Supplementary MaterialsS1 Table: Distribution of known HUVEC RELA transcription factor binding sites (TFBSs) across the GH elements of genes in modules

Supplementary MaterialsS1 Table: Distribution of known HUVEC RELA transcription factor binding sites (TFBSs) across the GH elements of genes in modules. the absolute value of the sum of estimated coefficients for the region; L = the number of probes in the region; clusterL = the number of probes in the cluster (not absolutely all probes in the cluster are always contained in the area); p.worth = p worth for differential methylation; fwer = p worth for differential methylation corrected to take into account the family-wise mistake rate. The rest of the columns recognize genes that (1) include a DMR in the gene body or (2) possess 5 untranslated locations (5 UTRs) within or near a GH promoter formulated with a DMR. The next sheet shows attributes connected with SNPs in genes with DMRs within their promoters (promoter DMRs, or pDMRs).(XLSX) pone.0230884.s003.xlsx (57K) GUID:?E2D2AB07-D7C2-4A94-966C-AAC5D5F75482 TH-302 tyrosianse inhibitor S3 Document: Locations of geneHancer elements mapped to genes in each WGCNA module that overlap a RELA TFBS (sheet 1), or that overlap a RELA TFBS and a DMR (sheet 2). Desk TH-302 tyrosianse inhibitor columns will be the GH chromosome, begin position, TH-302 tyrosianse inhibitor end placement, WGCNA gene mapped, and WGCNA component.(XLSX) pone.0230884.s004.xlsx (1.1M) GUID:?1F2C7D0F-E40C-462D-9E14-55CBB3274A0A S4 Document: Complete disease ontology results for PR52B the green, dark, and cyan modules. Columns consist of Disease Ontology identifier; disease name; amount of genes annotated for the condition; amount of genes in module that overlap the condition annotated genes; enrichment flip modification, z-score, p-value, FDR-adjusted p-value, chances ratio, 95% self-confidence interval higher and lower bounds; set of annotated genes for the condition, and set of in module that overlap the condition annotated genes.(XLSX) pone.0230884.s005.xlsx (71K) GUID:?F4BABDD3-AEDE-4E8B-8B49-07C089683CF6 S1 Fig: Directed acyclic graph showing the condition ontology structure of the very best 15 terms (of 136 with FDR-adjusted p-value 0.05) through the green module. Conditions with significant enrichment are in box-shaped nodes, and darker color signifies a far more significant p-value. The entire list of illnesses enriched for genes in the green module and linked gene brands are in S3 Document. The interactions of green module Disease Ontology conditions in not really pictured could be explored interactively at http://disease-ontology.org/.(DOCX) pone.0230884.s006.docx (2.8M) GUID:?6A5DC5C5-1E0B-4B4F-AF50-FAE41205B66A S2 Fig: Directed acyclic graph showing the condition ontology structure of most terms with FDR-adjusted p-value 0.05 (n = 11) through the black module. Conditions with significant enrichment are in box-shaped nodes, and darker color signifies a far more significant p-value. The full list of diseases enriched for genes in the black module and associated gene names are in S3 File.(DOCX) pone.0230884.s007.docx (3.0M) GUID:?E9539C28-9D0E-4A69-99C6-023968753B26 S3 Fig: Directed acyclic graph showing the disease ontology structure of all terms with FDR-adjusted p-value 0.05 (n = 6) from the cyan module. Terms with significant enrichment are in box-shaped nodes, and darker color indicates a more significant p-value. The full list of diseases enriched for genes in the cyan module and associated gene names are in S3 File.(DOCX) pone.0230884.s008.docx (2.8M) GUID:?93C92FB0-96BB-404A-8146-45FED1C2F9A5 Data Availability StatementAll expression and methylation data are available in the Gene Expression Omnibus (GEO) at https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144810. There are two SubSeries linked to GSE144810: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144803 (expression data) and https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE144804 (methylation data). Abstract Endothelial cells are a primary site of leukocyte recruitment during inflammation. An increase in tumor necrosis factor-alpha (TNFa) levels as a result of contamination or some autoimmune diseases can trigger this process. Several autoimmune diseases are now treated with TNFa inhibitors. However, genomic alterations that occur as a result of TNF-mediated inflammation are not well comprehended. TH-302 tyrosianse inhibitor To investigate molecular targets and networks resulting from increased TNFa, we measured DNA methylation and gene expression in 40 human umbilical vein endothelial cell primary cell lines before and 24 hours after stimulation with TNFa via microarray. Weighted TH-302 tyrosianse inhibitor gene co-expression network analysis identified 15 gene groups (modules) with comparable expression correlation patterns; four modules showed a strong association with TNFa treatment. Genes in the top TNFa-associated module were all up-regulated, had the highest proportion of hypomethylated regions, and were associated with 136 Disease Ontology terms, including autoimmune/inflammatory, infectious and cardiovascular diseases, and cancers. They included chemokines and and and and is the intramodular connectivity, or connectivity of a particular gene.