title: Isoform-specific knockout of endothelial myosin light chain kinase: closing the gap on inflammatory lung disease.
abstract: Inflammatory lung diseases result in high rates of morbidity and mortality. Central to the pathogenesis of these diseases is disruption of endothelial barrier function. Activation of myosin light chain kinase (MLCK) is a key regulatory step in the modulation of endothelial permeability. Recent studies show that mice with selective knockout of the endothelial MLCK are less susceptible to endotoxin-induced acute lung injury and that a new small-molecule inhibitor of MLCK also protects against lung injury.
authors.affiliation: Department of Medical Physiology and Cardiovascular Research Institute, Texas A&M University System Health Science Center, College of Medicine, College Station, 77843, USA.
authors.forename: John H
authors.initials: JH
authors.lastname: Tinsley
authors.forename: Sarah Y
authors.initials: SY
authors.lastname: Yuan
authors.forename: Emily
authors.initials: E
authors.lastname: Wilson
mesh_terms: D000818:Animals; D006801:Humans; D007527:Isoenzymes; D051379:Mice; D009219:Myosin-Light-Chain Kinase / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000502:physiology; D010766:Phosphorylation; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000517:prevention & control
chemical_list: D007527:Isoenzymes; D009219:Myosin-Light-Chain Kinase