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Your search keyword '"Yamada, Ryo"' showing total 9 results
Start Over Author "Yamada, Ryo" Journal nature genetics
9 results on '"Yamada, Ryo"'

1. Meta-analysis identifies nine new loci associated with rheumatoid arthritis in the Japanese population

Author

Okada, Yukinori, primary, Terao, Chikashi, additional, Ikari, Katsunori, additional, Kochi, Yuta, additional, Ohmura, Koichiro, additional, Suzuki, Akari, additional, Kawaguchi, Takahisa, additional, Stahl, Eli A, additional, Kurreeman, Fina A S, additional, Nishida, Nao, additional, Ohmiya, Hiroko, additional, Myouzen, Keiko, additional, Takahashi, Meiko, additional, Sawada, Tetsuji, additional, Nishioka, Yuichi, additional, Yukioka, Masao, additional, Matsubara, Tsukasa, additional, Wakitani, Shigeyuki, additional, Teshima, Ryota, additional, Tohma, Shigeto, additional, Takasugi, Kiyoshi, additional, Shimada, Kota, additional, Murasawa, Akira, additional, Honjo, Shigeru, additional, Matsuo, Keitaro, additional, Tanaka, Hideo, additional, Tajima, Kazuo, additional, Suzuki, Taku, additional, Iwamoto, Takuji, additional, Kawamura, Yoshiya, additional, Tanii, Hisashi, additional, Okazaki, Yuji, additional, Sasaki, Tsukasa, additional, Gregersen, Peter K, additional, Padyukov, Leonid, additional, Worthington, Jane, additional, Siminovitch, Katherine A, additional, Lathrop, Mark, additional, Taniguchi, Atsuo, additional, Takahashi, Atsushi, additional, Tokunaga, Katsushi, additional, Kubo, Michiaki, additional, Nakamura, Yusuke, additional, Kamatani, Naoyuki, additional, Mimori, Tsuneyo, additional, Plenge, Robert M, additional, Yamanaka, Hisashi, additional, Momohara, Shigeki, additional, Yamada, Ryo, additional, Matsuda, Fumihiko, additional, and Yamamoto, Kazuhiko, additional

Published
2012
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2. Polygenic burdens on cell-specific pathways underlie the risk of rheumatoid arthritis

Author

Ishigaki, Kazuyoshi, Kochi, Yuta, Suzuki, Akari, Tsuchida, Yumi, Tsuchiya, Haruka, Sumitomo, Shuji, Yamaguchi, Kensuke, Nagafuchi, Yasuo, Nakachi, Shinichiro, Kato, Rika, Sakurai, Keiichi, Shoda, Hirofumi, Ikari, Katsunori, Taniguchi, Atsuo, Yamanaka, Hisashi, Miya, Fuyuki, Tsunoda, Tatsuhiko, Okada, Yukinori, Momozawa, Yukihide, Kamatani, Yoichiro, Yamada, Ryo, Kubo, Michiaki, Fujio, Keishi, and Yamamoto, Kazuhiko

Abstract

Recent evidence suggests that a substantial portion of complex disease risk alleles modify gene expression in a cell-specific manner. To identify candidate causal genes and biological pathways of immune-related complex diseases, we conducted expression quantitative trait loci (eQTL) analysis on five subsets of immune cells (CD4+T cells, CD8+T cells, B cells, natural killer (NK) cells and monocytes) and unfractionated peripheral blood from 105 healthy Japanese volunteers. We developed a three-step analytical pipeline comprising (i) prediction of individual gene expression using our eQTL database and public epigenomic data, (ii) gene-level association analysis and (iii) prediction of cell-specific pathway activity by integrating the direction of eQTL effects. By applying this pipeline to rheumatoid arthritis data sets, we identified candidate causal genes and a cytokine pathway (upregulation of tumor necrosis factor (TNF) in CD4+T cells). Our approach is an efficient way to characterize the polygenic contributions and potential biological mechanisms of complex diseases.

Published
2017
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3. A regulatory variant in CCR6 is associated with rheumatoid arthritis susceptibility

Author

Kochi, Yuta, primary, Okada, Yukinori, additional, Suzuki, Akari, additional, Ikari, Katsunori, additional, Terao, Chikashi, additional, Takahashi, Atsushi, additional, Yamazaki, Keiko, additional, Hosono, Naoya, additional, Myouzen, Keiko, additional, Tsunoda, Tatsuhiko, additional, Kamatani, Naoyuki, additional, Furuichi, Tatsuya, additional, Ikegawa, Shiro, additional, Ohmura, Koichiro, additional, Mimori, Tsuneyo, additional, Matsuda, Fumihiko, additional, Iwamoto, Takuji, additional, Momohara, Shigeki, additional, Yamanaka, Hisashi, additional, Yamada, Ryo, additional, Kubo, Michiaki, additional, Nakamura, Yusuke, additional, and Yamamoto, Kazuhiko, additional

Published
2010
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4. Functional SNPs in CD244 increase the risk of rheumatoid arthritis in a Japanese population

Author

Suzuki, Akari, primary, Yamada, Ryo, additional, Kochi, Yuta, additional, Sawada, Tetsuji, additional, Okada, Yukinori, additional, Matsuda, Koichi, additional, Kamatani, Yoichiro, additional, Mori, Mikako, additional, Shimane, Kenichi, additional, Hirabayashi, Yasuhiko, additional, Takahashi, Atsushi, additional, Tsunoda, Tatsuhiko, additional, Miyatake, Akihiko, additional, Kubo, Michiaki, additional, Kamatani, Naoyuki, additional, Nakamura, Yusuke, additional, and Yamamoto, Kazuhiko, additional

