scholarly journals Association of a nonsynonymous single-nucleotide polymorphism of matrix metalloproteinase 9 with giant cell arteritis

2008 ◽  
Vol 58 (6) ◽  
pp. 1849-1853 ◽  
Author(s):  
A. Rodríguez-Pla ◽  
T. H. Beaty ◽  
P. J. Savino ◽  
R. C. Eagle ◽  
P. Seo ◽  
...  
Keyword(s):  
Single Nucleotide Polymorphism ◽  
Matrix Metalloproteinase ◽  
Giant Cell Arteritis ◽  
Giant Cell ◽  
Matrix Metalloproteinase 9 ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Metalloproteinase 9

Elevated levels of 92-kd type IV collagenase (matrix metalloproteinase 9) in giant cell arteritis

1996 ◽  
Vol 39 (10) ◽  
pp. 1747-1753 ◽  
Author(s):  
D. Sorbi ◽  
D. L. French ◽  
G. J. Nuovo ◽  
R. R. Kew ◽  
L. A. Arbeit ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Giant Cell Arteritis ◽  
Giant Cell ◽  
Matrix Metalloproteinase 9 ◽  
Type Iv Collagenase ◽  
Type Iv ◽  
Metalloproteinase 9

Evaluation of a Shared Autoimmune Disease-associated Polymorphism of TRAF6 in Systemic Sclerosis and Giant Cell Arteritis

2012 ◽  
Vol 39 (6) ◽  
pp. 1275-1279 ◽  
Author(s):  
F. DAVID CARMONA ◽  
AURORA SERRANO ◽  
LUIS RODRÍGUEZ-RODRÍGUEZ ◽  
JOSÉ LUIS CALLEJAS ◽  
CARMEN P. SIMEÓN ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Giant Cell Arteritis ◽  
Giant Cell ◽  
Lupus Erythematosus ◽  
Genetic Network ◽  
Healthy Controls ◽  
Nucleotide Polymorphism ◽  
Common Risk Factor ◽  
Single Nucleotide

Objective.We evaluated whether a single-nucleotide polymorphism (SNP) of theTRAF6gene previously associated with systemic lupus erythematosus and rheumatoid arthritis may be a common risk factor for systemic sclerosis (SSc) and giant cell arteritis (GCA).Methods.A total of 1185 patients with SSc, 479 patients with biopsy-proven GCA, and 1442 unrelated healthy controls of white Spanish origin were genotyped for the rs540386 variant using a specifically designed TaqMan©allele discrimination assay.Results.No significant associations of this SNP with global SSc or GCA were found. This was also the case when the potential associations of theTRAF6polymorphism with the main clinical phenotypes of the 2 diseases (e.g., limited cutaneous and diffuse cutaneous SSc, or presence of polymyalgia rheumatica and visual ischemic manifestations in GCA) were assessed.Conclusion.Our data do not support a role of the rs540386TRAF6variant as a key component of the genetic network underlying SSc and GCA.

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