Details

Project TitleMouse Null for Endothelial Cell Myosin Light Chain Kinase (EC-MLCK)
Track Code2002-026
Short Description

Investigators have created a mouse model that is resistant to ventilation induced- and acute- lung injury. These mice are null for expression of endothelial cell-myosin light chain kinase (EC-MLCK) and are able to survive bacterial endotoxin lipopolysaccharide (LPS)-induced lung injury, unlike wild-type mice.

Abstract

These mice are useful models to investigate the role of EC-MLCK in various pathological conditions, including ventilation-induced lung injury, acute lung injury, sepsis, tumor-related angiogensis and metastasis, cardiovascular disease, and are a useful validation tool for drugs designed to inhibit EC-MLCK.

BACKGROUND

EC-MLCK has been implicated as a mediator of the processes that occur in acute lung injury (ALI) and ventilation-induced lung injury (VILI). Endothelial cell myosin light chain kinase (MLCK210 or EC-MLCK) is a member of the myosin light chain kinase family. Members of the MLCK family have been demonstrated to be important molecules in cytoskeleton regulation, programmed cell death (apoptosis), and tumor suppression. Members of this family, including EC-MLCK, are potential drug discovery targets. EC-MLCK is an endothelial regulator and appears to be involved in susceptibility to lung injury, angiogenesis and tumor growth. This mouse model offers the ability to investigate the role of EC-MLCK in a variety of physiological processes.

This animal model is available for licensing.

 
Tagsresearch tools, animal models
 
Posted DateMar 30, 2011 4:35 PM

Inventor(s)

James Schavocky

Daniel Martin Watterson

Contact Information

Gwendolyn Humphreys, PhD

Invention Associate

(p) 847-467-0308

(e) Gwendolyn.Humphreys@northwestern.edu