Published
2008
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5. A functional variant in FCRL3, encoding Fc receptor-like 3, is associated with rheumatoid arthritis and several autoimmunities

Author

Kochi, Yuta, primary, Yamada, Ryo, additional, Suzuki, Akari, additional, Harley, John B, additional, Shirasawa, Senji, additional, Sawada, Tetsuji, additional, Bae, Sang-Cheol, additional, Tokuhiro, Shinya, additional, Chang, Xiaotian, additional, Sekine, Akihiro, additional, Takahashi, Atsushi, additional, Tsunoda, Tatsuhiko, additional, Ohnishi, Yozo, additional, Kaufman, Kenneth M, additional, Kang, Changsoo Paul, additional, Kang, Changwon, additional, Otsubo, Shigeru, additional, Yumura, Wako, additional, Mimori, Akio, additional, Koike, Takao, additional, Nakamura, Yusuke, additional, Sasazuki, Takehiko, additional, and Yamamoto, Kazuhiko, additional

Published
2005
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6. An intronic SNP in a RUNX1 binding site of SLC22A4, encoding an organic cation transporter, is associated with rheumatoid arthritis

Author

Tokuhiro, Shinya, primary, Yamada, Ryo, additional, Chang, Xiaotian, additional, Suzuki, Akari, additional, Kochi, Yuta, additional, Sawada, Tetsuji, additional, Suzuki, Masakatsu, additional, Nagasaki, Miyuki, additional, Ohtsuki, Masahiko, additional, Ono, Mitsuru, additional, Furukawa, Hidehiko, additional, Nagashima, Masakazu, additional, Yoshino, Shinichi, additional, Mabuchi, Akihiko, additional, Sekine, Akihiro, additional, Saito, Susumu, additional, Takahashi, Atsushi, additional, Tsunoda, Tatsuhiko, additional, Nakamura, Yusuke, additional, and Yamamoto, Kazuhiko, additional

Published
2003
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7. Functional haplotypes of PADI4, encoding citrullinating enzyme peptidylarginine deiminase 4, are associated with rheumatoid arthritis

Author

Suzuki, Akari, primary, Yamada, Ryo, additional, Chang, Xiaotian, additional, Tokuhiro, Shinya, additional, Sawada, Tetsuji, additional, Suzuki, Masakatsu, additional, Nagasaki, Miyuki, additional, Nakayama-Hamada, Makiko, additional, Kawaida, Reimi, additional, Ono, Mitsuru, additional, Ohtsuki, Masahiko, additional, Furukawa, Hidehiko, additional, Yoshino, Shinichi, additional, Yukioka, Masao, additional, Tohma, Shigeto, additional, Matsubara, Tsukasa, additional, Wakitani, Shigeyuki, additional, Teshima, Ryota, additional, Nishioka, Yuichi, additional, Sekine, Akihiro, additional, Iida, Aritoshi, additional, Takahashi, Atsushi, additional, Tsunoda, Tatsuhiko, additional, Nakamura, Yusuke, additional, and Yamamoto, Kazuhiko, additional

Published
2003
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9. Functional SNPs in the lymphotoxin-alpha gene that are associated with susceptibility to myocardial infarction.

Author

Ozaki K, Ohnishi Y, Iida A, Sekine A, Yamada R, Tsunoda T, Sato H, Sato H, Hori M, Nakamura Y, and Tanaka T

Subjects
Aged, Amino Acid Substitution, Case-Control Studies, Cells, Cultured, Chromosome Mapping, Chromosomes, Human, Pair 6, Coronary Vessels metabolism, Databases, Genetic, Gene Frequency, Genetic Testing, Genotype, Haplotypes, Homozygote, Humans, Introns, Jurkat Cells, Linkage Disequilibrium, Middle Aged, Muscle, Smooth, Vascular cytology, Muscle, Smooth, Vascular physiology, Recombinant Fusion Proteins metabolism, Sequence Analysis, DNA, Transcription, Genetic, Vascular Cell Adhesion Molecule-1 biosynthesis, Genetic Predisposition to Disease, Lymphotoxin-alpha genetics, Myocardial Infarction genetics, Polymorphism, Single Nucleotide
Abstract

By means of a large-scale, case-control association study using 92,788 gene-based single-nucleotide polymorphism (SNP) markers, we identified a candidate locus on chromosome 6p21 associated with susceptibility to myocardial infarction. Subsequent linkage-disequilibrium (LD) mapping and analyses of haplotype structure showed significant associations between myocardial infarction and a single 50 kb halpotype comprised of five SNPs in LTA (encoding lymphotoxin-alpha), NFKBIL1 (encoding nuclear factor of kappa light polypeptide gene enhancer in B cells, inhibitor-like 1) and BAT1 (encoding HLA-B associated transcript 1). Homozygosity with respect to each of the two SNPs in LTA was significantly associated with increased risk for myocardial infarction (odds ratio = 1.78, chi(2) = 21.6, P = 0.00000033; 1,133 affected individuals versus 1,006 controls). In vitro functional analyses indicated that one SNP in the coding region of LTA, which changed an amino-acid residue from threonine to asparagine (Thr26Asn), effected a twofold increase in induction of several cell-adhesion molecules, including VCAM1, in vascular smooth-muscle cells of human coronary artery. Moreover, the SNP, in intron 1 of LTA, enhanced the transcriptional level of LTA. These results indicate that variants in the LTA are risk factors for myocardial infraction and implicate LTA in the pathogenesis of the disorder.

Published
2002
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