Fig. 6.
Fig. 6. s-FKN–induced MonoMac6 cells adhesion to fibronectin is partially dependent on ERKs, SAPKs, PI3K, and Go/Gi proteins-mediated signaling pathways. / [3H]-Methyl thymidine-labeled MonoMac6 cells were washed and pretreated for 16 hours with either 100 ng/mL pertussis toxin (PTX) or for 2 hours with 30 μM SB202190, or PD98059, or 10 μM LY294002, or with combined inhibitors. Cells were then placed in the upper well of migration chambers in presence of 60 nM s-FKN and tested for their ability to adhere to fibronectin-coated filters. After a 3-hour period, filters were collected and washed twice in phosphate buffer saline. The amount of adherent cells to fibronectin was evaluated by liquid scintillation β counts as described in “Materials and methods.” Data are mean ± SD from triplicates of a single experiment representative of 3 others.

s-FKN–induced MonoMac6 cells adhesion to fibronectin is partially dependent on ERKs, SAPKs, PI3K, and Go/Gi proteins-mediated signaling pathways.

[3H]-Methyl thymidine-labeled MonoMac6 cells were washed and pretreated for 16 hours with either 100 ng/mL pertussis toxin (PTX) or for 2 hours with 30 μM SB202190, or PD98059, or 10 μM LY294002, or with combined inhibitors. Cells were then placed in the upper well of migration chambers in presence of 60 nM s-FKN and tested for their ability to adhere to fibronectin-coated filters. After a 3-hour period, filters were collected and washed twice in phosphate buffer saline. The amount of adherent cells to fibronectin was evaluated by liquid scintillation β counts as described in “Materials and methods.” Data are mean ± SD from triplicates of a single experiment representative of 3 others.

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