EC Number   |
General Information |
Reference |
|---|
   2.7.11.18 | malfunction |
decreasing MLCK activity in 4-dpf cells results in longer edge lifetimes and wider edges. Enzyme inhibition causes no change in the lateral propagation rate, but an increase in edge lifetime, which suggests that MLCK activity regulates edge size by controlling edge lifetime |
-, 740793 |
| 2.7.11.18 | malfunction |
in cultured cardiomyocytes, the knockdown of cMLCK impaired epinephrine-induced activation of sarcomere reassemble and overexpression of cMLCK promoted sarcomere organization. The lack of MLC2 phosphorylation in heart induces reduction in cardiac performance in genetically modified cMLCK knockout mice. Reduced levels of MLC2 phosphorylation induces cardiac dysfunction |
-, 741247 |
| 2.7.11.18 | malfunction |
in knockout mice, the lack of MLCK-mediated phosphorylation of myosin in tracheal, bronchial, and gastrointestinal smooth muscle cannot be rescued by other kinases |
740266 |
| 2.7.11.18 | malfunction |
in meiosis I, MLCK inhibition and other myosin perturbations impair spindle migration and first polar body emission. Inhibition of the MEK1/2-MAPK pathway with U0126 leads to reduced levels of phosphorylated myosin-regulatory light chain (pMRLC) and causes a reduction in cortical tension, effects that are mimicked by treatment with the myosin light chain kinase (MLCK) inhibitor ML-7. MAPK or MLCK inhibition induces loss of normal cortical spindle localization or parthenogenetic egg activation. This parthenogenesis is dependent on cytosolic and extracellular calcium and can be rescued by hyperloading eggs with zinc, suggesting that these effects of inhibition of MLCK or the MAPK pathway are linked with dysregulation of ion homeostasis, overview |
-, 740131 |
| 2.7.11.18 | malfunction |
induced endocytosis is slowed by acute inhibition of MLCK and by downregulation of MLCK via RNA interference while the total amount of vesicle exocytosis and somatic Ca2+channel current does not change with MLCK down-regulation. Downregulation of MLCK prevents depolarization-induced phosphorylation of myosin light chain, an effect shared by blockers of Ca2+ channels and calmodulin. Downregulation of MLCK does not decrease the amount of exocytosis |
740887 |
| 2.7.11.18 | malfunction |
mice harboring a deletion of the nmMLCK gene exhibit protection from radiation-induced lung injury, as assessed by attenuated vascular leakage and leukocyte infiltration |
762357 |
| 2.7.11.18 | malfunction |
MLCK activates myosin Mg-ATPase activity by phosphorylating Thr-18/Ser-19 on the RLC of myosin II, thereby initiating cross-bridge movements of both smooth muscle and non-muscle. MLCK deletion causes enhanced cell protrusion along with a reduction of membrane tension and is rescued by kinase-dead MLCK or five-DFRXXL motif. The deletion of MLCK results in fast cell migration, enhanced protrusion formation, but no alteration of myosin light chain phosphorylation. The mutant cells show reduced membrane tether force and fewer membrane F-actin filaments, as well as a higher average migrating velocity and protrusion compared to wild-type |
740727 |
| 2.7.11.18 | malfunction |
MLCK depletion modifies voltage-operated Ca2+ channels. KCl- and AVP-induced Ca2+ signals and voltage-activated Ca2+ current are decreased in MLCK-depleted A7r5 cells. MLCK enzyme inhibition leads to a significant inhibition of cytosolic Ca2+ increase (64%) and contraction induced by 50 mM KCl (92%). Phenotype, detailed overview. Voltage-dependent Ca2+ channel gene expression is decreased by MLCK downregulation |
-, 740289 |
| 2.7.11.18 | malfunction |
MLCK enzyme inhibitors reduce paracellular barrier dysfunction in ischemic porcine ileum. Pharmacological inhibitions of MLCK significantly reduce paracellular permeability and occludin internalization in in vitro anoxia/reoxygenation injury and ex vivo porcine ischemic injury experimental models |
-, 739835 |
| 2.7.11.18 | malfunction |
MLCK-deficient mice lack bronchial constrictions in normal and asthmatic airways, while the asthmatic inflammation response is not affected |
709148 |
