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The 8-oxoguanine DNA N-glycosylase 1 (hOGG1) Ser326Cys variant affects the susceptibility to Graves' disease.

Authors: Tanrikulu, S  Dogru-Abbasoglu, S  Ozderya, A  Ademoglu, E  Karadag, B  Erbil, Y  Uysal, M 
Citation: Tanrikulu S, etal., Cell Biochem Funct. 2011 Apr;29(3):244-8. doi: 10.1002/cbf.1742. Epub 2011 Feb 24.
Pubmed: (View Article at PubMed) PMID:21465496
DOI: Full-text: DOI:10.1002/cbf.1742

Oxidative DNA damage, caused by either endogenous or exogenous sources of reactive oxygen species (ROS), has been linked several diseases including Graves' disease (GD). 7,8-Dihydro-8-oxoguanine (8-oxoG) is a major lesion produced by ROS and is considered a key biomarker of oxidative DNA damage. In humans, 8-oxoG is mainly repaired by 8-oxoguanine DNA N-glycosylase-1 (hOGG1), which is an essential component of the base excision repair (BER) pathway. The functional studies showed that hOGG1 Ser326Cys polymorphism is associated with the reduced DNA repair activity and increased risk for some oxidative stress-related diseases. In this study, we firstly investigated hOGG1 Ser326Cys polymorphism in GD. According to our results, Cys/Cys genotype frequency in the GD patients (23.4%) was significantly higher than the controls (9.2%). Cys/Cys genotype had an 3.5-fold [95% CI (confidence interval): 2.10-6.01, p < 0.001] the Cys allele had 1.83-fold (95% CI: 1.43-2.34, p < 0.001) increase in the risk for developing GD. Our results suggest that Ser326Cys polymorphism of the hOGG1 gene is associated with GD risk.


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RGD Object Information
RGD ID: 8657376
Created: 2014-06-06
Species: All species
Last Modified: 2014-06-06
Status: ACTIVE


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