Isoform-specific knockout of endothelial myosin light chain kinase: closing the gap on inflammatory lung disease. Academic Article

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

• Wilson, Emily

published proceedings

• Trends Pharmacol Sci

author list (cited authors)

• Tinsley, J. H., Yuan, S. Y., & Wilson, E.

citation count

• 9

complete list of authors

• Tinsley, John H||Yuan, Sarah Y||Wilson, Emily

publication date

• January 2004

publisher

• Elsevier  Publisher

published in

• Trends in Pharmacological Sciences  Journal

keywords

• Animals
• Humans
• Isoenzymes
• Mice
• Myosin-Light-Chain Kinase
• Phosphorylation
• Respiratory Distress Syndrome

Digital Object Identifier (DOI)

• 10.1016/j.tips.2003.12.003

start page

• 64

end page

• 66

volume

• 25

issue

• 2

URL

• http://dx.doi.org/10.1016/j.tips.2003.12.003