Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency
Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that in...
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| Autor*in: |
Kim, Woo Jin [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2012 |
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© Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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| Übergeordnetes Werk: |
Enthalten in: Respiratory research - London : BioMed Central, 2001, 13(2012), 1 vom: 22. Feb. |
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| Übergeordnetes Werk: |
volume:13 ; year:2012 ; number:1 ; day:22 ; month:02 |
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| DOI / URN: |
10.1186/1465-9921-13-16 |
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| Katalog-ID: |
SPR028513932 |
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| 100 | 1 | |a Kim, Woo Jin |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency |
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| 520 | |a Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. | ||
| 650 | 4 | |a Chronic obstructive pulmonary disease |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Genetic association analysis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Genetic modifiers |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Wood, Alice M |4 aut | |
| 700 | 1 | |a Barker, Alan F |4 aut | |
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| 700 | 1 | |a Eden, Edward |4 aut | |
| 700 | 1 | |a McElvaney, Gerard |4 aut | |
| 700 | 1 | |a Rennard, Stephen I |4 aut | |
| 700 | 1 | |a Sandhaus, Robert A |4 aut | |
| 700 | 1 | |a Stocks, James M |4 aut | |
| 700 | 1 | |a Stoller, James K |4 aut | |
| 700 | 1 | |a Strange, Charlie |4 aut | |
| 700 | 1 | |a Turino, Gerard |4 aut | |
| 700 | 1 | |a Silverman, Edwin K |4 aut | |
| 700 | 1 | |a Stockley, Robert A |4 aut | |
| 700 | 1 | |a DeMeo, Dawn L |4 aut | |
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10.1186/1465-9921-13-16 doi (DE-627)SPR028513932 (SPR)1465-9921-13-16-e DE-627 ger DE-627 rakwb eng Kim, Woo Jin verfasserin aut Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. Chronic obstructive pulmonary disease (dpeaa)DE-He213 Genetic association analysis (dpeaa)DE-He213 Genetic modifiers (dpeaa)DE-He213 Wood, Alice M aut Barker, Alan F aut Brantly, Mark L aut Campbell, Edward J aut Eden, Edward aut McElvaney, Gerard aut Rennard, Stephen I aut Sandhaus, Robert A aut Stocks, James M aut Stoller, James K aut Strange, Charlie aut Turino, Gerard aut Silverman, Edwin K aut Stockley, Robert A aut DeMeo, Dawn L aut Enthalten in Respiratory research London : BioMed Central, 2001 13(2012), 1 vom: 22. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:13 year:2012 number:1 day:22 month:02 https://dx.doi.org/10.1186/1465-9921-13-16 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1 22 02 |
| spelling |
10.1186/1465-9921-13-16 doi (DE-627)SPR028513932 (SPR)1465-9921-13-16-e DE-627 ger DE-627 rakwb eng Kim, Woo Jin verfasserin aut Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. Chronic obstructive pulmonary disease (dpeaa)DE-He213 Genetic association analysis (dpeaa)DE-He213 Genetic modifiers (dpeaa)DE-He213 Wood, Alice M aut Barker, Alan F aut Brantly, Mark L aut Campbell, Edward J aut Eden, Edward aut McElvaney, Gerard aut Rennard, Stephen I aut Sandhaus, Robert A aut Stocks, James M aut Stoller, James K aut Strange, Charlie aut Turino, Gerard aut Silverman, Edwin K aut Stockley, Robert A aut DeMeo, Dawn L aut Enthalten in Respiratory research London : BioMed Central, 2001 13(2012), 1 vom: 22. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:13 year:2012 number:1 day:22 month:02 https://dx.doi.org/10.1186/1465-9921-13-16 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1 22 02 |
| allfields_unstemmed |
10.1186/1465-9921-13-16 doi (DE-627)SPR028513932 (SPR)1465-9921-13-16-e DE-627 ger DE-627 rakwb eng Kim, Woo Jin verfasserin aut Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. Chronic obstructive pulmonary disease (dpeaa)DE-He213 Genetic association analysis (dpeaa)DE-He213 Genetic modifiers (dpeaa)DE-He213 Wood, Alice M aut Barker, Alan F aut Brantly, Mark L aut Campbell, Edward J aut Eden, Edward aut McElvaney, Gerard aut Rennard, Stephen I aut Sandhaus, Robert A aut Stocks, James M aut Stoller, James K aut Strange, Charlie aut Turino, Gerard aut Silverman, Edwin K aut Stockley, Robert A aut DeMeo, Dawn L aut Enthalten in Respiratory research London : BioMed Central, 2001 13(2012), 1 vom: 22. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:13 year:2012 number:1 day:22 month:02 https://dx.doi.org/10.1186/1465-9921-13-16 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1 22 02 |
