Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology

1.Pinart, M. et al. Comorbidity of eczema, rhinitis, and bronchial asthma in IgE-sensitised and non-IgE-sensitised youngsters in MeDALL: a population-based cohort research. Lancet Respir. Med. 2, 131–140 (2014).2.Thomsen, S.F. et al. Findings on the atopic triad from a Danish twin registry. Int. J. Tuberc. Lung Dis. 10, 1268–1272 (2006).three.van Beijsterveldt, C.E. & Boomsma, D.I. Genetics of parentally reported bronchial asthma, eczema and rhinitis in 5-yr-old twins. Eur. Respir. J. 29, 516–521 (2007).four.Loh, P.R. et al. Contrasting genetic architectures of schizophrenia and different advanced ailments utilizing quick variance-components evaluation. Nat. Genet. 47, 1385–1392 (2015).5.Yang, J. et al. Conditional and joint multiple-SNP evaluation of GWAS abstract statistics identifies extra variants influencing advanced traits. Nat. Genet. 44, 369–375, S1–S3 (2012).6.Ferreira, M.A. Bettering the facility to detect danger variants for allergic illness by defining case–management standing based mostly on each bronchial asthma and hay fever. Twin Res. Hum. Genet. 17, 505–511 (2014).7.Bulik-Sullivan, B.Ok. et al. LD Rating regression distinguishes confounding from polygenicity in genome-wide affiliation research. Nat. Genet. 47, 291–295 (2015).eight.GTEx Consortium. The Genotype-Tissue Expression (GTEx) pilot evaluation: multitissue gene regulation in people. Science 348, 648–660 (2015).9.Wells, A. et al. The anatomical distribution of genetic associations. Nucleic Acids Res. 43, 10804–10820 (2015).10.Finucane, H.Ok. et al. Partitioning heritability by useful annotation utilizing genome-wide affiliation abstract statistics. Nat. Genet. 47, 1228–1235 (2015).11.Farh, Ok.Ok. et al. Genetic and epigenetic nice mapping of causal autoimmune illness variants. Nature 518, 337–343 (2015).12.Fehrmann, R.S. et al. Gene expression evaluation identifies international gene dosage sensitivity in most cancers. Nat. Genet. 47, 115–125 (2015).13.Thomsen, S.F., Kyvik, Ok.O. & Backer, V. Etiological relationships in atopy: a evaluation of dual research. Twin Res. Hum. Genet. 11, 112–120 (2008).14.Sanseau, P. et al. Use of genome-wide affiliation research for drug repositioning. Nat. Biotechnol. 30, 317–320 (2012).15.Bonder, M.J. et al. Illness variants alter transcription issue ranges and methylation of their binding websites. Nat. Genet. 49, 131–138 (2017).16.Joehanes, R. et al. Epigenetic signatures of cigarette smoking. Circ Cardiovasc Genet 9, 436–447 (2016).17.Lev, S. et al. Identification of a novel household of targets of PYK2 associated to Drosophila retinal degeneration B (rdgB) protein. Mol. Cell. Biol. 19, 2278–2288 (1999).18.Yan, S.R. & Novak, M.J. β2 integrin–dependent phosphorylation of protein-tyrosine kinase Pyk2 stimulated by tumor necrosis issue α and fMLP in human neutrophils adherent to fibrinogen. FEBS Lett. 451, 33–38 (1999).19.Kamen, L.A., Schlessinger, J. & Lowell, C.A. Pyk2 is required for neutrophil degranulation and host protection responses to bacterial an infection. J. Immunol. 186, 1656–1665 (2011).20.Willer, C.J., Li, Y. & Abecasis, G.R. METAL: quick and environment friendly meta-analysis of genomewide affiliation scans. Bioinformatics 26, 2190–2191 (2010).21.Fadista, J., Manning, A.Ok., Florez, J.C. & Groop, L. The (in)well-known GWAS P-value threshold revisited and up to date for low-frequency variants. Eur. J. Hum. Genet. 24, 1202–1205 (2016).22.Gough, H. et al. Allergic multimorbidity of bronchial asthma, rhinitis and eczema over 20 years within the German start cohort MAS. Pediatr. Allergy Immunol. 26, 431–437 (2015).23.Mortz, C.G., Andersen, Ok.E., Dellgren, C., Barington, T. & Bindslev-Jensen, C. Atopic dermatitis from adolescence to maturity within the TOACS cohort: prevalence, persistence and comorbidities. Allergy 70, 836–845 (2015).24.Sarnowski, C. et al. Identification of a brand new locus at 16q12 related to time to bronchial asthma onset. J. Allergy Clin. Immunol. 