Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profile of hemin induced erythroid differentiation, over-expressing and knocking-down GATA-1, EKLF and NF-E2 in K562s

ABSTRACT: we profiled miRNA gene expression with the Illumina hybridization system in K562 cells induced by hemin and K562 cells with over-expressing or knocking-down GATA-1, EKLF or NF-E2 treatments.

ORGANISM(S): Homo sapiens

PROVIDER: GSE30380 | GEO | 2011/12/31

SECONDARY ACCESSION(S): PRJNA154841

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression profile of hemin induced erythroid differentiation, over-expressing and knocking-down GATA-1, EKLF and NF-E2 in K562s

Project description:we profiled miRNA gene expression with the Illumina hybridization system in K562 cells induced by hemin and K562 cells with over-expressing or knocking-down GATA-1, EKLF or NF-E2 treatments. To find differential expression miRNAs, we profiled miRNA gene expression with the Illumina hybridization system in untreated, hemin-treated 48h and 72h K562 cells. To define GATA-1, EKLF or NF-E2 directly targeted miRNA genes, a comprehensive analysis of TF induced miRNA gene expression changes was performed using over-expressing or knocking-down TFs in K562 cells and illumina miRNA profiling Beadchip system.

2011-12-31 | E-GEOD-30380 | biostudies-arrayexpress

ChIP-chip from 48h hemin induced K562 cells with GATA-1, EKLF, and NF-E2 antibodies

Project description:The transcription factor GATA-1, EKLF and NF-E2 promotes erythroid differentition by regulating their target genes, however, the intricate interplays between these key TFs and microRNA genes are largely unknown. Chromatin immunoprecipitation (ChIP) of GATA-1, EKLF and NF-E2 together with microRNA genomic promoter profiling by ChIP-on-chip analysis demonstrated that GATA-1, EKLF and NF-E2 collaborately regulate a series of microRNA genes. Comparison of microRNA promoter arrays of GATA-1 VS EKLF VS NF-E2 in K562 cells suffering with hemin induced erythroid differentiation

2011-12-31 | E-GEOD-30808 | biostudies-arrayexpress

Systematical identification of GATA-1, EKLF, and NF-E2 regulated miRNAs by ChIP-on chip and microRNA microarray in K562 cells into erythroid differentiation

Project description:This SuperSeries is composed of the following subset Series: GSE30380: Expression profile of hemin induced erythroid differentiation, over-expressing and knocking-down GATA-1, EKLF and NF-E2 in K562s GSE30808: ChIP-chip from 48h hemin induced K562 cells with GATA-1, EKLF, and NF-E2 antibodies Refer to individual Series

2011-12-31 | E-GEOD-30809 | biostudies-arrayexpress

ChIP-chip from 48h hemin induced K562 cells with GATA-1, EKLF, and NF-E2 antibodies

2011-12-31 | GSE30808 | GEO

Mechanisms of terminal erythroid differentiation defect in EKLF-deficient mice

Project description:EKLF is a Krüppel-like transcription factor identified as a transcriptional activator and chromatin modifier in erythroid cells. EKLF-deficient (Eklf -/-) mice die at day 14.5 of gestation from severe anemia. In this study, we demonstrate that early progenitor cells fail to undergo terminal erythroid differention in Eklf -/- embryos. To discover potential EKLF target genes responsible for the failure of erythropoiesis, transcriptional profiling was performed with RNA from wild type and Eklf -/- early erythroid progenitor cells. These analyses identified significant perturbation of a network of genes involved in cell cycle regulation, with the critical regulator of the cell cycle, E2f2, at a hub. E2f2 mRNA and protein levels were markedly decreased in Eklf -/- early erythroid progenitor cells, which showed a delay in the G1-to-S-phase transition. Chromatin immunoprecipitation analysis demonstrated EKLF occupancy at the proximal E2f2 promoter in vivo. Consistent with the role of EKLF as a chromatin modifier, EKLF binding-sites in the E2f2 promoter were located in a region of EKLF-dependent DNase I sensitivity in early erythroid progenitor cells. We propose a model in which EKLF-dependent activation and modification of the E2f2 locus is required for cell cycle progression preceding terminal erythroid differentiation.

2012-03-20 | GSE36618 | GEO

Mechanisms of terminal erythroid differentiation defect in EKLF-deficient mice

2012-03-20 | E-GEOD-36618 | biostudies-arrayexpress

Systematical identification of GATA-1, EKLF, and NF-E2 regulated miRNAs by ChIP-on chip and microRNA microarray in K562 cells into erythroid differentiation

Project description:Systematical identification of GATA-1, EKLF, and NF-E2 regulated miRNAs by ChIP-on chip and microRNA microarray in K562 cells into erythroid differentiation

| PRJNA144211 | ENA

Expression data from K562 hemin differentiation

Project description:Expression data from K562 hemin differentiation

| PRJNA972618 | ENA

EKLF/Klf1 regulates erythroid transcription by its pioneering activity and selective control of RNA Pol II pause-release

Project description:EKLF/Klf1 is a Zinc-finger transcription activator essential for erythroid lineage commitment and terminal differentiation. Using ChIP-Seq, we investigate EKLF DNA binding and transcription activation mechanisms during mouse embryonic erythropoiesis. Our study focuses on global EKLF binding dynamics during embryonic erythropoiesis in primary WT and Nan/+ mouse fetal liver, and its correlation with chromatin accessibility, CBP occupancy, histone acetylation, and finally its effect on RNA Polymerase II pausing and elongation. Our goal is to elucidate the mechanisms of transcription activation by EKLF/Klf1 during embryonic erythropoiesis in vivo and in the context of RNA pol II pause-release control. Additionally, we aim to understand the unusually severe effects of conservative E to D change in Nan-EKLF and the molecular mechanisms leading to dominant anemia through global gene dysregulation.

2023-01-18 | GSE210779 | GEO

GATA-1-regulated erythroid microRNAs

Project description:We employed a gene complementation strategy combined with microarray screening to identify miRNAs involved in the formation of erythroid (red blood) cells. To search for GATA-1-regulated erythroid miRNAs, we used the Gata-1– erythroblast line G1E. These cells proliferate in culture as immature erythroid precursors and undergo terminal maturation when GATA-1 activity is restored. G1E-ER4 is a sub-line stably expressing an estrogen-activated form of GATA-1 (GATA-1 fused to the ligand binding domain of the estrogen receptor). Treatment of G1E-ER4 cells with estradiol induces a GATA-1-regulated program of gene expression with concomitant cellular maturation. We used a microarray to evaluate the expression of 292 different miRNAs in G1E-ER4 cells at 0 versus 24 hours after GATA-1 activation. Affymetrix gene expression profiling has previously been deposited (GEO accession no. GSE628). Keywords: microRNA analysis of a cell-line model of erythroid maturation

2008-02-05 | GSE10134 | 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