TY - JOUR
T1 - Association Study of ARMC9 Gene Variants with Vogt-Koyanagi-Harada Disease in Japanese Patients
AU - Ohno, Tomoko
AU - Meguro, Akira
AU - Takeuchi, Masaki
AU - Yamane, Takahiro
AU - Teshigawara, Takeshi
AU - Kitaichi, Nobuyoshi
AU - Horie, Yukihiro
AU - Namba, Kenichi
AU - Ohno, Shigeaki
AU - Nakao, Kumiko
AU - Sakamoto, Taiji
AU - Sakai, Tsutomu
AU - Nakano, Tadashi
AU - Keino, Hiroshi
AU - Okada, Annabelle A.
AU - Takeda, Atsunobu
AU - Fukuhara, Takako
AU - Mashimo, Hisashi
AU - Ohguro, Nobuyuki
AU - Oono, Shinichirou
AU - Enaida, Hiroshi
AU - Okinami, Satoshi
AU - Mizuki, Nobuhisa
N1 - Publisher Copyright:
© 2019, © 2019 Taylor & Francis Group, LLC.
PY - 2019
Y1 - 2019
N2 - Purpose: To investigate whether variants in the ARMC9 gene encoding KU-MEL-1 are associated with Vogt-Koyanagi-Harada (VKH) disease in a Japanese population. Methods: We recruited 380 Japanese patients with VKH disease and 744 Japanese healthy controls to genotype seven single-nucleotide polymorphisms (SNPs) in ARMC9. We also performed imputation analysis of the ARMC9 region and 195 imputed SNPs were included in the statistical analysis. Results: We observed an increased frequency of the A allele of rs28690417 in patients compared with controls (P = 0.0097, odds ratio (OR) = 1.46). The A allele had a dominant effect on VKH disease risk (P = 0.011, OR = 1.51). However, these significant differences disappeared after Bonferroni correction (corrected P > 0.05). The remaining 201 SNPs did not show any significant association with disease risk. Conclusions: Our study suggests that ARMC9 variants do not play a critical role in the development of VKH disease.
AB - Purpose: To investigate whether variants in the ARMC9 gene encoding KU-MEL-1 are associated with Vogt-Koyanagi-Harada (VKH) disease in a Japanese population. Methods: We recruited 380 Japanese patients with VKH disease and 744 Japanese healthy controls to genotype seven single-nucleotide polymorphisms (SNPs) in ARMC9. We also performed imputation analysis of the ARMC9 region and 195 imputed SNPs were included in the statistical analysis. Results: We observed an increased frequency of the A allele of rs28690417 in patients compared with controls (P = 0.0097, odds ratio (OR) = 1.46). The A allele had a dominant effect on VKH disease risk (P = 0.011, OR = 1.51). However, these significant differences disappeared after Bonferroni correction (corrected P > 0.05). The remaining 201 SNPs did not show any significant association with disease risk. Conclusions: Our study suggests that ARMC9 variants do not play a critical role in the development of VKH disease.
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U2 - 10.1080/09273948.2018.1523438
DO - 10.1080/09273948.2018.1523438
M3 - Article
C2 - 30395750
AN - SCOPUS:85056100244
VL - 27
SP - 699
EP - 705
JO - Ocular Immunology and Inflammation
JF - Ocular Immunology and Inflammation
SN - 0927-3948
IS - 5
ER -