Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study

A. E. Dijkstra, J. Smolonska, M. van den Berge, C. Wijmenga, P. Zanen, M. A. Luinge, M. Platteel, J. W. Lammers, M. Dahlback, K. Tosh, P. S. Hiemstra, P. J. Sterk, A. Spira, Jørgen Vestbo, B. G. Nordestgaard, M. Benn, S. F. Nielsen, M. Dahl, W. M. Verschuren, H. S. J. Picavet & 34 andre H. A. Smit, M. Owsijewitsch, H. U. Kauczor, H. J. de Koning, E. Nizankowska-Mogilnicka, F. Mejza, P. Nastalek, C. C. van Diemen, M. H. Cho, E. K. Silverman, J. D. Crapo, T. H. Beaty, D. A. Lomas, P. Bakke, A. Gulsvik, Y. Bosse, M. A. Obeidat, D. W. Loth, L. Lahousse, F. Rivadeneira, A. G. Uitterlinden, A. Hofman, B. H. Stricker, G. G. Brusselle, C. van Duijn, U. Brouwer, G. H. Koppelman, J. M. Vonk, M. C. Nawijn, H. J. M. Groen, W. Timens, H. M. Boezen, D. S. Postma, Study LifeLines Cohort

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Background: Chronic mucus hypersecretion (CMH) is associated with an increased frequency of respiratory infections, excess lung function decline, and increased hospitalisation and mortality rates in the general population. It is associated with smoking, but it is unknown why only a minority of smokers develops CMH. A plausible explanation for this phenomenon is a predisposing genetic constitution. Therefore, we performed a genome wide association (GWA) study of CMH in Caucasian populations. Methods: GWA analysis was performed in the NELSON-study using the Illumina 610 array, followed by replication and metaanalysis in 11 additional cohorts. In total 2,704 subjects with, and 7,624 subjects without CMH were included, all current or former heavy smokers (>= 20 pack-years). Additional studies were performed to test the functional relevance of the most significant single nucleotide polymorphism (SNP). Results: A strong association with CMH, consistent across all cohorts, was observed with rs6577641 (p = 4.25610(-6), OR = 1.17), located in intron 9 of the special AT-rich sequence-binding protein 1 locus (SATB1) on chromosome 3. The risk allele (G) was associated with higher mRNA expression of SATB1 (4.3610 29) in lung tissue. Presence of CMH was associated with increased SATB1 mRNA expression in bronchial biopsies from COPD patients. SATB1 expression was induced during differentiation of primary human bronchial epithelial cells in culture. Conclusions: Our findings, that SNP rs6577641 is associated with CMH in multiple cohorts and is a cis-eQTL for SATB1, together with our additional observation that SATB1 expression increases during epithelial differentiation provide suggestive evidence that SATB1 is a gene that affects CMH.
OriginalsprogEngelsk
TidsskriftP L o S One
Vol/bind9
Udgave nummer4
Sider (fra-til)13
Antal sider1
ISSN1932-6203
DOI
StatusUdgivet - 2014

Emneord

  • OBSTRUCTIVE PULMONARY-DISEASE CHRONIC-BRONCHITIS GENETIC EPIDEMIOLOGY GENERAL-POPULATION BINDING-PROTEIN RISK-FACTORS COPD CHROMATIN SATB1 EXPRESSION

