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. 2012 Apr 27;287(25):20975–20985. doi: 10.1074/jbc.M112.341479

FIGURE 4.

FIGURE 4.

A and B, recombinant S13D telokin completely abolishes the contraction induced by GST-MYPT1(654–880) fragment in β-escin-permeabilized mouse ileum SM without a significant change in the Thr-696 phosphorylation of GST-MYPT1(654–880). A paradoxical increase in Thr-853 phosphorylation level occurred. Addition of S13A telokin, known to be 2-fold less effective than S13D telokin, also relaxed the contraction induced by GST-MYPT1(654–880) fragment to a lesser extent (data not shown) without a significant change in either the Thr-696 or Thr-853 phosphorylation of GST-MYPT1(654–880). Phosphorylation levels after S13D telokin treatment normalized to the levels at pCa 6.3 + GST-MYPT1(654–880). C, relaxation induced by S13D or S13A telokin did not alter the phosphorylation level of endogenous MYPT1 at Thr-696 or Thr-853.