Molecular mechanisms underlying variations in lung function: a systems genetics analysisTools Obeidat, Ma'en and Hao, Ke and Bossé, Yohan and Nickle, David C. and Nie, Yunlong and Postma, Dirkje S. and Laviolette, Michel and Sandford, Andrew J. and Daley, Denise D. and Hogg, James C. and Elliott, W. Mark and Fishbane, Nick and Timens, Wim and Hysi, Pirro G. and Kaprio, Jaakko and Wilson, James F. and Hui, Jennie and Rawal, Rajesh and Schulz, Holger and Stubbe, Beate and Hayward, Caroline and Polasek, Ozren and Järvelin, Marjo-Riitta and Zhao, Jing Hua and Jarvis, Deborah and Kähönen, Mika and Franceschini, Nora and North, Kari E. and Loth, Daan W. and Brusselle, Guy G. and Smith, Albert Vernon and Gudnason, Vilmundur and Bartz, Traci M and Wilk, Jemma B. and O'Connor, George T. and Cassano, Patricia A. and Tang, Wenbo and Wain, Louise V. and Artigas, María Soler and Gharib, Sina A. and Strachan, David P. and Sin, Don D. and Tobin, Martin D. and London, Stephanie J. and Hall, Ian P. and Paré, Peter D. (2015) Molecular mechanisms underlying variations in lung function: a systems genetics analysis. Lancet Respiratory Medicine, 3 (10). pp. 782-795. ISSN 2213-2619 Full text not available from this repository.AbstractBackground: Lung function measures reflect the physiological state of the lung, and are essential to the diagnosis of chronic obstructive pulmonary disease (COPD). The SpiroMeta-CHARGE consortium undertook the largest genome wide association study (GWAS) so far (n=48 201) for forced expiratory volume in 1 s (FEV1) and the ratio of FEV1 to forced vital capacity (FEV1/FVC) in the general population. The lung expression quantitative trait loci (eQTLs) study mapped the genetic architecture of gene expression in lung tissue from 1111 individuals. We used a systems genetics approach to identify single nucleotide polymorphisms (SNPs) associated with lung function that act as eQTLs and change the level of expression of their target genes in lung tissue; termed eSNPs.
Actions (Archive Staff Only)
|