Citer dette

Dijkstra, A. E., Smolonska, J., van den Berge, M., Wijmenga, C., Zanen, P., Luinge, M. A., ... LifeLines Cohort, S. (2014). Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study. P L o S One, 9(4), 13. https://doi.org/10.1371/journal.pone.0091621
Dijkstra, A. E. ; Smolonska, J. ; van den Berge, M. ; Wijmenga, C. ; Zanen, P. ; Luinge, M. A. ; Platteel, M. ; Lammers, J. W. ; Dahlback, M. ; Tosh, K. ; Hiemstra, P. S. ; Sterk, P. J. ; Spira, A. ; Vestbo, Jørgen ; Nordestgaard, B. G. ; Benn, M. ; Nielsen, S. F. ; Dahl, M. ; Verschuren, W. M. ; Picavet, H. S. J. ; Smit, H. A. ; Owsijewitsch, M. ; Kauczor, H. U. ; de Koning, H. J. ; Nizankowska-Mogilnicka, E. ; Mejza, F. ; Nastalek, P. ; van Diemen, C. C. ; Cho, M. H. ; Silverman, E. K. ; Crapo, J. D. ; Beaty, T. H. ; Lomas, D. A. ; Bakke, P. ; Gulsvik, A. ; Bosse, Y. ; Obeidat, M. A. ; Loth, D. W. ; Lahousse, L. ; Rivadeneira, F. ; Uitterlinden, A. G. ; Hofman, A. ; Stricker, B. H. ; Brusselle, G. G. ; van Duijn, C. ; Brouwer, U. ; Koppelman, G. H. ; Vonk, J. M. ; Nawijn, M. C. ; Groen, H. J. M. ; Timens, W. ; Boezen, H. M. ; Postma, D. S. ; LifeLines Cohort, Study. / Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study. I: P L o S One. 2014 ; Bind 9, Nr. 4. s. 13.
@article{b302852eecf64df993d6b3174b387369,
title = "Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study",
abstract = "Background: Chronic mucus hypersecretion (CMH) is associated with an increased frequency of respiratory infections, excess lung function decline, and increased hospitalisation and mortality rates in the general population. It is associated with smoking, but it is unknown why only a minority of smokers develops CMH. A plausible explanation for this phenomenon is a predisposing genetic constitution. Therefore, we performed a genome wide association (GWA) study of CMH in Caucasian populations. Methods: GWA analysis was performed in the NELSON-study using the Illumina 610 array, followed by replication and metaanalysis in 11 additional cohorts. In total 2,704 subjects with, and 7,624 subjects without CMH were included, all current or former heavy smokers (>= 20 pack-years). Additional studies were performed to test the functional relevance of the most significant single nucleotide polymorphism (SNP). Results: A strong association with CMH, consistent across all cohorts, was observed with rs6577641 (p = 4.25610(-6), OR = 1.17), located in intron 9 of the special AT-rich sequence-binding protein 1 locus (SATB1) on chromosome 3. The risk allele (G) was associated with higher mRNA expression of SATB1 (4.3610 29) in lung tissue. Presence of CMH was associated with increased SATB1 mRNA expression in bronchial biopsies from COPD patients. SATB1 expression was induced during differentiation of primary human bronchial epithelial cells in culture. Conclusions: Our findings, that SNP rs6577641 is associated with CMH in multiple cohorts and is a cis-eQTL for SATB1, together with our additional observation that SATB1 expression increases during epithelial differentiation provide suggestive evidence that SATB1 is a gene that affects CMH.",
keywords = "OBSTRUCTIVE PULMONARY-DISEASE CHRONIC-BRONCHITIS GENETIC EPIDEMIOLOGY GENERAL-POPULATION BINDING-PROTEIN RISK-FACTORS COPD CHROMATIN SATB1 EXPRESSION",
author = "Dijkstra, {A. E.} and J. Smolonska and {van den Berge}, M. and C. Wijmenga and P. Zanen and Luinge, {M. A.} and M. Platteel and Lammers, {J. W.} and M. Dahlback and K. Tosh and Hiemstra, {P. S.} and Sterk, {P. J.} and A. Spira and J{\o}rgen Vestbo and Nordestgaard, {B. G.} and M. Benn and Nielsen, {S. F.} and M. Dahl and Verschuren, {W. M.} and Picavet, {H. S. J.} and Smit, {H. A.} and M. Owsijewitsch and Kauczor, {H. U.} and {de Koning}, {H. J.} and E. Nizankowska-Mogilnicka and F. Mejza and P. Nastalek and {van Diemen}, {C. C.} and Cho, {M. H.} and Silverman, {E. K.} and Crapo, {J. D.} and Beaty, {T. H.} and Lomas, {D. A.} and P. Bakke and A. Gulsvik and Y. Bosse and Obeidat, {M. A.} and Loth, {D. W.} and L. Lahousse and F. Rivadeneira and Uitterlinden, {A. G.} and A. Hofman and Stricker, {B. H.} and Brusselle, {G. G.} and {van Duijn}, C. and U. Brouwer and Koppelman, {G. H.} and Vonk, {J. M.} and Nawijn, {M. C.} and Groen, {H. J. M.} and W. Timens and Boezen, {H. M.} and Postma, {D. S.} and {LifeLines Cohort}, Study",
