EC Number   |
Natural Substrates |
|---|
   2.7.11.18 | ATP + myosin light chain |
activated MLCK then phosphorylates the regulatory myosin light chains, triggering cross-bridge cycling and contraction, in aortic rings from mice in which alpha1, the major catalytic subunit isoform in arterial smooth muscle, is deleted, KCl- or phenylephrine-induced contraction is increased, overview |
| 2.7.11.18 | ATP + myosin light chain |
activated MLCK then phosphorylates the regulatory myosin light chains, triggering cross-bridge cycling and contraction, myosin light chain phosphorylation is increased under these conditions, suggesting that contraction would be potentiated by ablation of AMPK |
| 2.7.11.18 | ATP + [myosin light chain] |
activation of the enzyme is a key regulatory step in the modulation of endothelial permeability, central to parthogenesis of inflammatory lung disease is disruption of the endothelial barrier function |
| 2.7.11.18 | ATP + light chain myosin II |
cardiac-MLCK is essential for normal cardiac development and function in zebrafish embryos, deletion of the gene encoding cardiac-MLCK is lethal for embryos |
| 2.7.11.18 | ATP + light chain myosin II |
causes endothelial contraction |
| 2.7.11.18 | more |
cytochalasin-induced increases in paracellular permeability are also mediated by MLC in Caco-2 monolayers |
| 2.7.11.18 | ATP + light chain myosin II |
cytokine-induced epithelial barrier dysfunction can be mediated by increased MLCK expression and subsequent myosin II regulatory light chain phosphorylation, the enzyme is involved in the inflammatory bowel disease |
| 2.7.11.18 | ATP + [myosin light chain] |
enzyme is regulating cytoskeletal rearrangement and cell motility |
| 2.7.11.18 | ATP + myosin light chain |
event in initiation of smooth-muscle contraction |
| 2.7.11.18 | more |
Human T cell leukemia virus 1-infected lymphocytes can cause a breakdown of the blood-brain barrier inducing an increase in paracellular endothelial permeability and transcellular migration, this disruption is associated with tight junction disorganization between endothelial cells and altered tight junction proteinexpression involving the enzyme MLCK, enzyme inhibition prevents the changes in endothelial cells, overview |
