TYK2 Promoter Variant and Diabetes Mellitus in the Japanese
Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is loc...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Seiho Nagafuchi [verfasserIn] Yumi Kamada-Hibio [verfasserIn] Kanako Hirakawa [verfasserIn] Nobutaka Tsutsu [verfasserIn] Masae Minami [verfasserIn] Akira Okada [verfasserIn] Katsuya Kai [verfasserIn] Miho Teshima [verfasserIn] Arisa Moroishi [verfasserIn] Yoshikazu Murakami [verfasserIn] Yoshikazu Umeno [verfasserIn] Yasushi Yokogawa [verfasserIn] Kazuhiko Kogawa [verfasserIn] Kenichi Izumi [verfasserIn] Keizo Anzai [verfasserIn] Ryuichi Iwakiri [verfasserIn] Kazuyuki Hamaguchi [verfasserIn] Nobuhiro Sasaki [verfasserIn] Sakae Nohara [verfasserIn] Eiko Yoshida [verfasserIn] Mine Harada [verfasserIn] Koichi Akashi [verfasserIn] Toshihiko Yanase [verfasserIn] Junko Ono [verfasserIn] Toshimitsu Okeda [verfasserIn] Ryoji Fujimoto [verfasserIn] Kenji Ihara [verfasserIn] Toshiro Hara [verfasserIn] Yohei Kikuchi [verfasserIn] Masanori Iwase [verfasserIn] Takanari Kitazono [verfasserIn] Fumiko Kojima [verfasserIn] Suminori Kono [verfasserIn] Hironori Kurisaki [verfasserIn] Shiori Kondo [verfasserIn] Hitoshi Katsuta [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: EBioMedicine - Elsevier, 2015, 2(2015), 7, Seite 744-749 |
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| Übergeordnetes Werk: |
volume:2 ; year:2015 ; number:7 ; pages:744-749 |
| Links: |
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| DOI / URN: |
10.1016/j.ebiom.2015.05.004 |
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| Katalog-ID: |
DOAJ032449925 |
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| 100 | 0 | |a Seiho Nagafuchi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a TYK2 Promoter Variant and Diabetes Mellitus in the Japanese |
| 264 | 1 | |c 2015 | |
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| 520 | |a Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. | ||
| 650 | 4 | |a Tyrosine kinase 2 (TYK2) | |
| 650 | 4 | |a Promoter variant | |
| 650 | 4 | |a Diabetes mellitus | |
| 650 | 4 | |a Virus | |
| 650 | 4 | |a Polymorphism | |
| 653 | 0 | |a Medicine | |
| 653 | 0 | |a R | |
| 653 | 0 | |a Medicine (General) | |
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| 700 | 0 | |a Yoshikazu Murakami |e verfasserin |4 aut | |
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| 700 | 0 | |a Yasushi Yokogawa |e verfasserin |4 aut | |
| 700 | 0 | |a Kazuhiko Kogawa |e verfasserin |4 aut | |
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| 700 | 0 | |a Kazuyuki Hamaguchi |e verfasserin |4 aut | |
| 700 | 0 | |a Nobuhiro Sasaki |e verfasserin |4 aut | |
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| 700 | 0 | |a Koichi Akashi |e verfasserin |4 aut | |
| 700 | 0 | |a Toshihiko Yanase |e verfasserin |4 aut | |
| 700 | 0 | |a Junko Ono |e verfasserin |4 aut | |
| 700 | 0 | |a Toshimitsu Okeda |e verfasserin |4 aut | |
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| 700 | 0 | |a Takanari Kitazono |e verfasserin |4 aut | |
| 700 | 0 | |a Fumiko Kojima |e verfasserin |4 aut | |
| 700 | 0 | |a Suminori Kono |e verfasserin |4 aut | |
| 700 | 0 | |a Hironori Kurisaki |e verfasserin |4 aut | |
| 700 | 0 | |a Shiori Kondo |e verfasserin |4 aut | |
| 700 | 0 | |a Hitoshi Katsuta |e verfasserin |4 aut | |
