Further Evidence for Asthma Susceptibility Gene on Chromosome 11 in African Americans

2006 ◽  
Vol 117 (2) ◽  
pp. S324
Author(s):  
P.S. Gao ◽  
R.A. Mathias ◽  
J. Goldstein ◽  
W. Alexander F ◽  
E.W. Pugh ◽  
...  
Keyword(s):  
African Americans ◽  
Susceptibility Gene ◽  
Chromosome 11 ◽  
Asthma Susceptibility

scholarly journals The ORMDL3 asthma susceptibility gene regulates systemic ceramide levels without altering key asthma features in mice

2019 ◽  
Vol 144 (6) ◽  
pp. 1648-1659.e9 ◽  
Author(s):  
Nincy Debeuf ◽  
Assem Zhakupova ◽  
Regula Steiner ◽  
Sofie Van Gassen ◽  
Kim Deswarte ◽  
...  
Keyword(s):  
Susceptibility Gene ◽  
Asthma Susceptibility

Positional Identification of an Asthma Susceptibility Gene on Human Chromosome 5q33

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

scholarly journals Positionally cloned asthma susceptibility gene polymorphisms and disease risk in the British 1958 Birth Cohort

Thorax ◽  
2009 ◽  
Vol 64 (5) ◽  
pp. 381-387 ◽  
Author(s):  
J D Blakey ◽  
I Sayers ◽  
S M Ring ◽  
D P Strachan ◽  
I P Hall
Keyword(s):  
Birth Cohort ◽  
Gene Polymorphisms ◽  
Disease Risk ◽  
Susceptibility Gene ◽  
Asthma Susceptibility

scholarly journals Genome wide-association study identifies novel loci in the Primary Open-Angle African American Glaucoma Genetics (POAAGG) study

2020 ◽  
Author(s):  
Harini V. Gudiseva ◽  
Shefali Setia Verma ◽  
Venkata R. M. Chavali ◽  
Rebecca J. Salowe ◽  
Anastasia Lucas ◽  
...  
Keyword(s):  
African American ◽  
African Americans ◽  
Large Scale ◽  
Genome Wide Association Study ◽  
Open Angle Glaucoma ◽  
Retinal Ganglion ◽  
Open Angle ◽  
Chromosome 11 ◽  
Disease Biology ◽  
Genome Wide

AbstractPrimary open-angle glaucoma (POAG), the leading cause of irreversible blindness worldwide, disproportionately affects African Americans. Large-scale POAG genetic studies have focused on individuals of European and Asian ancestry, limiting our understanding of disease biology. Here we report genetic analysis of the largest-ever deeply phenotyped African American population (n=5950), identifying a novel POAG-associated SNP on chromosome 11 near the TRIM66 gene (rs112369934). POAG trait association also implicated SNPs in genes involved in trabecular meshwork homeostasis and retinal ganglion cell maintenance. These new loci deepen our understanding of the pathophysiology of POAG in African Americans.

Analysis of the asthma susceptibility gene ORMDL3 using the model organism Drosophila melanogaster

Pneumologie ◽  
2012 ◽  
Vol 66 (06) ◽  
Author(s):  
K Kallsen ◽  
N Zehethofer ◽  
B Lindner ◽  
H Heine ◽  
T Roeder
Keyword(s):  
Drosophila Melanogaster ◽  
Susceptibility Gene ◽  
Model Organism ◽  
Asthma Susceptibility

scholarly journals ADAM33 Is Not Essential for Growth and Development and Does Not Modulate Allergic Asthma in Mice

2006 ◽  
Vol 26 (18) ◽  
pp. 6950-6956 ◽  
Author(s):  
Chun Chen ◽  
Xiaozhu Huang ◽  
Dean Sheppard
Keyword(s):  
Animal Model ◽  
Allergic Asthma ◽  
Growth And Development ◽  
Immunoglobulin E ◽  
Susceptibility Gene ◽  
Airway Hyperreactivity ◽  
Mammalian Development ◽  
Asthma Susceptibility ◽  
Integrin Ligand ◽  
Mucus Metaplasia

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.

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