TY - JOUR
T1 - Association of Forced Vital Capacity with the Developmental Gene NCOR2
AU - Generation Scotland
AU - Minelli, Cosetta
AU - Dean, Charlotte H.
AU - Hind, Matthew
AU - Alves, Alexessander Couto
AU - Amaral, André F S
AU - Siroux, Valerie
AU - Huikari, Ville
AU - Artigas, María Soler
AU - Evans, David M.
AU - Loth, Daan W.
AU - Bossé, Yohan
AU - Postma, Dirkje S.
AU - Sin, Don
AU - Thompson, John
AU - Demenais, Florence
AU - Henderson, John
AU - Bouzigon, Emmanuelle
AU - Jarvis, Deborah
AU - Järvelin, Marjo Riitta
AU - Burney, Peter
AU - Gharib, Sina A.
AU - Wain, Louise V.
AU - Franceschini, Nora
AU - Koch, Beate
AU - Pottinger, Tess D.
AU - Smith, Albert Vernon
AU - Duan, Qing
AU - Oldmeadow, Chris
AU - Lee, Mi Kyeong
AU - Strachan, David P.
AU - James, Alan L.
AU - Huffman, Jennifer E.
AU - Ramasamy, Adaikalavan
AU - Wareham, Nicholas J.
A2 - Vitart, Veronique
A2 - Lopez, Lorna M.
A2 - Joshi, Peter K.
A2 - Wright, Alan F.
A2 - Hastie, Nicholas D.
A2 - Campbell, Susan
A2 - Davies, Gail
A2 - Wild, Sarah H.
A2 - Navarro, Pau
A2 - Rudan, Igor
A2 - Campbell, Harry
A2 - Polasek, Ozren
A2 - Porteous, David J.
A2 - Deary, Ian J.
A2 - Wilson, James F.
A2 - Hayward, Caroline
PY - 2016/2/2
Y1 - 2016/2/2
N2 - Background Forced Vital Capacity (FVC) is an important predictor of all-cause mortality in the absence of chronic respiratory conditions. Epidemiological evidence highlights the role of early life factors on adult FVC, pointing to environmental exposures and genes affecting lung development as risk factors for low FVC later in life. Although highly heritable, a small number of genes have been found associated with FVC, and we aimed at identifying further genetic variants by focusing on lung development genes. Methods Per-allele effects of 24,728 SNPs in 403 genes involved in lung development were tested in 7,749 adults from three studies (NFBC1966, ECRHS, EGEA). The most significant SNP for the top 25 genes was followed-up in 46,103 adults (CHARGE and SpiroMeta consortia) and 5,062 children (ALSPAC). Associations were considered replicated if the replication p-value survived Bonferroni correction (p
AB - Background Forced Vital Capacity (FVC) is an important predictor of all-cause mortality in the absence of chronic respiratory conditions. Epidemiological evidence highlights the role of early life factors on adult FVC, pointing to environmental exposures and genes affecting lung development as risk factors for low FVC later in life. Although highly heritable, a small number of genes have been found associated with FVC, and we aimed at identifying further genetic variants by focusing on lung development genes. Methods Per-allele effects of 24,728 SNPs in 403 genes involved in lung development were tested in 7,749 adults from three studies (NFBC1966, ECRHS, EGEA). The most significant SNP for the top 25 genes was followed-up in 46,103 adults (CHARGE and SpiroMeta consortia) and 5,062 children (ALSPAC). Associations were considered replicated if the replication p-value survived Bonferroni correction (p
UR - http://www.scopus.com/inward/record.url?scp=84959440364&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0147388
DO - 10.1371/journal.pone.0147388
M3 - Article
AN - SCOPUS:84959440364
SN - 1932-6203
VL - 11
JO - PLoS ONE
JF - PLoS ONE
IS - 2
M1 - e0147388
ER -