note = "ISI Document Delivery No.: AE7FA Times Cited: 6 Cited Reference Count: 35 Dijkstra, Akkelies E. Smolonska, Joanna van den Berge, Maarten Wijmenga, Ciska Zanen, Pieter Luinge, Marjan A. Platteel, Mathieu Lammers, Jan-Willem Dahlback, Magnus Tosh, Kerrie Hiemstra, Pieter S. Sterk, Peter J. Spira, Avi Vestbo, Jorgen Nordestgaard, Borge G. Benn, Marianne Nielsen, Sune F. Dahl, Morten Verschuren, W. Monique Picavet, H. Susan J. Smit, Henriette A. Owsijewitsch, Michael Kauczor, Hans U. de Koning, Harry J. Nizankowska-Mogilnicka, Eva Mejza, Filip Nastalek, Pawel van Diemen, Cleo C. Cho, Michael H. Silverman, Edwin K. Crapo, James D. Beaty, Terri H. Lomas, David A. Bakke, Per Gulsvik, Amund Bosse, Yohan Obeidat, M. A. Loth, Daan W. Lahousse, Lies Rivadeneira, Fernando Uitterlinden, Andre G. Hofman, Andre Stricker, Bruno H. Brusselle, Guy G. van Duijn, CorneliaM. Brouwer, Uilke Koppelman, Gerard H. Vonk, Judith M. Nawijn, Martijn C. Groen, Harry J. M. Timens, Wim Boezen, H. Marike Postma, Dirkje S. Wijmenga, Cisca/D-2173-2009 EU FP7 [201379]; 'Zorg Onderzoek Nederland-Medische Wetenschappen (ZONMW)'; KWF Kankerbestrijiding; 'Stichting Centraal Fonds Reserves van Voormalig Vrijwillige Ziekenfondsverzekeringen' (RvvZ); Netherlands Organization for Scientific Research; Netherlands Asthma Foundation; University of Groningen; Leiden University Medical Center; GlaxoSmithKline; Dutch ministry of Health, Welfare and Sport; ministry of Economic Affairs, Agriculture and Innovation; province of Groningen; European Union (regional development fund); Northern Netherlands Provinces (SNN); Netherlands Organisation for Scientific Research (NWO); University Medical Center Groningen (UMCG); de Nierstichting (the Dutch Kidney Foundation); Diabetes Fonds (the Diabetic Foundation); GSK; NIH [RO I HL089897, RO I HL089856]; COPD foundation; Dutch Lung Foundation The COPACETIC study was funded by EU FP7 grant 201379. The NELSON study was supported by 'Zorg Onderzoek Nederland-Medische Wetenschappen (ZONMW),' KWF Kankerbestrijiding,' and 'Stichting Centraal Fonds Reserves van Voormalig Vrijwillige Ziekenfondsverzekeringen' (RvvZ). The GLUCOLD study was supported by the Netherlands Organization for Scientific Research, Netherlands Asthma Foundation, University of Groningen, Leiden University Medical Center, and GlaxoSmithKline. The LifeLines cohort study was sponsored by the Dutch ministry of Health, Welfare and Sport, the ministry of Economic Affairs, Agriculture and Innovation, the province of Groningen, the European Union (regional development fund), the Northern Netherlands Provinces (SNN), the Netherlands Organisation for Scientific Research (NWO), University Medical Center Groningen (UMCG), University of Groningen, de Nierstichting (the Dutch Kidney Foundation), and the Diabetes Fonds (the Diabetic Foundation). The ECLIPSE study was funded by GSK and NIH grants RO I HL089897 and by a grant from GlaxoSmithKline. The COPDGene study was funded by NIH grants RO I HL089856 and by the COPD foundation through contributions made to an Industry Advisory Board comprised of AstraZeneca, Boehringer Ingelheim, Novartis, Pfizer, and Sunovion. Data sampling for the Norway study was funded by GlaxoSmithKline. The Dutch Lung Foundation supported the cell culture work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 6 PUBLIC LIBRARY SCIENCE SAN FRANCISCO PLOS ONE",
year = "2014",
doi = "10.1371/journal.pone.0091621",
language = "English",
volume = "9",
pages = "13",
journal = "P L o S One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "4",

