Boletín de Segovia: Número 3 - 1913 enero 6

Copia digital. Madrid : Ministerio de Cultura. Subdirección General de Coordinación Bibliotecaria, 200

Additional file 8: Figure S6. of Glucocorticoid receptor and nuclear factor kappa-b affect three-dimensional chromatin organization

(A) Histogram depicting the genomic proximity (localization) of P300 binding sites identified by ChIP-seq in relation to those identified by using ChIA-PET self-ligation PETs. Identical comparison is performed for both DMSO-treated and TA + TNFα-treated data sets. (B) P300 ChIP-seq signal at P300 binding sites commonly identified by ChIP-seq and ChIA-PET and those binding sites that were uniquely detected in the ChIP-seq data set. (C) P300 ChIP-seq signal at P300 binding sites that were either involved (anchor) or not involved (non-anchor) in long-range interaction as identified by ChIA-PET analysis. (D) An example screenshot depicting the P300 interaction subdomains, P300 ChIP-seq binding sites in relation to topological domains as defined by replication timing data ( www.replicationdomain.org ). (E) Localization of all the interaction subdomains identified by ChIA-PET analysis (P300 and POLII) in relation to topological domains. (PDF 1041 kb

Additional file 2: Figure S2. of Glucocorticoid receptor and nuclear factor kappa-b affect three-dimensional chromatin organization

Activated p65 induces de novo P300 depositions to latent genomic loci. (A) Pile-up heat map depicting the H3K4me1 and H3K4me3 signal around (±12 kb) all p65-bound promoters and DBSs. (B) Pile-up heat map depicting the p65 and P300 signal at all p65-bound enhancers upon vehicle, DMSO (−), and TNFα (+) treatment. (C) Example screenshot depicting TNFα-induced P300 recruitment at genomic regions (red box) and recruitment of p65 at genomic loci that are pre-marked by P300. (D) Motif occurrence at all p65-bound DBS presented as a function of TNFα-dependent P300 recruitment (x-axis) (top-panel). Level of shared binding of p65 and other TFs at all p65-bound DBS, presented as a function of TNFα-dependent P300 recruitment (bottom panel). (E) Level of H3K27ac, DNase I hypersensitivity, and H3K4me1 at all p65-bound DBSs (induced and constitutive P300 sites). (PDF 909 kb

Additional file 11: Figure S8. of Glucocorticoid receptor and nuclear factor kappa-b affect three-dimensional chromatin organization

Direct comparison of long-range interactions identified by P300 ChIA-PET and 4C-seq analyses at FKBP5, DUSP1, and BIRC3 loci. (PDF 1037 kb

Additional file 3: Figure S3. of Glucocorticoid receptor and nuclear factor kappa-b affect three-dimensional chromatin organization

Large numbers of P300-bound loci are not co-occupied by GR or p65. (A) Average ChIP-seq signal of GR and P300 around (Âą10 kb) all the P300 binding sites that do not show a significant GR occupancy. (B) Average ChIP-seq signal of p65 and P300 around (Âą10 kb) all the P300 binding sites that do not show a significant p65 occupancy. (PDF 168 kb

Additional file 9: Table S2. of Glucocorticoid receptor and nuclear factor kappa-b affect three-dimensional chromatin organization

List of all significant long-range interactions identified by P300 and POLII ChIA-PET analysis. (XLS 2165 kb

Additional file 12: Figure S9. of Glucocorticoid receptor and nuclear factor kappa-b affect three-dimensional chromatin organization

Direct comparison of long-range interactions identified by P300 ChIA-PET and 4C-seq analyses at PTPN1, SULF1 and ZFHX3 loci. (PDF 1147 kb

Additional file 15: Table S5. of Glucocorticoid receptor and nuclear factor kappa-b affect three-dimensional chromatin organization

Overview of sequenced and mapped reads of 4C-seq libraries. (XLS 31 kb