Convergent Evidence Supports TH2LCRR as a Novel Asthma Susceptibility Gene

Author(s):  
Yi-Kun Li ◽  
Xin-Xin Zhang ◽  
Yuan Yang ◽  
Jing Gao ◽  
Qiang Shi ◽  
...  
2019 ◽  
Vol 144 (6) ◽  
pp. 1648-1659.e9 ◽  
Author(s):  
Nincy Debeuf ◽  
Assem Zhakupova ◽  
Regula Steiner ◽  
Sofie Van Gassen ◽  
Kim Deswarte ◽  
...  

2005 ◽  
Vol 172 (2) ◽  
pp. 183-188 ◽  
Author(s):  
Emiko Noguchi ◽  
Yukako Yokouchi ◽  
Jiang Zhang ◽  
Kazuko Shibuya ◽  
Akira Shibuya ◽  
...  

Thorax ◽  
2009 ◽  
Vol 64 (5) ◽  
pp. 381-387 ◽  
Author(s):  
J D Blakey ◽  
I Sayers ◽  
S M Ring ◽  
D P Strachan ◽  
I P Hall

Pneumologie ◽  
2012 ◽  
Vol 66 (06) ◽  
Author(s):  
K Kallsen ◽  
N Zehethofer ◽  
B Lindner ◽  
H Heine ◽  
T Roeder

2006 ◽  
Vol 26 (18) ◽  
pp. 6950-6956 ◽  
Author(s):  
Chun Chen ◽  
Xiaozhu Huang ◽  
Dean Sheppard

ABSTRACT 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.


2006 ◽  
Vol 117 (2) ◽  
pp. S324
Author(s):  
P.S. Gao ◽  
R.A. Mathias ◽  
J. Goldstein ◽  
W. Alexander F ◽  
E.W. Pugh ◽  
...  

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