}

Dijkstra, AE, Smolonska, J, van den Berge, M, Wijmenga, C, Zanen, P, Luinge, MA, Platteel, M, Lammers, JW, Dahlback, M, Tosh, K, Hiemstra, PS, Sterk, PJ, Spira, A, Vestbo, J, Nordestgaard, BG, Benn, M, Nielsen, SF, Dahl, M, Verschuren, WM, Picavet, HSJ, Smit, HA, Owsijewitsch, M, Kauczor, HU, de Koning, HJ, Nizankowska-Mogilnicka, E, Mejza, F, Nastalek, P, van Diemen, CC, Cho, MH, Silverman, EK, Crapo, JD, Beaty, TH, Lomas, DA, Bakke, P, Gulsvik, A, Bosse, Y, Obeidat, MA, Loth, DW, Lahousse, L, Rivadeneira, F, Uitterlinden, AG, Hofman, A, Stricker, BH, Brusselle, GG, van Duijn, C, Brouwer, U, Koppelman, GH, Vonk, JM, Nawijn, MC, Groen, HJM, Timens, W, Boezen, HM, Postma, DS & LifeLines Cohort, S 2014, 'Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study', P L o S One, bind 9, nr. 4, s. 13. https://doi.org/10.1371/journal.pone.0091621

Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study. / Dijkstra, A. E.; Smolonska, J.; van den Berge, M.; Wijmenga, C.; Zanen, P.; Luinge, M. A.; Platteel, M.; Lammers, J. W.; Dahlback, M.; Tosh, K.; Hiemstra, P. S.; Sterk, P. J.; Spira, A.; Vestbo, Jørgen; Nordestgaard, B. G.; Benn, M.; Nielsen, S. F.; Dahl, M.; Verschuren, W. M.; Picavet, H. S. J.; Smit, H. A.; Owsijewitsch, M.; Kauczor, H. U.; de Koning, H. J.; Nizankowska-Mogilnicka, E.; Mejza, F.; Nastalek, P.; van Diemen, C. C.; Cho, M. H.; Silverman, E. K.; Crapo, J. D.; Beaty, T. H.; Lomas, D. A.; Bakke, P.; Gulsvik, A.; Bosse, Y.; Obeidat, M. A.; Loth, D. W.; Lahousse, L.; Rivadeneira, F.; Uitterlinden, A. G.; Hofman, A.; Stricker, B. H.; Brusselle, G. G.; van Duijn, C.; Brouwer, U.; Koppelman, G. H.; Vonk, J. M.; Nawijn, M. C.; Groen, H. J. M.; Timens, W.; Boezen, H. M.; Postma, D. S.; LifeLines Cohort, Study.

I: P L o S One, Bind 9, Nr. 4, 2014, s. 13.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study

AU - Dijkstra, A. E.

AU - Smolonska, J.

AU - van den Berge, M.

AU - Wijmenga, C.

AU - Zanen, P.

AU - Luinge, M. A.

AU - Platteel, M.

AU - Lammers, J. W.

AU - Dahlback, M.

AU - Tosh, K.

AU - Hiemstra, P. S.

AU - Sterk, P. J.

AU - Spira, A.

AU - Vestbo, Jørgen

AU - Nordestgaard, B. G.

AU - Benn, M.

AU - Nielsen, S. F.

AU - Dahl, M.

AU - Verschuren, W. M.

AU - Picavet, H. S. J.

AU - Smit, H. A.

AU - Owsijewitsch, M.

AU - Kauczor, H. U.

AU - de Koning, H. J.

AU - Nizankowska-Mogilnicka, E.

AU - Mejza, F.

AU - Nastalek, P.

AU - van Diemen, C. C.

AU - Cho, M. H.

AU - Silverman, E. K.

AU - Crapo, J. D.

AU - Beaty, T. H.

AU - Lomas, D. A.

AU - Bakke, P.

AU - Gulsvik, A.

AU - Bosse, Y.

AU - Obeidat, M. A.

AU - Loth, D. W.

AU - Lahousse, L.

AU - Rivadeneira, F.

AU - Uitterlinden, A. G.