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10.1016/j.ebiom.2015.05.004 doi (DE-627)DOAJ032449925 (DE-599)DOAJ4513be54d16f42ffa11cc8aeca0b66f5 DE-627 ger DE-627 rakwb eng R5-920 Seiho Nagafuchi verfasserin aut TYK2 Promoter Variant and Diabetes Mellitus in the Japanese 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. Tyrosine kinase 2 (TYK2) Promoter variant Diabetes mellitus Virus Polymorphism Medicine R Medicine (General) Yumi Kamada-Hibio verfasserin aut Kanako Hirakawa verfasserin aut Nobutaka Tsutsu verfasserin aut Masae Minami verfasserin aut Akira Okada verfasserin aut Katsuya Kai verfasserin aut Miho Teshima verfasserin aut Arisa Moroishi verfasserin aut Yoshikazu Murakami verfasserin aut Yoshikazu Umeno verfasserin aut Yasushi Yokogawa verfasserin aut Kazuhiko Kogawa verfasserin aut Kenichi Izumi verfasserin aut Keizo Anzai verfasserin aut Ryuichi Iwakiri verfasserin aut Kazuyuki Hamaguchi verfasserin aut Nobuhiro Sasaki verfasserin aut Sakae Nohara verfasserin aut Eiko Yoshida verfasserin aut Mine Harada verfasserin aut Koichi Akashi verfasserin aut Toshihiko Yanase verfasserin aut Junko Ono verfasserin aut Toshimitsu Okeda verfasserin aut Ryoji Fujimoto verfasserin aut Kenji Ihara verfasserin aut Toshiro Hara verfasserin aut Yohei Kikuchi verfasserin aut Masanori Iwase verfasserin aut Takanari Kitazono verfasserin aut Fumiko Kojima verfasserin aut Suminori Kono verfasserin aut Hironori Kurisaki verfasserin aut Shiori Kondo verfasserin aut Hitoshi Katsuta verfasserin aut In EBioMedicine Elsevier, 2015 2(2015), 7, Seite 744-749 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:2 year:2015 number:7 pages:744-749 https://doi.org/10.1016/j.ebiom.2015.05.004 kostenfrei https://doaj.org/article/4513be54d16f42ffa11cc8aeca0b66f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396415300128 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2015 7 744-749 |
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10.1016/j.ebiom.2015.05.004 doi (DE-627)DOAJ032449925 (DE-599)DOAJ4513be54d16f42ffa11cc8aeca0b66f5 DE-627 ger DE-627 rakwb eng R5-920 Seiho Nagafuchi verfasserin aut TYK2 Promoter Variant and Diabetes Mellitus in the Japanese 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. Tyrosine kinase 2 (TYK2) Promoter variant Diabetes mellitus Virus Polymorphism Medicine R Medicine (General) Yumi Kamada-Hibio verfasserin aut Kanako Hirakawa verfasserin aut Nobutaka Tsutsu verfasserin aut Masae Minami verfasserin aut Akira Okada verfasserin aut Katsuya Kai verfasserin aut Miho Teshima verfasserin aut Arisa Moroishi verfasserin aut Yoshikazu Murakami verfasserin aut Yoshikazu Umeno verfasserin aut Yasushi Yokogawa verfasserin aut Kazuhiko Kogawa verfasserin aut Kenichi Izumi verfasserin aut Keizo Anzai verfasserin aut Ryuichi Iwakiri verfasserin aut Kazuyuki Hamaguchi verfasserin aut Nobuhiro Sasaki verfasserin aut Sakae Nohara verfasserin aut Eiko Yoshida verfasserin aut Mine Harada verfasserin aut Koichi Akashi verfasserin aut Toshihiko Yanase verfasserin aut Junko Ono verfasserin aut Toshimitsu Okeda verfasserin aut Ryoji Fujimoto verfasserin aut Kenji Ihara verfasserin aut Toshiro Hara verfasserin aut Yohei Kikuchi verfasserin aut Masanori Iwase verfasserin aut Takanari Kitazono verfasserin aut Fumiko Kojima verfasserin aut Suminori Kono verfasserin aut Hironori Kurisaki verfasserin aut Shiori Kondo verfasserin aut Hitoshi Katsuta verfasserin aut In EBioMedicine Elsevier, 2015 2(2015), 7, Seite 744-749 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:2 year:2015 number:7 pages:744-749 https://doi.org/10.1016/j.ebiom.2015.05.004 kostenfrei https://doaj.org/article/4513be54d16f42ffa11cc8aeca0b66f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396415300128 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2015 7 744-749 |
