ChIP-seq of H3K4me3 and H3K27ac of dermal fibroblasts
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB22016 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Dermal fibroblasts from human, rhesus macaque, mouse and rat with and without dsRNA (poly I:C) stimulation (1ug/mL for 4 hours).<br>The innate immune response - the expression programme that is initiated once a pathogen is sensed - is known to be variable among responding cells, as well as to rapidly evolve in the course of mammal evolution. To study the transcriptional divergence and cell-to-cell variability of this response, we stimulated dermal fibroblast cells from two primates (human and macaque) and two rodents (mouse and rat) with dsRNA - a mimic of viral RNA that elicits a rapid innate immune response. Subsequently, we profiled the response using bulk RNA-seq, scRNA-seq and ChIP-seq across the four species and across different time points.
2018-07-06 | E-MTAB-5918 | biostudies-arrayexpress
Project description:We report changes in enrichment at chromatin of p63, KLF4 and H3K27ac following ectopic expression of wildtype or mutant p63+/- KLF4 for 72 hours in dermal BJ fibroblasts.
2019-02-15 | GSE126390 | GEO
Project description:ChIP-seq of AJSZ in human dermal fibroblasts
| PRJNA759229 | ENA
Project description:Tissue stem cells preserve a certain level of potency to maintain intact tissue integrity after various injury. Postnatal dermal fibroblasts lose differentiation potential for regenerative healing that recreates normal tissue including functional hair follicles (HFs), however, their intrinsic cellular changes are not understood yet. Here, we uncover a postnatal maturation process in papillary fibroblasts (PFs) mediated by Twist2-driven chromatin and transcriptional remodeling. Within 4 days after birth, dermal PFs lost WNT transcription factors (TFs) and target gene expressions accompanied by loss of H3K27ac expression. Through single-cell transcriptomics, ATAC-seq and ChIP-seq profiling, we define a postnatal maturation trajectory of PFs, in addition to loss of regenerative trajectory, triggered by decrease of H3K27ac and chromatic accessibility. In vivo inhibition of histone deacetylation delays the postnatal chromatin remodeling and maintains developmental signaling and differentiation potential in PFs. TF motif analysis on the chromatin regions losing accessibility identifies TWIST as a potential regulator specifying these regions. Using Twist2 conditional knock-out mouse model, we unearth a postnatal role of Twist2 TF as governing the postnatal maturation process resulting in switch-off of developmental pathways after birth. Together, our findings expose a comprehensive intracellular mechanism driving postnatal maturation in dermal fibroblasts with profound implications for regenerative medicine.
2022-05-17 | GSE181394 | GEO
Project description:Skeletal muscle myonuclei-specific ChIP-Seq of H3K4me3 and H3K27ac
| PRJNA757393 | ENA
Project description:Considered as fundamental epigenetic regulators controlling many key cellular processes, histone modifications are a well-conserved and widely studied class of epigenetic modifications. Genome-wide studies have identified enhancers as DNA sequences that bind to H3K4me1 and H3K27ac and promoters as DNA sequences that bind to H3K4me3. To explore how the Twist1 complex (Twist1/YY1/p300) regulates miR-9 expression, we performed ChIP-seq in PLC-PRF-5 cells, providing a panorama of p300, H3K4me3, H3K4me1, and H3K27ac.
2022-07-21 | GSE208334 | GEO
Project description:This dataset contains ChIP-seq data profiling genomic binding of H3K27ac and H3K4me3 in single cell-derived control, as well as CRISPR/Cas9 induced tRNA gene deletion clones and intergenic region deletion clones in human cancer cell lines HAP1. In this study, we found a large genomic deletion of 10q23 in Cas9 modified clones and further investigate the effect of H3K27ac binding.
2023-10-24 | E-MTAB-11859 | biostudies-arrayexpress
Project description:Tissue stem cells preserve a certain level of potency to maintain intact tissue integrity after various injury. Postnatal dermal fibroblasts lose differentiation potential for regenerative healing that recreates normal tissue including functional hair follicles (HFs), however, their intrinsic cellular changes are not understood yet. Here, we uncover a postnatal maturation process in papillary fibroblasts (PFs) mediated by Twist2-driven chromatin and transcriptional remodeling. Within 4 days after birth, dermal PFs lost WNT transcription factors (TFs) and target gene expressions accompanied by loss of H3K27ac expression. Through single-cell transcriptomics, ATAC-seq and ChIP-seq profiling, we define a postnatal maturation trajectory of PFs, in addition to loss of regenerative trajectory, triggered by decrease of H3K27ac and chromatic accessibility. In vivo inhibition of histone deacetylation delays the postnatal chromatin remodeling and maintains developmental signaling and differentiation potential in PFs. TF motif analysis on the chromatin regions losing accessibility identifies TWIST as a potential regulator specifying these regions. Using Twist2 conditional knock-out mouse model, we unearth a postnatal role of Twist2 TF as governing the postnatal maturation process resulting in switch-off of developmental pathways after birth. Together, our findings expose a comprehensive intracellular mechanism driving postnatal maturation in dermal fibroblasts with profound implications for regenerative medicine.
2022-05-17 | GSE181390 | GEO
Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription of HNF1A, preventing silencing or overexpression. We have generated a mouse model where the promoter of Haster has been specifically deleted in liver (Haster loxP/loxP; AlbCre). In liver the prevailing consequence is upregulation of HNF1A. We performed HNF1A, H3K4me3 and H3K27ac ChIP-seq to assess the impact of HNF1A upregulation on the chromatin landscape of Haster KO liver.
2022-05-01 | E-MTAB-11471 | biostudies-arrayexpress