AU - Hofman, A.

AU - Stricker, B. H.

AU - Brusselle, G. G.

AU - van Duijn, C.

AU - Brouwer, U.

AU - Koppelman, G. H.

AU - Vonk, J. M.

AU - Nawijn, M. C.

AU - Groen, H. J. M.

AU - Timens, W.

AU - Boezen, H. M.

AU - Postma, D. S.

AU - LifeLines Cohort, Study

N1 - ISI Document Delivery No.: AE7FA Times Cited: 6 Cited Reference Count: 35 Dijkstra, Akkelies E. Smolonska, Joanna van den Berge, Maarten Wijmenga, Ciska Zanen, Pieter Luinge, Marjan A. Platteel, Mathieu Lammers, Jan-Willem Dahlback, Magnus Tosh, Kerrie Hiemstra, Pieter S. Sterk, Peter J. Spira, Avi Vestbo, Jorgen Nordestgaard, Borge G. Benn, Marianne Nielsen, Sune F. Dahl, Morten Verschuren, W. Monique Picavet, H. Susan J. Smit, Henriette A. Owsijewitsch, Michael Kauczor, Hans U. de Koning, Harry J. Nizankowska-Mogilnicka, Eva Mejza, Filip Nastalek, Pawel van Diemen, Cleo C. Cho, Michael H. Silverman, Edwin K. Crapo, James D. Beaty, Terri H. Lomas, David A. Bakke, Per Gulsvik, Amund Bosse, Yohan Obeidat, M. A. Loth, Daan W. Lahousse, Lies Rivadeneira, Fernando Uitterlinden, Andre G. Hofman, Andre Stricker, Bruno H. Brusselle, Guy G. van Duijn, CorneliaM. Brouwer, Uilke Koppelman, Gerard H. Vonk, Judith M. Nawijn, Martijn C. Groen, Harry J. M. Timens, Wim Boezen, H. Marike Postma, Dirkje S. Wijmenga, Cisca/D-2173-2009 EU FP7 [201379]; 'Zorg Onderzoek Nederland-Medische Wetenschappen (ZONMW)'; KWF Kankerbestrijiding; 'Stichting Centraal Fonds Reserves van Voormalig Vrijwillige Ziekenfondsverzekeringen' (RvvZ); Netherlands Organization for Scientific Research; Netherlands Asthma Foundation; University of Groningen; Leiden University Medical Center; GlaxoSmithKline; Dutch ministry of Health, Welfare and Sport; ministry of Economic Affairs, Agriculture and Innovation; province of Groningen; European Union (regional development fund); Northern Netherlands Provinces (SNN); Netherlands Organisation for Scientific Research (NWO); University Medical Center Groningen (UMCG); de Nierstichting (the Dutch Kidney Foundation); Diabetes Fonds (the Diabetic Foundation); GSK; NIH [RO I HL089897, RO I HL089856]; COPD foundation; Dutch Lung Foundation The COPACETIC study was funded by EU FP7 grant 201379. The NELSON study was supported by 'Zorg Onderzoek Nederland-Medische Wetenschappen (ZONMW),' KWF Kankerbestrijiding,' and 'Stichting Centraal Fonds Reserves van Voormalig Vrijwillige Ziekenfondsverzekeringen' (RvvZ). The GLUCOLD study was supported by the Netherlands Organization for Scientific Research, Netherlands Asthma Foundation, University of Groningen, Leiden University Medical Center, and GlaxoSmithKline. The LifeLines cohort study was sponsored by the Dutch ministry of Health, Welfare and Sport, the ministry of Economic Affairs, Agriculture and Innovation, the province of Groningen, the European Union (regional development fund), the Northern Netherlands Provinces (SNN), the Netherlands Organisation for Scientific Research (NWO), University Medical Center Groningen (UMCG), University of Groningen, de Nierstichting (the Dutch Kidney Foundation), and the Diabetes Fonds (the Diabetic Foundation). The ECLIPSE study was funded by GSK and NIH grants RO I HL089897 and by a grant from GlaxoSmithKline. The COPDGene study was funded by NIH grants RO I HL089856 and by the COPD foundation through contributions made to an Industry Advisory Board comprised of AstraZeneca, Boehringer Ingelheim, Novartis, Pfizer, and Sunovion. Data sampling for the Norway study was funded by GlaxoSmithKline. The Dutch Lung Foundation supported the cell culture work. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 6 PUBLIC LIBRARY SCIENCE SAN FRANCISCO PLOS ONE

