Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: ChIP-seq analysis of AF9 and TET2 enrichment in day 12 neural cells

PROVIDER: PRJNA282457 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR2000232.fastq.gz	Fastqsanger.gz
	SRR2000233.fastq.gz	Fastqsanger.gz
	SRR2000234.fastq.gz	Fastqsanger.gz

Items per page:

1 - 3 of 3

Similar Datasets

ChIP-seq analysis of AF9 and TET2 enrichment in day 12 neural cells

Project description:AF9 and TET2 were enriched in neural gene loci

2016-04-19 | GSE68332 | GEO

ChIP-seq of histone marks H3K36, H3K27, and H3K9 in JMJD1C knockout or mutated MLL-AF9 leukemia cells

Project description:We performed genome-wide profiling of H3K9me3, H3K9me1, H3K27me3, and H3K36me3 by ChIP-seq in JMJD1C knockout or mutated MLL-AF9 leukemia cells. For ChIP-seq in JMJD1C mutated cells, we transduced sgRNA targeting the zinc finger, jumonji domain of JMJD1C or Renilla control and sorted on day 6 for GFP (MLL-AF9) Tdtomato (sgRNA) double positive cells. For ChIP-seq in JMJD1C knockout cells, we transduced Jmjd1c flox/flox MLL-AF9 leukemia cells with CRE TdTomato and sorted on day 6 for GFP (MLL-AF9) Tdtomato (CRE) double positive cells. These cells were subjected to ChIP-seq analysis with either H3K27me3, H3K9me3, H3K9me1 (JMJD1C knockout cells) or H3K36me3 (both knockout and mutated cells) antibody. We found increased H3K36me3 level at promoters of differentially expressed genes between control and JMJD1C loss or mutated leukemia cells.

2019-04-12 | GSE129661 | GEO

Homo sapiens

Project description:ChIP-seq analysis of H3K9 acetylation enrichment in hESCs and day 8 neural progenitor cells

| PRJNA277946 | ENA

ChIP-seq analysis of COUP-TFI enrichment in neural retina.

Project description:ChIP-seq analysis of COUP-TFI enrichment in neural retina.

| PRJNA787928 | ENA

Homo sapiens

Project description:DIP-seq analysis of 5mC and 5hmC distributions in hESCs and day 12 neural cells

| PRJNA282456 | ENA

Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis (eRRBS)

Project description:DNA methylation is tightly regulated throughout mammalian development and altered methylation patterns are a hallmark of cancer. The methylcytosine dioxygenase TET2 is frequently mutated in acute myeloid leukemia (AML) and has been suggested to protect CpG islands and promoters from aberrant methylation. By generating a novel mouse model of Tet2-deficient AML we show that loss of Tet2 in hematopoietic cells leads to progressive hypermethylation of active enhancer elements and altered expression of genes implicated in tumorigenesis. In contrast, CpG island and promoter methylation does not change in a Tet2-dependent manner. Furthermore, we confirm this specific enhancer hypermethylation phenotype in human AML patients. Thus, we propose that TET2 prevents leukemic transformation of hematopoietic cells by protecting enhancers from aberrant DNA methylation. Enhanced Reduced Representation Bisulfite Sequencing (eRRBS) analysis of in vitro-grown hematopoietic cells transduced with AML1-ETO or MLL-AF9

2015-04-22 | E-GEOD-59584 | biostudies-arrayexpress

Degree of Recruitment of DOT1L to MLL-AF9 Defines Level of H3K79 Di- and Tri-methylation on Target Genes and Transformation Potential

Project description:The MLL gene is a common target of chromosomal translocations found in human leukemia. MLL-fusion leukemias are consistently poor prognosis. One of the most common translocation partners is AF9 (a.k.a. MLLT3). MLL-AF9 recruits DOT1L, a histone 3 lysine 79 methyltransferase (H3K79me1/me2/me3), leading to aberrant gene transcription. We show that DOT1L has three AF9 binding sites, and present the NMR solution structure of a DOT1L-AF9 complex. We generated structure-guided point mutations with graded effects on recruitment of DOT1L to MLL-AF9. ChIP-Seq analyses of H3K79me2 and H3K79me3 show that graded reduction of the DOT1L interaction with MLL-AF9 results in selective losses in H3K79me2 and me3 marks at MLL-AF9 target genes. Furthermore, the degree of DOT1L recruitment defines the level of MLL-AF9 hematopoietic transformation. Hematopoietic progenitor cells isolated from mouse bone marrow were transduced with retrovirus expressing either wildtype MLL-AF9 (WT), mutants, MLL-AF9 (D544R) and MLL-AF9 (D546R). ChIP-Seq analyses were performed on these wildtype and mutant cells using H3K79me2 and H3K79me3 antibodies. 3 samples corresponding to ChIP-Seq with H3K79me2 antibody: 1) MLL-AF9 (WT) 2) MLL-AF9 (D544R) 3) MLL-AF9 (D546R) 3 Samples Corresponding to ChIP-Seq with H3K79me3 antibody: 4) MLL-AF9 (WT) 5) MLL-AF9 (D544R) 6) MLL-AF9 (D546R)

2015-04-30 | E-GEOD-64365 | biostudies-arrayexpress

Genome-wide anaylsis of histone acetylation during mouse ESC differentiation [ChIP-seq]

Project description:Using acetylated histone H3 ChIP-seq, we reveal that the histone H3 acetylation level is gradually increased on the neural gene loci while decreased on the neural-inhibitory gene loci during mouse ESC neural differentiation. By overlapping with the targets of HDAC1 ChIP-seq, we identify Nodal as a target gene repressed by histone deacetylation. Thus, our study reveals an intrinsic mechanism that epigenetic histone deacetylation ensures neural fate commitment by restricting Nodal signaling. Examination of HDAC1 in differentiated day 2 cells and acetylated histone H3 in day 2, day 4 and day 6 cells.

2015-02-19 | E-GEOD-66025 | biostudies-arrayexpress

Reproducibility of standard and micro-scaled H3K4me2 ChIP-Seq assay in mouse derived lymphoblastic cell line (D10.G4.1 cells, ATCC)

Project description:To estimate the reproducibility of standard and micro-scaled H3K4me2 ChIP-Seq assay we performed the genome-wide correlation analysis of H3K4me2 enrichment patterns from 7 independent standard ChIP-Seq assays (2 million D10 cells), and micro-scaled ChIP-Seq 100,000 cells sample –(N=12), 10,000 cells sample–(N=3), and 1000 cell sample – (N=4)

2014-07-05 | GSE53644 | GEO

Transcriptomic analysis of hyperglycemic stress induced myeloid neoplasms associated with Tet2 haploinsufficiency

Project description:Purpose: To identify potential mediators of myeloid neoplasms driven by Tet2 haploinsufficiency and hyperglycemic stress. Methods: Lin-negative bone marrow cells from WT, Tet2+/-, Ins2Akita/+ and Tet2+/-;Ins2Akita/+ were used for total RNA purification and RNA-seq. Results: Using unbiased Gene Set Enrichment Analysis (GSEA), we identified that innate immune pathway, IL-6 signaling pathway and TLR4-NFkB pathway were significantly enriched in the compound mutants (Tet2+/-;Ins2Akita/+) while controls (Tet2+/- or Ins2Akita/+) were similar to WT mice.

2020-09-23 | GSE158351 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data