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Association of Forced Vital Capacity with the Developmental Gene NCOR2

Authors :
Minelli, C. (Cosetta)
Dean, C. H. (Charlotte H.)
Hind, M. (Matthew)
Alves, A. C. (Alexessander Couto)
Amaral, A. F. (André F. S.)
Siroux, V. (Valerie)
Huikari, V. (Ville)
Soler Artigas, M. (María)
Evans, D. M. (David M.)
Loth, D. W. (Daan W.)
Bossé, Y. (Yohan)
Postma, D. S. (Dirkje S.)
Sin, D. (Don)
Thompson, J. (John)
Demenais, F. (Florence)
Henderson, J. (John)
S. c. (SpiroMeta consortium)
C. c. (CHARGE consortium)
Bouzigon, E. (Emmanuelle)
Jarvis, D. (Deborah)
Järvelin, M.-R. (Marjo-Riitta)
Burney, P. (Peter)
School of Medicine / Public Health
Latzin, Philipp
Source :
PLoS ONE 11:e0147388 (2016), PloS one, vol 11, iss 2, PLoS ONE, Vol 11, Iss 2, p e0147388 (2016)
Publication Year :
2016
Publisher :
Public Library of Science, 2016.

Abstract

Article<br />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<br />published version<br />peerReviewed

Details

Language :
English
Database :
OpenAIRE
Journal :
PLoS ONE 11:e0147388 (2016), PloS one, vol 11, iss 2, PLoS ONE, Vol 11, Iss 2, p e0147388 (2016)
Accession number :
edsair.dedup.wf.001..bb616ffe5eb5b41cfa63c6d3dacd887c