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«ARMS2

Below is an extended ARMS2 publications listing. Click here to return to the gene page.

Gene Information from Publications

Publication Link Summary of findings
18248681 Observational study of genotype prevalence. (HuGE Navigator)
18292785 Observational study of gene-disease association. (HuGE Navigator)
18325906 Observational study of gene-disease association. (HuGE Navigator)
17325155 Observational study of gene-disease association. (HuGE Navigator)
17347568 Observational study of gene-disease association and gene-environment interaction. (HuGE Navigator)
17352366 Observational study of genotype prevalence and gene-disease association. (HuGE Navigator)
17426452 Observational study of gene-disease association. (HuGE Navigator)
17456821 Observational study of gene-disease association, gene-gene interaction, and gene-environment interaction. (HuGE Navigator)
17884985 Observational study of gene-disease association. (HuGE Navigator)
18054635 Observational study of gene-environment interaction and pharmacogenomic / toxicogenomic. (HuGE Navigator)
18061132 Observational study of gene-disease association. (HuGE Navigator)
18079691 Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator)
18161619 Observational study of gene-disease association. (HuGE Navigator)
18162041 Observational study of gene-disease association, gene-gene interaction, and gene-environment interaction. (HuGE Navigator)
18164066 Observational study of gene-disease association, gene-gene interaction, and gene-environment interaction. (HuGE Navigator)
18079691 Although a role for PLEKHA1 could not be totally excluded, there was a four times higher age-related macular degeneration risk was associated with haplotype "A-T-A" involving "PLEKHA1-LOC387715-HTRA1" risk alleles.
18162041 Polymorphisms in the complement factor H gene, LOC387715, and the HTRA1 promoter are strongly associated with age-related macular degeneration.
18054635 The Age-related macular degeneration associated complement factor H Y402H and LOC387715 A69S variants were associated with differences in choroidal neovascular lesion size in this study.
17884985 SNP rs10490924 represents a major susceptibility variant for age-related macular degeneration. A likely biological mechanism is that the A69S change in the LOC387715/ARMS2 protein affects its presumptive function in mitochondria.
17692272 The LOC387715/HTRA1 variants are associated with polypoidal choroidal vasculopathy (PCV) and wet age-related macular degeneration (AMD) in the Japanese population.
17846368 Both ARMS2 polymorphism and complement factor H polymorphism are independently associated with progression of age-related macular degeneration.
16642439 Our results strongly implicate a coding change (Ala69Ser) in the LOC387715 gene as the second major identified AMD-susceptibility allele, confirming earlier suggestions. This variant's effect on AMD is statistically independent of CFH .
17285240 findings suggest that the combined effect of variants in the CFH and LOC 387715 genes may contribute to the age-related macular degeneration phenotype in this family
17000705 study provides additional support for the CFH and LOC387715 genes in age-related maculopathy (ARM) susceptibility via the evaluation of cohorts that had different ascertainment schemes regarding ARM status and through the meta-analyses
16174643 Hypothetical LOC387715 is a second major susceptibility gene for age-related macular degeneration, contributing independently of complement factor H to disease risk.
17194541 A polymorphism of LOC387715 gene is associated with age-related macular degeneration in the Japanese population.
16954704 Results further support the notion that CFH (complement factor H) and LOC387715 genes are the major risk factors for ARMD.
17347568 The number of risk alleles at the LOC387715 SNP was associated with advanced Age-related macular degeneration
17325155 AMD (age-related macular degeneration) genetic risk marker harbored within LOC387715, the nested case-control data from the population-based BMES samples showed lower estimates than from the clinic-based samples.

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