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. Author manuscript; available in PMC: 2026 Jul 25.
Published in final edited form as: Biophys J. 2025 Jul 25;124(17):2840–2853. doi: 10.1016/j.bpj.2025.07.026

Figure 2: Strain rate softening depends on actomyosin binding kinetics.

Figure 2:

Average axial PK1 stress during first cycle of stress relaxation for cells pretreated with 0.1 nM calyculin (a) to promote myosin activity, untreated cells (c), or 3 μM Y-27632 (e) to inhibit myosin activity and then subjected stress relaxation at slow (black) or fast (red) strain rates. Calyculin: n = 13 cells slow, 12 cells fast. Untreated: reproduced from Fig. 1f. Y-27632: n = 13 cells slow, 9 cells fast. Normalized peak and decay stress during first cycle of stress relaxation for cells pre-treated with calyculin (b), untreated (d), or pre-treated with Y-27632 (f). Stresses between cells stretched at the slow vs the fast rate are not significantly different for cells pre-treated with calyculin. Solid bars represent mean normalized axial PK1 stress, open circles represent individual measurements. Error bars represent s.e.m. *p < 0.05. g, Ratio of stress in cells stretched at fast rate vs slow rate for untreated (black), Y-27632-treated (blue), and calyuclin-treated (cyan) cells. Stimulating myosin activity with calyculin decreases strain rate softening, while inhibiting myosin with Y-27632 increases strain rate softening.