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AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency

ABSTRACT: AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency

PROVIDER: PRJNA495467 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14434013.fastq.gz	Fastqsanger.gz
	SRR14434014.fastq.gz	Fastqsanger.gz
	SRR14434015.fastq.gz	Fastqsanger.gz
	SRR14434016.fastq.gz	Fastqsanger.gz
	SRR14434020_1.fastq.gz	Fastqsanger.gz

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AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (ATAC-Seq)

Project description:AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (ATAC-Seq)

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AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (ChIP-Seq)

Project description:AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (ChIP-Seq)

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AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (RNA-Seq)

Project description:AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (RNA-Seq)

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AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (RNA-Seq)

Project description:Somatic cell transcription factors are critical to maintaining cellular identity and constitute a barrier to human somatic cell reprogramming, yet a comprehensive understanding of the mechanism of action is lacking. To gain insight, we examined epigenome remodeling at the onset of human nuclear reprogramming by profiling human fibroblasts after fusion with murine embryonic stem cells. By ATAC-seq and ChIP-seq we identified enrichment for the AP-1 transcription factor c Jun at regions of early transient accessibility at fibroblast-specific enhancers. Expression of a dominant negative AP-1 mutant (dnAP 1) reduced accessibility and expression of fibroblast genes, overcoming the barrier to reprogramming. Remarkably, efficient reprogramming of human fibroblasts to iPSC was achieved by transduction with vectors expressing SOX2, KLF4, and inducible dnAP 1 demonstrating that dnAP-1 can substitute for exogenous human OCT4. Mechanistically, we show that the AP-1 component c-Jun has two unexpected temporally distinct functions in human reprogramming: i) to potentiate fibroblast enhancer accessibility and fibroblast-specific gene expression and ii) to bind to and repress OCT4 as a complex with MBD3. Our findings highlight AP-1 as a previously unrecognized potent dual gatekeeper of the somatic cell state.

2021-05-21 | GSE121052 | GEO

AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (ATAC-Seq)

2021-05-21 | GSE120992 | GEO

AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency (ChIP-Seq)

2021-05-21 | GSE173937 | GEO

AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency.

Project description:Somatic cell transcription factors are critical to maintaining cellular identity and constitute a barrier to human somatic cell reprogramming; yet a comprehensive understanding of the mechanism of action is lacking. To gain insight, we examined epigenome remodeling at the onset of human nuclear reprogramming by profiling human fibroblasts after fusion with murine embryonic stem cells (ESCs). By assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) and chromatin immunoprecipitation sequencing we identified enrichment for the activator protein 1 (AP-1) transcription factor c-Jun at regions of early transient accessibility at fibroblast-specific enhancers. Expression of a dominant negative AP-1 mutant (dnAP-1) reduced accessibility and expression of fibroblast genes, overcoming the barrier to reprogramming. Remarkably, efficient reprogramming of human fibroblasts to induced pluripotent stem cells was achieved by transduction with vectors expressing SOX2, KLF4, and inducible dnAP-1, demonstrating that dnAP-1 can substitute for exogenous human OCT4. Mechanistically, we show that the AP-1 component c-Jun has two unexpected temporally distinct functions in human reprogramming: 1) to potentiate fibroblast enhancer accessibility and fibroblast-specific gene expression, and 2) to bind to and repress OCT4 as a complex with MBD3. Our findings highlight AP-1 as a previously unrecognized potent dual gatekeeper of the somatic cell state.

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AP-1 is a temporally regulated dual gatekeeper of reprogramming to pluripotency

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

2021-05-21 | GSE121053 | GEO

PRDM14 Ensures Naïve Pluripotency through Dual Regulation of Signaling and Epigenetic Pathways in Mouse Embryonic Stem Cells

Project description:Mouse embryonic stem cells (mESCs) fluctuate between a naïve inner cell mass (ICM)-like state and a primed epiblast-like state of pluripotency in serum, but are harnessed exclusively in a distinctive, naïve state of pluripotency that more faithfully captures the ICM state (the ground state) with inhibitors for mitogen-activated protein kinase (MAPK) and glycogen synthase kinase 3 pathways (2i). Understanding the mechanism ensuring the naïve states of pluripotency will be critical to realizing the full potential of ESCs. We show here that PRDM14, a PR domain-containing transcriptional regulator, ensures naïve pluripotency by a dual mechanism: Antagonizing fibroblast growth factor receptor (FGFR) signaling that is activated paradoxically by the core transcriptional circuitry for pluripotency and directs a primed state, and repressing de novo DNA methyltransferases that create a primed epiblast-like epigenome. PRDM14 exerts these functions by recruiting polycomb repressive complex 2 (PRC2) specifically to key targets and repressing their expression. ChIP-seq of PRDM14 and that of H3K27me3 and SUZ12 on Prdm14 wildtype and knockout ES cells

2013-01-18 | E-GEOD-42616 | biostudies-arrayexpress

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Project description:This phase I trial is studying the best dose of 3-AP and the side effects of giving 3-AP together with gemcitabine in treating patients with advanced solid tumors or lymphoma. Drugs used in chemotherapy, such as 3-AP and gemcitabine (GEM), work in different ways to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. 3-AP may help gemcitabine kill more cancer cells by making the cells more sensitive to the drug. 3-AP may also stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

| 2026481 | ecrin-mdr-crc

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