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Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [ATAC-seq]

ABSTRACT: Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [ATAC-seq]

PROVIDER: PRJNA825470 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18711614_1.fastq.gz	Fastqsanger.gz
	SRR18711614_2.fastq.gz	Fastqsanger.gz
	SRR18711615_1.fastq.gz	Fastqsanger.gz
	SRR18711615_2.fastq.gz	Fastqsanger.gz
	SRR18711616_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner

Project description:Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner

| PRJNA825465 | ENA

Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [RNA-seq]

Project description:Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [RNA-seq]

| PRJNA825471 | ENA

Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [ChIP-seq]

Project description:Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [ChIP-seq]

| PRJNA825472 | ENA

Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [RNA-seq]

Project description:Chromatin modifications are thought to provide additional context dependence for sequence-based gene activation. Binding sites of the transcription factor (TF) and important tumor suppressor p53 are unusually diverse with regards to their chromatin accessibility and histone modifications, suggesting different modes of binding. Here, we show that the ability of p53 to open chromatin and activate its target genes upon DNA damage is locally restricted by its cofactor Trim24. The histone-binding domains of Trim24 limit the role of p53 at closed chromatin but not at accessible chromatin where Trim24 is blocked by histone 3 methylation at lysine 4. In turn p53 regulates gene expression as a function of the naïve chromatin state prior to activation. These findings establish a set of p53 response genes in closed chromatin that are Trim24-regulated and illustrate how histone modification sensing cofactors bridge local chromatin state and TF potency.

2023-04-30 | GSE200581 | GEO

Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [ChIP-seq]

2023-04-30 | GSE200580 | GEO

Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner [ATAC-seq]

2023-04-30 | GSE200582 | GEO

Readout of histone methylation by Trim24 locally restricts chromatin opening by p53

Project description:The genomic binding sites of the transcription factor (TF) and tumour suppressor p53 are unusually diverse in regards to their chromatin features, including histone modifications, opening the possibility that chromatin provides context-dependence for p53 regulation. Here, we show that the ability of p53 to open chromatin and activate its target genes is indeed locally restricted by its cofactor Trim24. Trim24 binds to both p53 and unmethylated lysine 4 of histone H3, thereby preferentially locating to those p53 sites that reside in closed chromatin, while it is deterred from accessible chromatin by lysine 4 methylation. The presence of Trim24 increases cell viability upon stress and enables p53 to impact gene expression as a function of the local chromatin state. These findings link histone methylation to p53 function and illustrate how specificity in chromatin can be achieved, not by TF-intrinsic sensitivity to histone modifications, but by employing chromatin-sensitive cofactors which locally modulate TF function.

2023-05-05 | PXD039553 | Pride

Chromatin opening by p53 is confined by Trim24 in a histone methylation-dependent manner

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

2023-04-29 | GSE200586 | GEO

Trim24 knock down in the 2i-state of the mouse ES cells

Project description:Differentially expressed genes were determined by single-end sequencing (stranded protocol) following Trim24 and/or p53 knock down in the mouse ES cells grown in 2i media. Triplicates were generated for treatment and control samples but for p53 knock down (duplicate).

2017-11-08 | E-MTAB-4893 | biostudies-arrayexpress

TRIM28 protects TRIM24 from SPOP-mediated degradation and promotes prostate cancer progression [microarray]

Project description:In this study, proteomic profiling of TRIM24 interactome in conjunction with shRNA screening of TRIM24 top-interactors nominated that TRIM28 is indispensable for TRIM24 protein stability. We showed that TRIM28 stabilizes TRIM24 against SPOP-mediated ubiquitination and degradation. TRIM28 promotes TRIM24 and AR transcription activity, androgen-dependent and -independent PCa growth. In addition, we demonstrated that TRIM28 level in high in advanced PCa, which drives TRIM24/AR transcription activity in a similar manner to SPOP mutation, which implies that TRIM28 potentially dictates the therapeutic outcome of TRIM24-targeted therapy.

2018-10-05 | GSE108145 | GEO

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