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Figure 6 shows that control adhesion of TK-1 cells was about 57.68 ± 3.77 of the maximal adhesion induced by TNF-α.
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This speculation is mostly in line with findings from a study on adhesion induced GUV deformation28.
Adhesion induced differential expression of pFAK, pMEK and pERK.
Liu, Y. J. et al. Confinement and low adhesion induce fast amoeboid migration of slow mesenchymal cells.
Normal cells rely on adhesion to appropriate ECM for survival and loss of this adhesion induces anoikis.
TNF-α induced maximal adhesion (100 ± 2.1%) which was significantly elevated compared to controls (p < 0.01TNF-α vs. control).
Figure 4 showed that control adhesion of TK-1 cells was 12.3 ± 0.98%; TNF-α induced maximal adhesion (29.8 ± 1.30%, p < 0.001 vs. untreated control) at 24 h.
Mitogenesis, cell migration, and loss of focal adhesions induced by tenascin-C interacting with its cell surface receptor, annexin II.
These characteristic patterns follow the maximal adhesion peak and are defined by a phase of increasing force or a force-plateau, prior to a sharp reduction of the recorded force.
We find that maximal adhesion occurs at intermediate densities of both sialyl Lewis X and anti-ICAM-1, owing to synergistic binding effects between the two ligands.
Maximal adhesion was observed to CRP.
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