PY - 2014

Y1 - 2014

N2 - Background: Chronic mucus hypersecretion (CMH) is associated with an increased frequency of respiratory infections, excess lung function decline, and increased hospitalisation and mortality rates in the general population. It is associated with smoking, but it is unknown why only a minority of smokers develops CMH. A plausible explanation for this phenomenon is a predisposing genetic constitution. Therefore, we performed a genome wide association (GWA) study of CMH in Caucasian populations. Methods: GWA analysis was performed in the NELSON-study using the Illumina 610 array, followed by replication and metaanalysis in 11 additional cohorts. In total 2,704 subjects with, and 7,624 subjects without CMH were included, all current or former heavy smokers (>= 20 pack-years). Additional studies were performed to test the functional relevance of the most significant single nucleotide polymorphism (SNP). Results: A strong association with CMH, consistent across all cohorts, was observed with rs6577641 (p = 4.25610(-6), OR = 1.17), located in intron 9 of the special AT-rich sequence-binding protein 1 locus (SATB1) on chromosome 3. The risk allele (G) was associated with higher mRNA expression of SATB1 (4.3610 29) in lung tissue. Presence of CMH was associated with increased SATB1 mRNA expression in bronchial biopsies from COPD patients. SATB1 expression was induced during differentiation of primary human bronchial epithelial cells in culture. Conclusions: Our findings, that SNP rs6577641 is associated with CMH in multiple cohorts and is a cis-eQTL for SATB1, together with our additional observation that SATB1 expression increases during epithelial differentiation provide suggestive evidence that SATB1 is a gene that affects CMH.

AB - Background: Chronic mucus hypersecretion (CMH) is associated with an increased frequency of respiratory infections, excess lung function decline, and increased hospitalisation and mortality rates in the general population. It is associated with smoking, but it is unknown why only a minority of smokers develops CMH. A plausible explanation for this phenomenon is a predisposing genetic constitution. Therefore, we performed a genome wide association (GWA) study of CMH in Caucasian populations. Methods: GWA analysis was performed in the NELSON-study using the Illumina 610 array, followed by replication and metaanalysis in 11 additional cohorts. In total 2,704 subjects with, and 7,624 subjects without CMH were included, all current or former heavy smokers (>= 20 pack-years). Additional studies were performed to test the functional relevance of the most significant single nucleotide polymorphism (SNP). Results: A strong association with CMH, consistent across all cohorts, was observed with rs6577641 (p = 4.25610(-6), OR = 1.17), located in intron 9 of the special AT-rich sequence-binding protein 1 locus (SATB1) on chromosome 3. The risk allele (G) was associated with higher mRNA expression of SATB1 (4.3610 29) in lung tissue. Presence of CMH was associated with increased SATB1 mRNA expression in bronchial biopsies from COPD patients. SATB1 expression was induced during differentiation of primary human bronchial epithelial cells in culture. Conclusions: Our findings, that SNP rs6577641 is associated with CMH in multiple cohorts and is a cis-eQTL for SATB1, together with our additional observation that SATB1 expression increases during epithelial differentiation provide suggestive evidence that SATB1 is a gene that affects CMH.

KW - OBSTRUCTIVE PULMONARY-DISEASE CHRONIC-BRONCHITIS GENETIC EPIDEMIOLOGY GENERAL-POPULATION BINDING-PROTEIN RISK-FACTORS COPD CHROMATIN SATB1 EXPRESSION

U2 - 10.1371/journal.pone.0091621

DO - 10.1371/journal.pone.0091621

M3 - Journal article

VL - 9

SP - 13

JO - P L o S One

JF - P L o S One

SN - 1932-6203

IS - 4

ER -

Dijkstra AE, Smolonska J, van den Berge M, Wijmenga C, Zanen P, Luinge MA et al. Susceptibility to Chronic Mucus Hypersecretion, a Genome Wide Association Study. P L o S One. 2014;9(4):13. https://doi.org/10.1371/journal.pone.0091621