Additional file 2 of multi-method genome- and epigenome-wide studies of inflammatory protein levels in healthy older adults

Hillary RF, Trejo-Banos D, Kousathanas A, McCartney DL, Harris SE, Stevenson AJ, Patxot M, Ojavee SE, Zhang Q, Liewald DC, Ritchie CW, Evans KL, Tucker-Drob EM, Wray NR, McRae AF, Visscher PM, Deary IJ, Robinson MR, Marioni RE. 2020. Additional file 2 of multi-method genome- and epigenome-wide studies of inflammatory protein levels in healthy older adults, Springer Nature, 10.6084/m9.figshare.12629697.v1.

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Hillary, Robert F.; Trejo-Banos, Daniel; Kousathanas, Athanasios; McCartney, Daniel L.; Harris, Sarah E.; Stevenson, Anna J.; Patxot, Marion; Ojavee, Sven Erik; Zhang, Qian; Liewald, David C.; Ritchie, Craig W.; Evans, Kathryn L.
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Abstract
Additional file 2: Supplementary Tables. The association of pre-adjusted protein levels with biological and technical covariates. Protein levels were adjusted for age, sex, array plate and four genetic principal components (population structure) prior to analyses. Significant associations are emboldened. (Table S1). pQTLs associated with inflammatory biomarker levels from Bayesian penalised regression model (Posterior Inclusion Probability > 95%). (Table S2). All pQTLs associated with inflammatory biomarker levels from ordinary least squares regression model (P < 7.14 × 10− 10). (Table S3). Summary of lambda values relating to ordinary least squares GWAS and EWAS performed on inflammatory protein levels (n = 70) in Lothian Birth Cohort 1936 study. (Table S4). Conditionally significant pQTLs associated with inflammatory biomarker levels from ordinary least squares regression model (P < 7.14 × 10− 10). (Table S5). Comparison of variance explained by ordinary least squares and Bayesian penalised regression models for concordantly identified SNPs. (Table S6). Estimate of heritability for blood protein levels as well as proportion of variance explained attributable to different prior mixtures. (Table S7). Comparison of heritability estimates from Ahsan et al. (maximum likelihood) and Hillary et al. (Bayesian penalised regression). (Table S8). List of concordant SNPs identified by linear model and Bayesian penalised regression and whether they have been previously identified as eQTLs. (Table S9). Bayesian tests of colocalisation for cis pQTLs and cis eQTLs. (Table S10). Sherlock algorithm: Genes whose expression are putatively associated with circulating inflammatory proteins that harbour pQTLs. (Table S11). CpGs associated with inflammatory protein biomarkers as identified by Bayesian model (Bayesian model; Posterior Inclusion Probability > 95%). (Table S12). CpGs associated with inflammatory protein biomarkers as identified by linear model (limma) at P < 5.14 × 10− 10. (Table S13). CpGs associated with inflammatory protein biomarkers as identified by mixed linear model (OSCA) at P < 5.14 × 10− 10. (Table S14). Estimate of variance explained for blood protein levels by DNA methylation as well as proportion of explained attributable to different prior mixtures - BayesR+. (Table S15). Comparison of variance in protein levels explained by genome-wide DNA methylation data by mixed linear model (OSCA) and Bayesian penalised regression model (BayesR+). (Table S16). Variance in circulating inflammatory protein biomarker levels explained by common genetic and methylation data (joint and conditional estimates from BayesR+). Ordered by combined variance explained by genetic and epigenetic data - smallest to largest. Significant results from t-tests comparing distributions for variance explained by methylation or genetics alone versus combined estimate are emboldened. (Table S17). Genetic and epigenetic factors identified by BayesR+ when conditioning on all SNPs and CpGs together. (Table S18). Mendelian Randomisation analyses to assess whether proteins with concordantly identified genetic signals are causally associated with Alzheimer’s disease risk. (Table S19).
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2020-07-09
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Hillary RF, Trejo-Banos D, Kousathanas A, et al. Additional file 2 of multi-method genome- and epigenome-wide studies of inflammatory protein levels in healthy older adults. 2020. doi:10.6084/m9.figshare.12629697.v1
Hillary, R. F., Trejo-Banos, D., Kousathanas, A., McCartney, D. L., Harris, S. E., Stevenson, A. J., … Marioni, R. E. (2020). Additional file 2 of multi-method genome- and epigenome-wide studies of inflammatory protein levels in healthy older adults. Springer Nature. https://doi.org/10.6084/m9.figshare.12629697.v1
Hillary, Robert F., Daniel Trejo-Banos, Athanasios Kousathanas, Daniel L. McCartney, Sarah E. Harris, Anna J. Stevenson, Marion Patxot, et al. “Additional File 2 of Multi-Method Genome- and Epigenome-Wide Studies of Inflammatory Protein Levels in Healthy Older Adults.” Springer Nature, 2020. https://doi.org/10.6084/m9.figshare.12629697.v1.
R. F. Hillary et al., “Additional file 2 of multi-method genome- and epigenome-wide studies of inflammatory protein levels in healthy older adults.” Springer Nature, 2020.
Hillary RF, Trejo-Banos D, Kousathanas A, McCartney DL, Harris SE, Stevenson AJ, Patxot M, Ojavee SE, Zhang Q, Liewald DC, Ritchie CW, Evans KL, Tucker-Drob EM, Wray NR, McRae AF, Visscher PM, Deary IJ, Robinson MR, Marioni RE. 2020. Additional file 2 of multi-method genome- and epigenome-wide studies of inflammatory protein levels in healthy older adults, Springer Nature, 10.6084/m9.figshare.12629697.v1.
Hillary, Robert F., et al. Additional File 2 of Multi-Method Genome- and Epigenome-Wide Studies of Inflammatory Protein Levels in Healthy Older Adults. Springer Nature, 2020, doi:10.6084/m9.figshare.12629697.v1.

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