H3K27ac ChIP-Seq in REH and 697
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE79870 | GEO | 2016/09/26
SECONDARY ACCESSION(S): PRJNA317297
REPOSITORIES: GEO
Similar Datasets
Project description:H3K27ac ChIP-Seq data of the T-ALL cell line LOUCY was obtained to find active regions in the genome and to correlate that with expression profiling of lncRNAs in the LOUCY cell line. ChIP-sequencing data was generated for H3K27ac in the T-ALL cell line LOUCY.
2016-05-17 | E-GEOD-74311 | biostudies-arrayexpress
Project description:H3K27ac ChIP-Seq data of the T-ALL cell line LOUCY was obtained to find active regions in the genome and to correlate that with expression profiling of lncRNAs in the LOUCY cell line.
2016-05-17 | GSE74311 | GEO
Project description:Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their expression and role in pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we conducted a comprehensive analysis of the long non-coding RNA transcriptome in ETV6/RUNX1 positive BCP-ALL, one of the most frequent subtypes of pediatric leukemia. An ETV6/RUNX1 expression signature was established, consisting of 596 lncRNAs (434 up and 162 down) using expression analysis of a series of primary patient samples. Subsequently, RNA sequencing from BCP-ALL cell lines and shRNA-mediated silencing of ETV6/RUNX1, illustrated that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 are bona fide ETV6/RUNX1 targets and could serve as novel biomarkers of this prevalent subtype of human leukemia.
2016-09-26 | GSE79871 | GEO
Project description:Enterococcus faecium 697 Genome sequencing
| PRJNA211807 | ENA
Project description:MLL-fusion proteins are potent inducers of cancer in hematopoietic cells, where they are known to cause changes in global gene expression. How MLL-fusion proteins interact with the genome has not been established, so we have limited understanding of the pathway by which these proteins generate aberrant gene expression programs. Here we describe how the MLL-AF4 protein occupies the genome in human leukemia cells and its striking effects on chromatin states. We find that the MLL-AF4 fusion protein selectively occupies regions of the genome that contain developmental regulatory genes important for hematopoietic stem cell identity and self-renewal. These MLL-AF4 bound regions have grossly altered chromatin structure, with histone modifications catalyzed by Trithorax Group (TrxG) proteins and Dot1 extending across unusually large domains. This indicates that a key feature of MLL-associated leukemogenesis is aberrant targeting of chromatin modifiers to regions of the genome controlling hematopoietic development. Our results define the direct targets of the MLL-fusion protein, reveal the global role of epigenetic misregulation in leukemia, and identify new targets for therapeutic intervention in human cancer. This dataset includes expression data for two replicates each of SEM and REH leukemia cell lines, ChIP-chip data targeting RNAP2, H3K4me3, H3K79me2, ENL, AF4-C, and MLL-N in SEM and REH leukemia cell lines, and ChIP-Seq data of H3K79me2, H3K4me3, ans WCE in SEM and REH cell lines. This Series contains the ChIP-Seq data only. The expression and ChIP-chip data are provided in GEO Series GSE13313.
2012-05-31 | E-GEOD-38338 | biostudies-arrayexpress
Project description:MLL-fusion proteins are potent inducers of cancer in hematopoietic cells, where they are known to cause changes in global gene expression. How MLL-fusion proteins interact with the genome has not been established, so we have limited understanding of the pathway by which these proteins generate aberrant gene expression programs. Here we describe how the MLL-AF4 protein occupies the genome in human leukemia cells and its striking effects on chromatin states. We find that the MLL-AF4 fusion protein selectively occupies regions of the genome that contain developmental regulatory genes important for hematopoietic stem cell identity and self-renewal. These MLL-AF4 bound regions have grossly altered chromatin structure, with histone modifications catalyzed by Trithorax Group (TrxG) proteins and Dot1 extending across unusually large domains. This indicates that a key feature of MLL-associated leukemogenesis is aberrant targeting of chromatin modifiers to regions of the genome controlling hematopoietic development. Our results define the direct targets of the MLL-fusion protein, reveal the global role of epigenetic misregulation in leukemia, and identify new targets for therapeutic intervention in human cancer. Keywords: cell type comparison This dataset includes expression data for two replicates each of SEM and REH leukemia cell lines and ChIP-chip data targeting RNAP2, H3K4me3, H3K79me2, ENL, AF4-C, and MLL-N in SEM and REH leukemia cell lines.
2008-12-14 | E-GEOD-13313 | biostudies-arrayexpress
Project description:CRISPR/Cas9 system was used to generate mediator complex subunit 1 (MED1) knockout human pre-B ALL cell line 697. RNA-seq was performed to observe the effects of MED1 deletion on gene expression in 697.
2020-05-13 | E-MTAB-8178 | biostudies-arrayexpress
Project description:ARHGEF4 expression is associated with t(12;21) acute lymphoblastic leukaemia (ALL). Our study investigated the substrate specificity of ARHGEF4, a member of the diffuse B-cell lymphoma (DBL) family of guanine nucleotide exchange factors (GEFs), in t(12;21) ALL REH cells. ARHGEF4 was found to activate the small guanine nucleotide binding protein (GTPase) CDC42. In order to determine the function of CDC42 in t(12;21) ALL cells, we performed RNAseq analysis on REH cells treated for 24 hours with DMSO vehicle control in comparison to 25uM ML141, a CDC42 inhibitor.
2020-06-20 | GSE152836 | GEO