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. 2015 Feb 12;3:5. doi: 10.1186/s40635-014-0037-7

Figure 6.

Figure 6

ROK-dependent myosin phosphatase activity was unchanged in platelets isolated from patients with septic shock. (A) The proportion of the myosin phosphatase regulatory subunit (MYPT) phosphorylated at the ROK substrate site Thr855 did not differ between unstimulated platelets taken from patients with septic shock compared to those taken from non-septic shock controls (n = 22 to 24 in each patient group). (B) Rat mesenteric artery samples were transferred with platelet samples as controls. Treatment with the stable thromboxane A2 mimetic U46619 increased ROK-dependent Thr855 phosphorylation of MYPT that was attenuated with the ROK antagonist Y-27632; representative data from n = 3.