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10.1016/j.ebiom.2015.05.004 doi (DE-627)DOAJ032449925 (DE-599)DOAJ4513be54d16f42ffa11cc8aeca0b66f5 DE-627 ger DE-627 rakwb eng R5-920 Seiho Nagafuchi verfasserin aut TYK2 Promoter Variant and Diabetes Mellitus in the Japanese 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. Tyrosine kinase 2 (TYK2) Promoter variant Diabetes mellitus Virus Polymorphism Medicine R Medicine (General) Yumi Kamada-Hibio verfasserin aut Kanako Hirakawa verfasserin aut Nobutaka Tsutsu verfasserin aut Masae Minami verfasserin aut Akira Okada verfasserin aut Katsuya Kai verfasserin aut Miho Teshima verfasserin aut Arisa Moroishi verfasserin aut Yoshikazu Murakami verfasserin aut Yoshikazu Umeno verfasserin aut Yasushi Yokogawa verfasserin aut Kazuhiko Kogawa verfasserin aut Kenichi Izumi verfasserin aut Keizo Anzai verfasserin aut Ryuichi Iwakiri verfasserin aut Kazuyuki Hamaguchi verfasserin aut Nobuhiro Sasaki verfasserin aut Sakae Nohara verfasserin aut Eiko Yoshida verfasserin aut Mine Harada verfasserin aut Koichi Akashi verfasserin aut Toshihiko Yanase verfasserin aut Junko Ono verfasserin aut Toshimitsu Okeda verfasserin aut Ryoji Fujimoto verfasserin aut Kenji Ihara verfasserin aut Toshiro Hara verfasserin aut Yohei Kikuchi verfasserin aut Masanori Iwase verfasserin aut Takanari Kitazono verfasserin aut Fumiko Kojima verfasserin aut Suminori Kono verfasserin aut Hironori Kurisaki verfasserin aut Shiori Kondo verfasserin aut Hitoshi Katsuta verfasserin aut In EBioMedicine Elsevier, 2015 2(2015), 7, Seite 744-749 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:2 year:2015 number:7 pages:744-749 https://doi.org/10.1016/j.ebiom.2015.05.004 kostenfrei https://doaj.org/article/4513be54d16f42ffa11cc8aeca0b66f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396415300128 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2015 7 744-749 |
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10.1016/j.ebiom.2015.05.004 doi (DE-627)DOAJ032449925 (DE-599)DOAJ4513be54d16f42ffa11cc8aeca0b66f5 DE-627 ger DE-627 rakwb eng R5-920 Seiho Nagafuchi verfasserin aut TYK2 Promoter Variant and Diabetes Mellitus in the Japanese 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. Tyrosine kinase 2 (TYK2) Promoter variant Diabetes mellitus Virus Polymorphism Medicine R Medicine (General) Yumi Kamada-Hibio verfasserin aut Kanako Hirakawa verfasserin aut Nobutaka Tsutsu verfasserin aut Masae Minami verfasserin aut Akira Okada verfasserin aut Katsuya Kai verfasserin aut Miho Teshima verfasserin aut Arisa Moroishi verfasserin aut Yoshikazu Murakami verfasserin aut Yoshikazu Umeno verfasserin aut Yasushi Yokogawa verfasserin aut Kazuhiko Kogawa verfasserin aut Kenichi Izumi verfasserin aut Keizo Anzai verfasserin aut Ryuichi Iwakiri verfasserin aut Kazuyuki Hamaguchi verfasserin aut Nobuhiro Sasaki verfasserin aut Sakae Nohara verfasserin aut Eiko Yoshida verfasserin aut Mine Harada verfasserin aut Koichi Akashi verfasserin aut Toshihiko Yanase verfasserin aut Junko Ono verfasserin aut Toshimitsu Okeda verfasserin aut Ryoji Fujimoto verfasserin aut Kenji Ihara verfasserin aut Toshiro Hara verfasserin aut Yohei Kikuchi verfasserin aut Masanori Iwase verfasserin aut Takanari Kitazono verfasserin aut Fumiko Kojima verfasserin aut Suminori Kono verfasserin aut Hironori Kurisaki verfasserin aut Shiori Kondo verfasserin aut Hitoshi Katsuta verfasserin aut In EBioMedicine Elsevier, 2015 2(2015), 7, Seite 744-749 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:2 year:2015 number:7 pages:744-749 https://doi.org/10.1016/j.ebiom.2015.05.004 kostenfrei https://doaj.org/article/4513be54d16f42ffa11cc8aeca0b66f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396415300128 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2015 7 744-749 |
