Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE26397
PROVIDER: PRJNA136845 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR039137.fastq.gz | Fastqsanger.gz | |||
| SRR039138.fastq.gz | Fastqsanger.gz | |||
| SRR039152.fastq.gz | Fastqsanger.gz | |||
| SRR039153.fastq.gz | Fastqsanger.gz | |||
| SRR039154.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:HL-1 cells treated with two different siRNAs against Gata4, Mef2a, Nkx2.5 and Srf each in duplicate to identify downstream targets.
2011-01-05 | E-TABM-376 | biostudies-arrayexpress
Project description:The aim of the experiment was to identify genome wide binding sites for Gata4, Mef2a, Nkx2.5, Srf, p300, Pol_II, H3ac, H3K4me1 by using Chromatin Immunoprecipitation followed by microarray analysis (ChIP-chip) in HL1 cells.
2011-01-05 | E-TABM-378 | biostudies-arrayexpress
Project description:We investigated the cardiac transcription network driven by the DNA-binding key factor Srf in combination with epigenetic marks of histone 3 acetylation (H3ac). Srf has been shown to play a key role in cardiac cell growth and muscle gene regulation. However, we still have limited understanding of the global transcription network driven by this factor in a direct or indirect manner. Moreover, we lack knowledge to which extent epigenetic marks such as histone modifications interfere with the regulation of direct targets. To gain insights into the transcriptional regulatory network two independent chromatin immunoprecipitation (ChIP) samples were profiled. DNA fragments bound to Srf or modified with acetylated histone 3 in mouse cardiomyocytes (HL1-cells) were sequenced using ultra-high throughput DNA sequencing. ChIP-seq profile of a transcription factor (Srf) and a histone modification (H3ac)
2011-01-03 | E-GEOD-19065 | biostudies-arrayexpress
Project description:The aim of this study was to induce cardiomyogenic conversion of Human Umbilical Vein Endothelial Cells (HUVEC ) by triggering ectopic expression of the cardiac transcription factors Nkx2.5 and GATA4. Cells were cultured without cell myocardial co-culture system and transduced with lentivirus containing coding sequence of Nkx2.5, GATA4 or GFP as control. Cells were cultured in the EBM-2/ EGM-2 medium, 12 days before microarray analysis. We report in this study that over-expression of NKX2.5 and GATA4 in HUVECs stimulates the expression of some specific genes important in the cardiomyogenic differentiation process, leading to partial switch of these cells from the endothelial to the myocardial course. 12 arrays were analysed. Three competitive hybridizations to the arrays were performed in duplicate using each time, two dye-swap following this experimental design: AWA065 : CY5 (HUVEC+NKX2,5) / CY3 (HUVEC) AWA067 : CY5 (HUVEC) / CY3 (HUVEC+NKX2,5) AWA075 : CY5 (HUVEC+NKX2,5) / CY3 (HUVEC) AWA076 : CY5 (HUVEC) / CY3 (HUVEC+NKX2,5) AWA068 : CY5 ((HUVEC) / CY3 (HUVEC+GATA4) AWA070 : CY5 (HUVEC+GATA4) / CY3 ((HUVEC) AWA073 : CY5 (HUVEC+GATA4) / CY3 ((HUVEC) AWA002 : CY5 ((HUVEC) / CY3 (HUVEC+GATA4) AWA066 : CY5 (HUVEC) / CY3 (HUVEC+NKX2.5+GATA4) AWA069 : CY5 (HUVEC+NKX2.5+GATA4) / CY3 (HUVEC) AWA071 : CY5 (HUVEC+NKX2.5+GATA4) / CY3 (HUVEC) AWA074 ; CY5 (HUVEC) / CY3 (HUVEC+NKX2.5+GATA4)
2012-04-20 | E-GEOD-37459 | biostudies-arrayexpress
Project description:We investigated the cardiac transcription network driven by the DNA-binding key factor Srf in combination with epigenetic marks of histone 3 acetylation (H3ac). Srf has been shown to play a key role in cardiac cell growth and muscle gene regulation. However, we still have limited understanding of the global transcription network driven by this factor in a direct or indirect manner. Moreover, we lack knowledge to which extent epigenetic marks such as histone modifications interfere with the regulation of direct targets. To gain insights into the transcriptional regulatory network two independent chromatin immunoprecipitation (ChIP) samples were profiled. DNA fragments bound to Srf or modified with acetylated histone 3 in mouse cardiomyocytes (HL1-cells) were sequenced using ultra-high throughput DNA sequencing.
2011-01-03 | GSE19065 | GEO
Project description:The aim of this study was to induce cardiomyogenic conversion of Human Umbilical Vein Endothelial Cells (HUVEC ) by triggering ectopic expression of the cardiac transcription factors Nkx2.5 and GATA4. Cells were cultured without cell myocardial co-culture system and transduced with lentivirus containing coding sequence of Nkx2.5, GATA4 or GFP as control. Cells were cultured in the EBM-2/ EGM-2 medium, 12 days before microarray analysis. We report in this study that over-expression of NKX2.5 and GATA4 in HUVECs stimulates the expression of some specific genes important in the cardiomyogenic differentiation process, leading to partial switch of these cells from the endothelial to the myocardial course.
