Skip to main content
. 2010 May 17;87(2):272–280. doi: 10.1093/cvr/cvq144

Figure 1.

Figure 1

Control of actin–myosin contraction in endothelium. Increased MLC phosphorylation in response to MLCK activation by Ca2+-calmodulin binding and src kinase activity, or to inhibition of MLCP by ROCK activation downstream of RhoA, increases MLC ATPase-driven force generation relative to actin.