Letter to the EditorThe − 429 T>C polymorphism of the receptor for advanced glycation end products (RAGE) is associated with type 1 diabetes in a Brazilian population☆
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− 374 T/A polymorphism of the RAGE gene promoter in relation to severity of coronary atherosclerosis
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The HLA 8.1 ancestral haplotype is strongly linked to the C allele of − 429 T>C promoter polymorphism of receptor of the advanced glycation endproducts (RAGE). Haplotype-independent association of the − 429 C allele with high hemoglobinA1C levels in diabetic patients
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(2007)
Cited by (14)
Promoter methylation cooperates with SNPs to modulate RAGE transcription and alter UC risk
2019, Biochemistry and Biophysics ReportsCitation Excerpt :Conflicting results have also been reported. Picheth (2007) reported that the −429T>C, rather than the -374T>A, RAGE promoter polymorphism is associated with type 1 diabetes in a Brazilian population, and a 2-fold increase in the -429C allele frequency was observed among diabetic subjects compared with nondiabetic subjects [33]. Similarly, Peng et al. (2009) found that Chinese patients with type 2 diabetes mellitus who carry the C allele of -429T/C and G allele of G82S exhibited significantly higher sRAGE levels, while no such association was found in patients with different combinations of the -374T/A allele [34].
Genetic polymorphisms of RAGE and risk of ulcerative colitis in a Chinese population
2016, Immunology LettersCitation Excerpt :Considering the variation in the prevalence of RAGE G82S among different populations, the hypothesis that inherited variation in RAGE might contribute to UC should be tested in the future using larger and ethnically different populations. Because RAGE is upregulated in IBD [14,23], it is tempting to speculate that the −429 T/C and −374 T/A polymorphisms located at the promoter region could alter transcription, leading to an enhanced level of RAGE and a different disease outcome; indeed, there were reports that promoter polymorphisms could alter transcription in other diseases [35–38]. For example, Däbritz et al. [23] reported that a −374 T/A polymorphism that facilitated RAGE gene transcription may, to some degree, protect against development of a strict subphenotype of CD.
Functional promoter polymorphisms of the receptor for advanced glycation end products in children and adolescents with type 1 diabetes
2015, Molecular and Cellular ProbesAssociation of RAGE gene polymorphisms with sporadic Parkinson's disease in Chinese Han population
2014, Neuroscience LettersCitation Excerpt :The RAGE gene, comprising 11 exons, is located on chromosome 6p21.3 in the major histocompatibility complex locus in the class III region, which is a gene-dense region containing a number of inflammatory genes [24]. So far, the RAGE genes have been identified having several genetic variants including −429T/C(rs1800625),−374T/A(rs1800624), and 82G/S(2070600) which may affect the expression or function of RAGE [9,14,23]. Previous studies have reported association between the polymorphisms of RAGE gene and various disease including Alzheimer's disease [8] and inflammatory processes.
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We are thankful to Dr M.G. Yates for reading the manuscript and for the suggestions. This project was supported by CNPq.