138, 1071–1080 (2016).25.Dharmage, S.C. et al. Atopic dermatitis and the atopic march revisited. Allergy 69, 17–27 (2014).26.Chang, X. & Wang, Ok. wANNOVAR: annotating genetic variants for private genomes by way of the net. J. Med. Genet. 49, 433–436 (2012).27.1000 Genomes Mission Consortium. An built-in map of genetic variation from 1,092 human genomes. Nature 491, 56–65 (2012).28.Rebhan, M., Chalifa-Caspi, V., Prilusky, J. & Lancet, D. GeneCards: integrating details about genes, proteins and ailments. Developments Genet. 13, 163 (1997).29.Davis, J.R. et al. An environment friendly multiple-testing adjustment for eQTL research that accounts for linkage disequilibrium between variants. Am. J. Hum. Genet. 98, 216–224 (2016).30.Montgomery, S.B. et al. Transcriptome genetics utilizing second era sequencing in a Caucasian inhabitants. Nature 464, 773–777 (2010).31.Lappalainen, T. et al. Transcriptome and genome sequencing uncovers useful variation in people. Nature 501, 506–511 (2013).32.Westra, H.J. et al. Systematic identification of trans eQTLs as putative drivers of identified illness associations. Nat. Genet. 45, 1238–1243 (2013).33.Chun, S. et al. Restricted statistical proof for shared genetic results of eQTLs and autoimmune-disease-associated loci in three main immune-cell varieties. Nat. Genet. 49, 600–605 (2017).34.Sanyal, A., Lajoie, B.R., Jain, G. & Dekker, J. The long-range interplay panorama of gene promoters. Nature 489, 109–113 (2012).35.Mifsud, B. et al. Mapping long-range promoter contacts in human cells with high-resolution seize Hello-C. Nat. Genet. 47, 598–606 (2015).36.Li, G. et al. Intensive promoter-centered chromatin interactions present a topological foundation for transcription regulation. Cell 148, 84–98 (2012).37.Rao, S.S. et al. A 3D map of the human genome at kilobase decision reveals rules of chromatin looping. Cell 159, 1665–1680 (2014).38.Corradin, O. et al. Combinatorial results of a number of enhancer variants in linkage disequilibrium dictate ranges of gene expression to confer susceptibility to widespread traits. Genome Res. 24, 1–13 (2014).39.Hnisz, D. et al. Tremendous-enhancers within the management of cell id and illness. Cell 155, 934–947 (2013).40.He, B., Chen, C., Teng, L. & Tan, Ok. International view of enhancer–promoter interactome in human cells. Proc. Natl. Acad. Sci. USA 111, E2191–E2199 (2014).41.Andersson, R. et al. An atlas of lively enhancers throughout human cell varieties and tissues. Nature 507, 455–461 (2014).42.Welter, D. et al. The NHGRI GWAS Catalog, a curated useful resource of SNP–trait associations. Nucleic Acids Res. 42, D1001–D1006 (2014).43.Astle, W.J. et al. The allelic panorama of human blood cell trait variation and hyperlinks to widespread advanced illness. Cell 167, 1415–1429.e19 (2016).44.Zheng, J. et al. LD Hub: a centralized database and net interface to carry out LD rating regression that maximizes the potential of abstract stage GWAS knowledge for SNP heritability and genetic correlation evaluation. Bioinformatics 33, 272–279 (2017).45.Fairfax, B.P. et al. Genetics of gene expression in main immune cells identifies cell sort–particular grasp regulators and roles of HLA alleles. Nat. Genet. 44, 502–510 (2012).46.Fairfax, B.P. et al. Innate immune exercise situations the impact of regulatory variants upon monocyte gene expression. Science 343, 1246949 (2014).47.Fu, J. et al. Unraveling the regulatory mechanisms underlying tissue-dependent genetic variation of gene expression. PLoS Genet. eight, e1002431 (2012).48.Zhernakova, D.V. et al. Identification of context-dependent expression quantitative trait loci in entire blood. Nat. Genet. 49, 139–145 (2017).49.Willemsen, G. et al. The Netherlands Twin Register biobank: a useful resource for genetic epidemiological research. Twin Res. Hum. Genet. 13, 231–245 (2010).50.Tsai, P.C. et al. DNA methylation adjustments within the IGF1R gene in start weight discordant grownup monozygotic twins. Twin Res. Hum. Genet. 18, 635–646 (2015).

LEAVE A REPLY

Please enter your comment!
Please enter your name here