathogens." ?g. }

• _3 value "Figure 7 Model of PMN NADPH oxidaseâ�?��??derived oxidant signaling in mediating the TLR4-TLR2 cross talk in endothelial cells. LPS stimulation induces NADPH oxidase activation and production of reactive oxygen species (ROS) in PMNs as well as the initiation of MyD88-dependent NF-�?ºB signaling in endothelial cells and the consequent expression of TLR2 and ICAM-1. Adhesion of PMNs to endothelial cells is mediated by binding of constitutive ICAM-1 to CD18 integrin and provides the appropriate coupling required for PMNs to transmit oxidant signals to endothelial cells. The oxidants augment NF-�?ºB signaling and TLR2 expression (+), which results in the augmented response of the cell to PGN, thereby amplifying ICAM-1 expression (circled +) and promoting stable adhesion of PMNs to endothelial cells and increased PMN migration. Thus, the PMN NADPH oxidaseâ�?��??mediated TLR4-TLR2 cross talk activates a positive feedback signal leading to sustained and amplified endothelial activation in response to invading pathogens." provenance.
• _3 value "Figure 7 Model of PMN NADPH oxidaseâ�?��??derived oxidant signaling in mediating the TLR4-TLR2 cross talk in endothelial cells. LPS stimulation induces NADPH oxidase activation and production of reactive oxygen species (ROS) in PMNs as well as the initiation of MyD88-dependent NF-�?ºB signaling in endothelial cells and the consequent expression of TLR2 and ICAM-1. Adhesion of PMNs to endothelial cells is mediated by binding of constitutive ICAM-1 to CD18 integrin and provides the appropriate coupling required for PMNs to transmit oxidant signals to endothelial cells. The oxidants augment NF-�?ºB signaling and TLR2 expression (+), which results in the augmented response of the cell to PGN, thereby amplifying ICAM-1 expression (circled +) and promoting stable adhesion of PMNs to endothelial cells and increased PMN migration. Thus, the PMN NADPH oxidaseâ�?��??mediated TLR4-TLR2 cross talk activates a positive feedback signal leading to sustained and amplified endothelial activation in response to invading pathogens." provenance.
• _3 value "Figure 7 Model of PMN NADPH oxidaseâ�?��??derived oxidant signaling in mediating the TLR4-TLR2 cross talk in endothelial cells. LPS stimulation induces NADPH oxidase activation and production of reactive oxygen species (ROS) in PMNs as well as the initiation of MyD88-dependent NF-�?ºB signaling in endothelial cells and the consequent expression of TLR2 and ICAM-1. Adhesion of PMNs to endothelial cells is mediated by binding of constitutive ICAM-1 to CD18 integrin and provides the appropriate coupling required for PMNs to transmit oxidant signals to endothelial cells. The oxidants augment NF-�?ºB signaling and TLR2 expression (+), which results in the augmented response of the cell to PGN, thereby amplifying ICAM-1 expression (circled +) and promoting stable adhesion of PMNs to endothelial cells and increased PMN migration. Thus, the PMN NADPH oxidaseâ�?��??mediated TLR4-TLR2 cross talk activates a positive feedback signal leading to sustained and amplified endothelial activation in response to invading pathogens." provenance.
• _3 value "Figure 7 Model of PMN NADPH oxidaseâ�?��??derived oxidant signaling in mediating the TLR4-TLR2 cross talk in endothelial cells. LPS stimulation induces NADPH oxidase activation and production of reactive oxygen species (ROS) in PMNs as well as the initiation of MyD88-dependent NF-�?ºB signaling in endothelial cells and the consequent expression of TLR2 and ICAM-1. Adhesion of PMNs to endothelial cells is mediated by binding of constitutive ICAM-1 to CD18 integrin and provides the appropriate coupling required for PMNs to transmit oxidant signals to endothelial cells. The oxidants augment NF-�?ºB signaling and TLR2 expression (+), which results in the augmented response of the cell to PGN, thereby amplifying ICAM-1 expression (circled +) and promoting stable adhesion of PMNs to endothelial cells and increased PMN migration. Thus, the PMN NADPH oxidaseâ�?��??mediated TLR4-TLR2 cross talk activates a positive feedback signal leading to sustained and amplified endothelial activation in response to invading pathogens." provenance.