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10.1186/1465-9921-13-16 doi (DE-627)SPR028513932 (SPR)1465-9921-13-16-e DE-627 ger DE-627 rakwb eng Kim, Woo Jin verfasserin aut Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. Chronic obstructive pulmonary disease (dpeaa)DE-He213 Genetic association analysis (dpeaa)DE-He213 Genetic modifiers (dpeaa)DE-He213 Wood, Alice M aut Barker, Alan F aut Brantly, Mark L aut Campbell, Edward J aut Eden, Edward aut McElvaney, Gerard aut Rennard, Stephen I aut Sandhaus, Robert A aut Stocks, James M aut Stoller, James K aut Strange, Charlie aut Turino, Gerard aut Silverman, Edwin K aut Stockley, Robert A aut DeMeo, Dawn L aut Enthalten in Respiratory research London : BioMed Central, 2001 13(2012), 1 vom: 22. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:13 year:2012 number:1 day:22 month:02 https://dx.doi.org/10.1186/1465-9921-13-16 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1 22 02 |
| allfieldsSound |
10.1186/1465-9921-13-16 doi (DE-627)SPR028513932 (SPR)1465-9921-13-16-e DE-627 ger DE-627 rakwb eng Kim, Woo Jin verfasserin aut Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. Chronic obstructive pulmonary disease (dpeaa)DE-He213 Genetic association analysis (dpeaa)DE-He213 Genetic modifiers (dpeaa)DE-He213 Wood, Alice M aut Barker, Alan F aut Brantly, Mark L aut Campbell, Edward J aut Eden, Edward aut McElvaney, Gerard aut Rennard, Stephen I aut Sandhaus, Robert A aut Stocks, James M aut Stoller, James K aut Strange, Charlie aut Turino, Gerard aut Silverman, Edwin K aut Stockley, Robert A aut DeMeo, Dawn L aut Enthalten in Respiratory research London : BioMed Central, 2001 13(2012), 1 vom: 22. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:13 year:2012 number:1 day:22 month:02 https://dx.doi.org/10.1186/1465-9921-13-16 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2012 1 22 02 |
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Kim, Woo Jin @@aut@@ Wood, Alice M @@aut@@ Barker, Alan F @@aut@@ Brantly, Mark L @@aut@@ Campbell, Edward J @@aut@@ Eden, Edward @@aut@@ McElvaney, Gerard @@aut@@ Rennard, Stephen I @@aut@@ Sandhaus, Robert A @@aut@@ Stocks, James M @@aut@@ Stoller, James K @@aut@@ Strange, Charlie @@aut@@ Turino, Gerard @@aut@@ Silverman, Edwin K @@aut@@ Stockley, Robert A @@aut@@ DeMeo, Dawn L @@aut@@ |
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. 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Kim, Woo Jin |
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Kim, Woo Jin misc Chronic obstructive pulmonary disease misc Genetic association analysis misc Genetic modifiers Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency |
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Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency Chronic obstructive pulmonary disease (dpeaa)DE-He213 Genetic association analysis (dpeaa)DE-He213 Genetic modifiers (dpeaa)DE-He213 |
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Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency |
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Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency |
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Kim, Woo Jin Wood, Alice M Barker, Alan F Brantly, Mark L Campbell, Edward J Eden, Edward McElvaney, Gerard Rennard, Stephen I Sandhaus, Robert A Stocks, James M Stoller, James K Strange, Charlie Turino, Gerard Silverman, Edwin K Stockley, Robert A DeMeo, Dawn L |
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association of ireb2 and chrna3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency |
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Association of IREB2 and CHRNA3polymorphisms with airflow obstruction in severe alpha-1 antitrypsin deficiency |
| abstract |
Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. © Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstractGer |
Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. © Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
| abstract_unstemmed |
Background The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2). We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. Methods The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. $ FEV_{1} $ percent of predicted and $ FEV_{1} $/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. Results Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator $ FEV_{1} $ percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator $ FEV_{1} $ percent of predicted and pre-bronchodilator $ FEV_{1} $/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. Conclusions IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact. © Kim et al; licensee BioMed Central Ltd. 2012. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( |
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