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Molecular and Cellular Biology, September 2006, p. 6950-6956, Vol. 26, No. 18
0270-7306/06/$08.00+0 doi:10.1128/MCB.00646-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Lung Biology Center, Department of Medicine, University of California, San Francisco, San Francisco, California 94158
Received 13 April 2006/ Returned for modification 16 June 2006/ Accepted 30 June 2006
A disintegrin and metalloprotease 33 (ADAM33) is a transmembrane protease and integrin ligand that has been identified as an asthma susceptibility gene product. To determine whether ADAM33 plays important roles in mammalian development and the modulation of allergic airway dysfunction, we generated ADAM33-null mice by gene targeting. ADAM33-null mice were born at expected Mendelian ratios, and both male and females developed normally and were fertile. No anatomical or histological abnormalities were detected in any tissues. In an animal model of allergic asthma, ADAM33-null mice showed normal allergen-induced airway hyperreactivity, immunoglobulin E production, mucus metaplasia, and airway inflammation. Our results demonstrate that ADAM33 is not essential for growth or reproduction in the mouse and does not modulate baseline or allergen-induced airway responsiveness.
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