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10.1016/j.ebiom.2015.05.004 doi (DE-627)DOAJ032449925 (DE-599)DOAJ4513be54d16f42ffa11cc8aeca0b66f5 DE-627 ger DE-627 rakwb eng R5-920 Seiho Nagafuchi verfasserin aut TYK2 Promoter Variant and Diabetes Mellitus in the Japanese 2015 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. Tyrosine kinase 2 (TYK2) Promoter variant Diabetes mellitus Virus Polymorphism Medicine R Medicine (General) Yumi Kamada-Hibio verfasserin aut Kanako Hirakawa verfasserin aut Nobutaka Tsutsu verfasserin aut Masae Minami verfasserin aut Akira Okada verfasserin aut Katsuya Kai verfasserin aut Miho Teshima verfasserin aut Arisa Moroishi verfasserin aut Yoshikazu Murakami verfasserin aut Yoshikazu Umeno verfasserin aut Yasushi Yokogawa verfasserin aut Kazuhiko Kogawa verfasserin aut Kenichi Izumi verfasserin aut Keizo Anzai verfasserin aut Ryuichi Iwakiri verfasserin aut Kazuyuki Hamaguchi verfasserin aut Nobuhiro Sasaki verfasserin aut Sakae Nohara verfasserin aut Eiko Yoshida verfasserin aut Mine Harada verfasserin aut Koichi Akashi verfasserin aut Toshihiko Yanase verfasserin aut Junko Ono verfasserin aut Toshimitsu Okeda verfasserin aut Ryoji Fujimoto verfasserin aut Kenji Ihara verfasserin aut Toshiro Hara verfasserin aut Yohei Kikuchi verfasserin aut Masanori Iwase verfasserin aut Takanari Kitazono verfasserin aut Fumiko Kojima verfasserin aut Suminori Kono verfasserin aut Hironori Kurisaki verfasserin aut Shiori Kondo verfasserin aut Hitoshi Katsuta verfasserin aut In EBioMedicine Elsevier, 2015 2(2015), 7, Seite 744-749 (DE-627)802540074 (DE-600)2799017-5 23523964 nnns volume:2 year:2015 number:7 pages:744-749 https://doi.org/10.1016/j.ebiom.2015.05.004 kostenfrei https://doaj.org/article/4513be54d16f42ffa11cc8aeca0b66f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352396415300128 kostenfrei https://doaj.org/toc/2352-3964 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 2 2015 7 744-749 |
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Seiho Nagafuchi @@aut@@ Yumi Kamada-Hibio @@aut@@ Kanako Hirakawa @@aut@@ Nobutaka Tsutsu @@aut@@ Masae Minami @@aut@@ Akira Okada @@aut@@ Katsuya Kai @@aut@@ Miho Teshima @@aut@@ Arisa Moroishi @@aut@@ Yoshikazu Murakami @@aut@@ Yoshikazu Umeno @@aut@@ Yasushi Yokogawa @@aut@@ Kazuhiko Kogawa @@aut@@ Kenichi Izumi @@aut@@ Keizo Anzai @@aut@@ Ryuichi Iwakiri @@aut@@ Kazuyuki Hamaguchi @@aut@@ Nobuhiro Sasaki @@aut@@ Sakae Nohara @@aut@@ Eiko Yoshida @@aut@@ Mine Harada @@aut@@ Koichi Akashi @@aut@@ Toshihiko Yanase @@aut@@ Junko Ono @@aut@@ Toshimitsu Okeda @@aut@@ Ryoji Fujimoto @@aut@@ Kenji Ihara @@aut@@ Toshiro Hara @@aut@@ Yohei Kikuchi @@aut@@ Masanori Iwase @@aut@@ Takanari Kitazono @@aut@@ Fumiko Kojima @@aut@@ Suminori Kono @@aut@@ Hironori Kurisaki @@aut@@ Shiori Kondo @@aut@@ Hitoshi Katsuta @@aut@@ |
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In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. 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Seiho Nagafuchi |
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R5-920 TYK2 Promoter Variant and Diabetes Mellitus in the Japanese Tyrosine kinase 2 (TYK2) Promoter variant Diabetes mellitus Virus Polymorphism |
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Elektronische Aufsätze |
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Seiho Nagafuchi |
