Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KLF3 promotes the 8-cell-like transcriptional state in pluripotent stem cells

ABSTRACT: KLF3 promotes the 8-cell-like transcriptional state in pluripotent stem cells

PROVIDER: PRJNA662786 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12622127_1.fastq.gz	Fastqsanger.gz
	SRR12622127_2.fastq.gz	Fastqsanger.gz
	SRR12622128_1.fastq.gz	Fastqsanger.gz
	SRR12622128_2.fastq.gz	Fastqsanger.gz
	SRR12622129_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

KLF3 promotes the 8-cell-like transcriptional state in pluripotent stem cells

Project description:This study identifies previously unrecognized heterogeneity due to KLF3 protein expression in mESCs.

2020-11-18 | GSE157790 | GEO

KLF3 promotes the 8-cell-like transcriptional state in pluripotent stem cells.

Project description:ObjectivesMouse embryonic stem cell (mESC) culture contains various heterogeneous populations, which serve as excellent models to study gene regulation in early embryo development. The heterogeneity is typically defined by transcriptional activities, for example, the expression of Nanog or Rex1 mRNA. Our objectives were to identify mESC heterogeneity that are caused by mechanisms other than transcriptional control.Materials and methodsKlf3 mRNA and protein were analysed by RT-qPCR, Western blotting or immunofluorescence in mESCs, C2C12 cells, early mouse embryos and various mouse tissues. An ESC reporter line expressing KLF3-GFP fusion protein was made to study heterogeneity of KLF3 protein expression in ESCs. GFP-positive mESCs were sorted for further analysis including RT-qPCR and RNA-seq.ResultsIn the majority of mESCs, KLF3 protein is actively degraded due to its proline-rich sequence and highly disordered structure. Interestingly, KLF3 protein is stabilized in a small subset of mESCs. Transcriptome analysis indicates that KLF3-positive mESCs upregulate genes that are initially activated in 8-cell embryos. Consistently, KLF3 protein but not mRNA is dramatically increased in 8-cell embryos. Forced expression of KLF3 protein in mESCs promotes the expression of 8-cell-embryo activated genes.ConclusionsOur study identifies previously unrecognized heterogeneity due to KLF3 protein expression in mESCs.

| S-EPMC7653263 | biostudies-literature

Microarray analysis of wildtype, Klf3 H275R homozygous and heterozygous, Klf3 CH gene trap homozygous and heterozygous E12.5 embryos

2013-01-31 | GSE43908 | GEO

Microarray analysis of wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt TER119+ E13.5 fetal liver cells

2013-01-17 | GSE43524 | GEO

Microarray analysis of wildtype, Klf3 H275R homozygous and heterozygous, Klf3 CH gene trap homozygous and heterozygous E12.5 embryos

Project description:The aim of this experiment was to investigate the dysregulation of gene expression in whole E12.5 embryos containing a gene trap (CH) or point mutation (H275R) within the Klf3 gene Affymetrix microarrays were performed on RNA from wildtype, Klf3 H275R/H275R, Klf3 H275R/+, Klf3 CH homozygous and Klf3 CH heterozygous E12.5 embryos Four wildtype replicates, three Klf3 H275R/H275R replicates, four Klf3 H275R/+ replicates, four Klf3 CH homozygous replicates and two Klf3 CH heterozygous replicates of whole E12.5 embryos, litter-matched where possible.

2013-01-31 | E-GEOD-43908 | biostudies-arrayexpress

Microarray analysis of wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt TER119+ E13.5 fetal liver cells

Project description:The aim of this experiment was to investigate the regulation of gene expression by KLF3 and KLF8 in fetal erythroid cells by analyzing single and double mutant mouse models. Affymetrix microarrays were performed on RNA from TER119+ fetal liver cells from E13.5 wildtype, Klf8gt/gt, Klf3-/- and Klf3-/- Klf8gt/gt mice. Four wildtype replicates, four Klf8gt/gt replicates, three Klf3-/- replicates and four Klf3-/- Klf8gt/gt replicates of E13.5 TER119+ fetal liver cell samples, litter-matched where possible.

2013-01-17 | E-GEOD-43524 | biostudies-arrayexpress

MPP8 is essential for sustaining self-renewal of ground-state pluripotent stem cells

Project description:Deciphering the mechanisms that control the pluripotent ground state is key for understanding embryonic development. Nonetheless, the epigenetic regulation of ground-state mouse embryonic stem cells (mESCs) is not fully understood. Here, we identify the epigenetic protein MPP8 as being essential for ground-state pluripotency. Its depletion leads to cell cycle arrest and spontaneous differentiation. MPP8 has been suggested to repress LINE1 elements by recruiting the human silencing hub (HUSH) complex to H3K9me3-rich regions. Unexpectedly, we find that LINE1 elements are efficiently repressed by MPP8 lacking the chromodomain, while the unannotated C-terminus is essential for its function. Moreover, we show that SETDB1 recruits MPP8 to its genomic target loci, whereas transcriptional repression of LINE1 elements is maintained without retaining H3K9me3 levels. Taken together our findings demonstrate that MPP8 protects the DNA-hypomethylated pluripotent ground state through its association with the HUSH core complex, however, independently of detectable chromatin binding and maintenance of H3K9me3.

2021-03-21 | PXD019345 | Pride

KLF3 mediates epidermal differentiation through the epigenomic writer CBP [ChIP-seq]

Project description:The differentiated layers of the epidermis protect the body from the outside environment. Impairments in the differentiation process can lead to skin diseases that can afflict ~20% of the population. Thus, it is of utmost importance to characterize and understand the factors that promote the differentiation process. Here we identify the transcription factor KLF3 as a novel regulator of epidermal differentiation. Knockdown of KLF3 results in reduced differentiation gene expression and increased cell cycle gene expression. Over 50% of KLF3’s genomic binding sites occur at regions containing H3K4me/H3K27ac with the vast majority at active enhancers. KLF3 bound to active enhancers proximal to differentiation genes that are dependent upon KLF3 for expression. Based on this association, we sought to investigate KLF3’s possible relationship with the enhancer associated proteins CBP and P300. Analysis of the transcriptome controlled by CBP and P300 showed that CBP and KLF3 control a similar gene expression program and are both essential for promoting differentiation. In addition, 35% of CBP’s genomic binding sites overlap with KLF3 and knockdown of KLF3 results in reduced CBP localization at enhancers proximal to differentiation gene clusters. Our results suggest that KLF3 regulates differentiation gene expression by promoting CBP localization at enhancers.

2020-07-22 | GSE140991 | GEO

KLF3 mediates epidermal differentiation through the epigenomic writer CBP [RNA-seq]

2020-07-22 | GSE140990 | GEO

Expression data of K562 cells with KLF3 deficiency and shRNA vector control

Project description:KLF3, a member of the Krüppel-like factor (KLF) family, is expressed in a wide range of cell types. It is involved in hematopoiesis of several blood cell lineages including erythrocyte and B lymphocyte. However, the research of regulatory roles on hematopoiesis of KLF3 in K562 cells has been still largely limited. To comprehensively assess the regulatory roles of KLF3 on hematopoiesis in K562 cells, a microarray analysis was performed in KLF3-deficient K562 cells. The differentially expressed genes were applied to IPA analysis to observe the perturbed hematopoiesis-associated functions, networks, and molecular pathways. This study will extensively assess the regulatory roles of KLF3 on hematopoiesis in K562 cells. We used microarrays to study the genome-wide expression profiles of KLF3-deficient K562 cells.

2017-01-25 | GSE54437 | 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