Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction [ChIP-Seq]

ABSTRACT: Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction [ChIP-Seq]

PROVIDER: PRJNA543515 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9083620_1.fastq.gz	Fastqsanger.gz
	SRR9083620_2.fastq.gz	Fastqsanger.gz
	SRR9083611_1.fastq.gz	Fastqsanger.gz
	SRR9083611_2.fastq.gz	Fastqsanger.gz
	SRR9083621_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 30

Similar Datasets

Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction [RNA-Seq]

Project description:Metabolic activity possess a crucial role during cell fate determination. Here, we show that maternal transcriptional factor Glis1 could not only promote normal MEF reprogramming but also enable aging MEF reprogramming. By association ChIP-seq and RNA-seq, we found that Glis1 could bind and activate glycolytic genes, and bind and suppress somatic state genes simultaneously during reprogramming. While knockdown phosphoglyceric kinase (Pgk1) impeded reprogramming efficiency which indicates that Glis1-glycolytic process axes is required for Glis1 function. Metabolic analysis indicated that the level of acetyl-CoA has a significant fluctuation upon Glis1 induction or silence. Acetate, a precursor of acetyl-CoA rescued the effects on reprogramming in a time-dependent manner when knockdown endogenous Glis1. The fluctuation of Ac-CoA changed the level of H3K27Ac, especially in pluripotent genes and “second wave” genes promoter, and activated the expression of endogenous pluripotency genes in advance subsequently. In conclusion, we demonstrate the exactly novel mechanism of Glis1 in pluripotency acquisition.

2020-06-24 | GSE131491 | GEO

Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction [ChIP-Seq]

2020-06-24 | GSE131426 | GEO

Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction

Project description:Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction

| PRJNA544443 | ENA

Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction [RNA-Seq]

Project description:Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction [RNA-Seq]

| PRJNA543849 | ENA

Glis1 Activate Glycolytic Process and Increase H3K27Ac Level on Pluripotent and Second Wave Genes Promoter Facilitating Pluripotency Induction

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-23 | GSE131692 | GEO

BV6 induces an early wave of gene expression via NF-κB and AP-1 and a second wave via TNFα/TNFR1 signaling

Project description:Smac mimetics are considered as promising cancer therapeutics, but little is yet known about how they alter gene expression. In this study we used an unbiased genome-wide expression array to investigate Smac mimetic BV6-induced gene regulation in breast cancer cell lines. Kinetic analysis revealed that BV6 alters gene expression in two waves. The first wave primarily involves NF-κB- and AP-1 families of transcription factors, while the second wave largely depends on tumor necrosis factor receptor 1 (TNFR1) signaling. Interestingly, disrupting auto-/paracrine tumor necrosis factor-α (TNFα)/ (TNFR1) signaling by knockdown of TNFR1 strongly attenuates the BV6-induced second wave of gene expression and upregulation of many pathways including NF-κB signaling, apoptosis and immune signalling, but not MAPK signaling pathways. Consistently, BV6 stimulates phosphorylation of cJun, a marker of MAPK cascade activation, irrespective of the presence or absence of the TNFα blocking antibody Enbrel. We show here in a comprehensive overview that BV6-induced gene expression in breast cancer cells takes place in a time- as well as TNFR1-dependent manner.

2018-02-05 | GSE107912 | GEO

Promotion of Direct Reprogramming by Glis1

Project description:Induced pluripotent stem cells (iPSC) are generated from somatic cells by the transgene expression of three transcription factors Oct3/4, Sox2, and Klf4 (OSK), albeit at a low efficiency. The protooncogene c-Myc enhances the efficiency of iPSC generation by OSK, but it also increases the tumorigenicity of the resulting iPSC. In the current study, we found the Gli-like transcription factor Glis1, when expressed together with OSK, to markedly enhance the generation of iPSC from both mouse and human fibroblasts. Mouse iPSC generated by OSK and Glis1 can form germline-competent chimeras. Glis1 is enriched in unfertilized oocytes and one cell-stage embryos. DNA microarray analyses revealed that Glis1 promotes multiple pro-reprogramming pathways, including Myc, Nanog, Lin28, Wnt, mesenchymal-epithelial transition (MET), and Esrrb. These results therefore demonstrated that oocyte transcription factor Glis1 effectively promote direct reprogramming during iPSC generation. p53-null mouse embryonic fibroblasts were transduced with OSK and OSK+Glis1 and were used for microarray analyses.

2011-06-10 | E-GEOD-26429 | biostudies-arrayexpress

Effect of Glis1 on human iPS cell generation

Project description:Induced pluripotent stem cells (iPSC) are generated from somatic cells by the transgene expression of three transcription factors Oct3/4, Sox2, and Klf4 (OSK), albeit at a low efficiency. The protooncogene c-Myc enhances the efficiency of iPSC generation by OSK, but it also increases the tumorigenicity of the resulting iPSC. In the current study, we found the Gli-like transcription factor Glis1, when expressed together with OSK, to markedly enhance the generation of iPSC from both mouse and human fibroblasts. Mouse iPSC generated by OSK and Glis1 can form germline-competent chimeras. Glis1 is enriched in unfertilized oocytes and one cell-stage embryos. DNA microarray analyses revealed that Glis1 promotes multiple pro-reprogramming pathways, including Myc, Nanog, Lin28, Wnt, mesenchymal-epithelial transition (MET), and Esrrb. These results therefore demonstrated that oocyte transcription factor Glis1 effectively promote direct reprogramming during iPSC generation. Adult human fibroblasts were transduced with OSKM and OSK+Glis1 and were used for microarray analyses.

2011-06-10 | E-GEOD-26428 | biostudies-arrayexpress

Promotion of Direct Reprogramming by Glis1

2011-06-10 | GSE26429 | GEO

Effect of Glis1, Dmrtb1, and Pitx2 on mouse iPS cell generation

Project description:Induced pluripotent stem cells (iPSC) are generated from somatic cells by the transgene expression of three transcription factors Oct3/4, Sox2, and Klf4 (OSK), albeit at a low efficiency. The protooncogene c-Myc enhances the efficiency of iPSC generation by OSK, but it also increases the tumorigenicity of the resulting iPSC. In the current study, we found the Gli-like transcription factor Glis1, when expressed together with OSK, to markedly enhance the generation of iPSC from both mouse and human fibroblasts. Mouse iPSC generated by OSK and Glis1 can form germline-competent chimeras. Glis1 is enriched in unfertilized oocytes and one cell-stage embryos. DNA microarray analyses revealed that Glis1 promotes multiple pro-reprogramming pathways, including Myc, Nanog, Lin28, Wnt, mesenchymal-epithelial transition (MET), and Esrrb. These results therefore demonstrated that oocyte transcription factor Glis1 effectively promote direct reprogramming during iPSC generation. Mouse embryonic fibroblasts were transduced with OSKM, OSM+Glis1, OSM+Dmrtb1, and OSM+Pitx2 and were used for microarray analyses.

2011-06-10 | E-GEOD-26430 | biostudies-arrayexpress

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