The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Epigenome-wide association data implicate DNA methylation as an intermediary of genetic risk in rheumatoid arthritis
Open accessAbstract
Epigenetic mechanisms integrate genetic and environmental causes of disease, but comprehensive genome-wide analyses of epigenetic modifications have not yet demonstrated robust association with common diseases. Using Illumina HumanMethylation450 arrays on 354 anti-citrullinated protein antibody–associated rheumatoid arthritis cases and 337 controls, we identified two clusters within the major histocompatibility complex (MHC) region whose differential methylation potentially mediates genetic risk for rheumatoid arthritis. To reduce confounding factors that have hampered previous epigenome-wide studies, we corrected for cellular heterogeneity by estimating and adjusting for cell-type proportions in our blood-derived DNA samples and used mediation analysis to filter out associations likely to be a consequence of disease. Four CpGs also showed an association between genotype and variance of methylation. The associations for both clusters replicated at least one CpG (P < 0.01), with the rest showing suggestive association, in monocyte cell fractions in an independent cohort of 12 cases and 12 controls. Thus, DNA methylation is a potential mediator of genetic risk.
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Cited by
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A survey of best practices for RNA-seq data analysis
Conesa, A., Madrigal, P., Tarazona, S., Gomez-Cabrero, D., Cervera, A., McPherson, A., Szcześniak, M. W., Gaffney, D. J., Elo, L. L., Zhang, X., et al. (2016) · Genome Biology · doi:10.1186/s13059-016-0881-8 · Cited by 2,794
Orienting the causal relationship between imprecisely measured traits using GWAS summary data.
Hemani, G., Tilling, K., & Davey Smith, G. (2017) · PLoS Genetics · doi:10.1371/journal.pgen.1007081 · Cited by 2,607
Methods of integrating data to uncover genotype-phenotype interactions
Ritchie, M. D., Holzinger, E. R., Li, R., Pendergrass, S. A., & Kim, D. (2015) · Nature Reviews Genetics · doi:10.1038/nrg3868 · Cited by 1,085
Metadata
- Authors
- Liu, Y., Aryee, M. J., Padyukov, L., Fallin, M. D., Hesselberg, E., Runarsson, A., Reinius, L., Acevedo, N., Taub, M., Ronninger, M., Shchetynsky, K., Scheynius, A., Kere, J., Alfredsson, L., Klareskog, L., Ekström, T. J., & Feinberg, A. P.
- Venue
- Nature Biotechnology
- Published
- 2013-01-20
- Volume
- 31
- Issue
- 2
- Pages
- 142-147
- ISSN
- 0733-222X (ISSN-L)
- 1087-0156
- 1546-1696
- OpenAlex
- W2028934624
- Cited by
- 969
- References
- 8
- FWCI
- 46.53
- Type
- journal article
- Language
- en
- Open access
- green
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- Liu, Y., Aryee, M. J., Padyukov, L., Fallin, M. D., Hesselberg, E., Runarsson, A., Reinius, L., Acevedo, N., Taub, M., Ronninger, M., Shchetynsky, K., Scheynius, A., Kere, J., Alfredsson, L., Klareskog, L., Ekström, T. J., & Feinberg, A. P. (2013). Epigenome-wide association data implicate DNA methylation as an intermediary of genetic risk in rheumatoid arthritis. Nature Biotechnology. https://doi.org/10.1038/nbt.2487
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