2012-04-21 | GSE37459 | GEO
Project description:[1] Gene expression profiling in Gata4, Mef2a knockdown in HL-1 cells. HL-1 cells infected with adenovirus expressing either control siRNA or Gata4, and Gata4 & Mef2a siRNA. [2] Genome-wide maps of cardiac transcription factors binding region in HL-1 cells. We performed bio-ChIP-seq using streptavidin beads immunoprecipitation of biotinylated 5 cardiac transcription factors (fbio) and P300 antibody ChIP-seq. We used a dox-inducible dual adenovirus system to express biotinylated Core Cardiac TFs in HL1. One adenovirus expressed the dox-activated reverse tet activator protein (rtTA) and the E. coli biotinylating enzyme BirA from the cardiac specific rat troponin T promoter. The second virus expressed a Core Cardiac TF fused to a C-terminal flag-bio epitope tag, where bio is the 15 amino acid substrate for BirA. This in vivo biotinylation approach permits pulldown of different factors to be performed under identical, stringent conditions, and circumvents limitations posed by available antibodies. We titrated adenovirus and dox doses to express GATA4flbio and MEF2Aflbio at near endogenous levels. The same conditions were then used to express SRFflbio, TBX5flbio, and NKX2-5flbio. Reference: 12. de Boer E, Rodriguez P, Bonte E, Krijgsveld J, Katsantoni E et al. (2003) Efficient biotinylation and single-step purification of tagged transcription factors in mammalian cells and transgenic mice. Proc Natl Acad Sci U S A 100: 7480-7485. [1] Gene expression profiling: Identify differentially expressed genes after siRNA Gata4 or Gata4_Mef2a double knockdown in HL-1 cells [2] Genome occupancy profiling: Identify cardiac active enhancers by identified 5 cardiac transcription factors and P300 peaks.
2011-03-02 | E-GEOD-21529 | biostudies-arrayexpress
Project description:Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering the transcriptional programs that orchestrate organ development and homeostasis. Here we used biotinylated knockin alleles of seven key TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) that regulate heart development and homeostasis to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult heart. Our results show that these TFs have dynamic chromatin occupancy between developmental stages. We observed that multiple TFs often co-occupy the same chromatin region, exhibiting collaborative binding that overall was most consistent with indirect cooperativity. Regions with multiple TF binding were more likely to exhibit features of functional regulatory elements, including evolutionary conservation, chromatin accessibility, and activity in transcriptional enhancer assays. Although histone H3 acetylation on lysine 27 (H3K27ac) has been used to identify active enhancers, many regions occupied by multiple TFs lacked H3K27ac, and TF-bound regions with or without H3K27ac co-occupancy had similar region conservation and enhancer activity. Specific studies of TEAD1 demonstrated that it is a core component of the cardiac transcriptional network: physically interacted with NKX2-5 and MEF2C and co-occupied regulatory loci with other cardiac TFs to regulate cardiomyocyte-specific gene functions. Our study shows that co-occupancy by multiple TFs is a hallmark of a subset of functional transcriptional regulatory elements and provides a rich resource for deciphering the cardiac transcriptional regulatory network.
2019-09-13 | GSE124008 | GEO
Project description:Background: Cardiac transcription factors are master regulators during heart development. Recently, some were shown to transdifferentiate noncardiac mesoderm cells and cardiac fibroblasts into cardiomyocytes. However, the individual roles of each transcription factors in activating cardiac gene program have not been elucidated. We examined cardiac-specific and genome-wide gene expression in fibroblasts induced with cardiac transcription factors Nkx2.5 (N), Tbx5 (T), Gata4 (G), Myocardin (M) alone or different combinations. Methodology/Principal Findings: We applied different combinations of human Nkx2.5 (N), Tbx5 (T), Gata4 (G) and Myocardin (M) lentiviruses into 10T1/2 fibroblasts. Immunostaining and quantitative reverse transcription polymerase chain reaction (qRT-PCR) showed that N, T, G or M alone did not induce expression of cardiac marker genes M-NM-1-myosin heavy chain (M-NM-1MHC) and cardiac troponin T (cTnT). Only T+M and T+G+M combinations induced M-NM-1MHC and cTnT expression. Microarray-based gene ontology analysis revealed that T alone inhibited most genes involved in cardiac-related processes and activated genes involved in Wnt receptor signaling pathway and in aberrant processes. M alone inhibited genes involved in Wnt receptor signaling pathway and activated genes involved in cardiac-related processes and in aberrant processes. G alone inhibited genes involved in ectoderm development. T+G+M combination was the most effective activator of genes associated with cardiac-related processes including muscle cell differentiation, sarcomere, striated muscle contraction, regulation of heart contraction, and glucose metabolism and fatty acid oxidation (two significant forms of cardiomyocyte energy metabolism). And unlike T, M, G alone or T+M, T+G+M did not activate genes associated with aberrant processes. Conclusions: Tbx5, Gata4 and Myocardin play different roles in activating cardiac gene program and in avoiding aberrant gene program activation. The combination of T+G+M activated cardiac gene program and avoided aberrant gene program activation. Two weeks after doxycline induction, total RNA was isolated from 10T1/2-tTA cells infected with different combinations of Tbx5, Gata4, and Myocardin lentiviruses. Biological triplicated.
2012-11-30 | E-GEOD-27329 | biostudies-arrayexpress
Project description:Through integration of GATA4 genome-wide occupancy and RNA-seq dataset in embryonic conditional knockout heart, we identified a class of the master cardiac regulator GATA4 bound enhancers. With combinatorial assembly of chromatin signatures, we further refined that a unique type of fetal distal GATA4 enhancers enriched for H3K27ac, H3K4me1, but not for H3K4me3 and RNA polymerase II, are reinstated in adult hypertrophic heart. Study Gata4 and histone modifications in E12.5, Adult, Banding and Sham, and to correlate to gene expression and heart function
2014-08-13 | E-GEOD-52123 | biostudies-arrayexpress