NmMlck is required for β-catenin and FoxO1 occupancy of the Cldn5 repressor. nmMlck is required for β-catenin and FoxO1 occupancy of the Cldn5 repressor.

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nmMlck is required for β-catenin and FoxO1 occupancy of the Cldn5 repressor. nmMlck is required for β-catenin and FoxO1 occupancy of the Cldn5 repressor. Primary BMVECs were isolated from cortices of wild-type (nmmlck+/+) and nmMlck homozygous knockout (nmmlck−/−) mice. (A) Treating BMVECs with IL-1β (100 ng/ml) acutely (within 15 minutes) activated nmMlck, as indicated by increased phosphorylation of Y464 in a time-dependent manner. (B) ICWs were used to assess IL-1β-mediated inactivation of the Akt–FoxO1 pathway in BMVECs, by using phosphospecific antibodies against T308 on Akt (pT308 Akt) and T24 on FoxO1 (pT24 FoxO1). Antibodies against total Akt and FoxO1 were used for co-labeling, and the measurements were used to normalize phosphospecific signals. (C) IL-1β (100 ng/ml, 1.5 hours) increased the ratio of active β-catenin (hypophosphorylated at GSK3β sites Ser37 and Thr41) to total β-catenin in BMVECs isolated from nmmlck+/+ mice, but not in those isolated from nmmlck−/− mice. *P<0.05 compared with control. (D,E) Consistent with the inactivation and activation signals on Akt, FoxO1 and β-catenin, nmMlck deficiency attenuated IL-1β-mediated nuclear accumulation of β-catenin, but not nuclear accumulation of FoxO1. (F) Although IL-1β treatment led to nuclear accumulation of FoxO1 in both nmmlck+/+ and nmmlck−/− BMVECs, the absence of β-catenin in the nuclei of nmmlck−/− BMVECs treated with IL-1β prevented the binding of FoxO1 to the Cldn5 repressor. Data represent the mean±s.e.m. *P<0.05 compared with all other groups; Student's t-test. Richard S. Beard, Jr et al. J Cell Sci 2014;127:1840-1853 © 2014. Published by The Company of Biologists Ltd