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10.1016/j.ebiom.2015.05.004 |
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verfasserin |
| title_sort |
tyk2 promoter variant and diabetes mellitus in the japanese |
| callnumber |
R5-920 |
| title_auth |
TYK2 Promoter Variant and Diabetes Mellitus in the Japanese |
| abstract |
Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. |
| abstractGer |
Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. |
| abstract_unstemmed |
Background: Recently, natural mutation of Tyrosine kinase 2 (Tyk2) gene has been shown to determine susceptibility to murine virus-induced diabetes. In addition, a previous human genome-wide study suggested the type 1 diabetes (T1D) susceptibility region to be 19p13, where the human TYK2 gene is located (19p13.2). Methods: Polymorphisms of TYK2 gene at the promoter region and exons were studied among 331 healthy controls, and 302 patients with T1D and 314 with type 2 diabetes (T2D) in the Japanese. Findings: A TYK2 promoter haplotype with multiple genetic polymorphisms, which are in complete linkage disequilibrium, named TYK2 promoter variant, presenting decreased promoter activity, is associated with an increased risk of not only T1D (odds ratio (OR), 2.4; 95% confidence interval (CI), 1.2 to 4.6; P = 0.01), but also T2D (OR, 2.1; 95% CI, 1.1 to 4.1; P = 0.03). The risk is high in patients with T1D associated with flu-like syndrome at diabetes onset and also those without anti-glutamic acid decarboxylase autoantibody. Interpretation: The TYK2 promoter variant is associated with an overall risk for diabetes, serving a good candidate as a virus-induced diabetes susceptibility gene in humans. Funding: Ministry of Education, Culture, Sports, Science and Technology and of Health, Labor and Welfare of Japan. |
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| title_short |
TYK2 Promoter Variant and Diabetes Mellitus in the Japanese |
| url |
https://doi.org/10.1016/j.ebiom.2015.05.004 https://doaj.org/article/4513be54d16f42ffa11cc8aeca0b66f5 http://www.sciencedirect.com/science/article/pii/S2352396415300128 https://doaj.org/toc/2352-3964 |
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Yumi Kamada-Hibio Kanako Hirakawa Nobutaka Tsutsu Masae Minami Akira Okada Katsuya Kai Miho Teshima Arisa Moroishi Yoshikazu Murakami Yoshikazu Umeno Yasushi Yokogawa Kazuhiko Kogawa Kenichi Izumi Keizo Anzai Ryuichi Iwakiri Kazuyuki Hamaguchi Nobuhiro Sasaki Sakae Nohara Eiko Yoshida Mine Harada Koichi Akashi Toshihiko Yanase Junko Ono Toshimitsu Okeda Ryoji Fujimoto Kenji Ihara Toshiro Hara Yohei Kikuchi Masanori Iwase Takanari Kitazono Fumiko Kojima Suminori Kono Hironori Kurisaki Shiori Kondo Hitoshi Katsuta |
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Yumi Kamada-Hibio Kanako Hirakawa Nobutaka Tsutsu Masae Minami Akira Okada Katsuya Kai Miho Teshima Arisa Moroishi Yoshikazu Murakami Yoshikazu Umeno Yasushi Yokogawa Kazuhiko Kogawa Kenichi Izumi Keizo Anzai Ryuichi Iwakiri Kazuyuki Hamaguchi Nobuhiro Sasaki Sakae Nohara Eiko Yoshida Mine Harada Koichi Akashi Toshihiko Yanase Junko Ono Toshimitsu Okeda Ryoji Fujimoto Kenji Ihara Toshiro Hara Yohei Kikuchi Masanori Iwase Takanari Kitazono Fumiko Kojima Suminori Kono Hironori Kurisaki Shiori Kondo Hitoshi Katsuta |
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R - General Medicine |
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10.1016/j.ebiom.2015.05.004 |
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2024-07-04T01:15:00.399Z |
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| score |
7.3994417 |