ArticleAge (Dordrecht, Netherlands)2014
In-depth analyses unveil the association and possible functional involvement of novel RAD51B polymorphisms in age-related macular degeneration.
Article in Age (Dordrecht, Netherlands), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions.Annual review of vision science · 2021Review
- Epistatic interactions of genetic loci associated with age-related macular degeneration.Scientific reports · 2021Article
- Analysis of genetic polymorphisms for age-related macular degeneration (AMD) in Chinese Tujia ethnic minority group.BMC medical genetics · 2019Article
- Article
- Functional single nucleotide polymorphism in IL-17A 3' untranslated region is targeted by miR-4480 in vitro and may be associated with age-related macular degeneration.Environmental and molecular mutagenesis · 2016Article
- Wnt signaling in age-related macular degeneration: human macular tissue and mouse model.Journal of translational medicine · 2015Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The contribution of DNA damage to the pathogenesis of age-related macular degeneration (AMD) has been reported. Recently, a genomewide association study detected the association of a single-nucleotide polymorphism (SNP) in RAD51B (rs8017304 A>G) with AMD. RAD51B is involved in recombinational repair of DNA double-strand breaks. We analyzed RAD51B influence on AMD using two cohorts from Caucasian and Han Chinese populations. The Caucasian set replicated the rs8017304 A>G association and revealed two novel AMD-associated SNPs in RAD51B, rs17105278 T>C and rs4902566 C>T. Under the dominant model, these two SNPs exhibit highly significant disease risk. SNP-SNP interaction analysis on rs17105278 T>C and rs4902566 C>T homozygous demonstrated a synergistic effect on AMD risk, reaching an odds ratio multifold higher than well-established AMD susceptibility loci in genes such as CFH, HTRA1, and ARMS2. Functional study revealed lower RAD51B mRNA expression in cultured primary human fetal retinal pigment epithelium (hfRPE) carrying rs17105278 T>C variants than in hfRPE carrying rs17105278 wild type. We concluded that the risk of developing AMD exhibits dose dependency as well as an epistatic combined effect in rs17105278 T>C and rs4902566 C>T carriers and that the elevated risk for rs17105278 T>C carriers may be due to decreased transcription of RAD51B. This study further confirms the role of DNA damage/DNA repair in AMD pathogenesis.
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