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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile

ABSTRACT: Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile

PROVIDER: PRJNA481463 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7529700_1.fastq.gz	Fastqsanger.gz
	SRR7529700_2.fastq.gz	Fastqsanger.gz
	SRR7529710_1.fastq.gz	Fastqsanger.gz
	SRR7529710_2.fastq.gz	Fastqsanger.gz
	SRR7529720_1.fastq.gz	Fastqsanger.gz

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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [Hi-C]

Project description:Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [Hi-C]

| PRJNA481464 | ENA

Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [RNA-seq]

Project description:Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [RNA-seq]

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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [ChIP-seq]

Project description:Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [ChIP-seq]

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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile

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

2018-07-18 | GSE117210 | GEO

Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [ChIP-seq]

Project description:The emerging 4D genome project aiming to map the dynamics of genomes in spatial and temporal dimension has put forward to developing the mechanisms of how the nucleus is organized and functions. Therefore, processes like cellular senescence characterized by complex events give rise to understanding the regulation network from 1D genome to dynamically organized 3D structure. Unfortunately, how spatial genome reorganization triggers cellular senescence and how it influences senescence-related downstream transcriptional profile remains unaddressed well. Here, we uncover that re re-orchestration of 3D chromatin architecture has occurred in cellular senescence, accompanied with remodeling of enhancer repertories, which in turn facilicate the recruitment of the chromatin reader C/EBPα to newly activated senescence enhancers (SAEs), leading to the expression of SAEs flanking SASP genes kinetics.

2018-07-18 | GSE117209 | GEO

Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [RNA-seq]

2018-07-18 | GSE117208 | GEO

Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [Hi-C]

2018-07-18 | GSE117207 | GEO

ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype

Project description:ADAM19 Mediates Cellular Senescence and the Senescence-Associated Secretory Phenotype

2020-04-03 | MSV000085224 | MassIVE

Establishment of Enhancer Repertoires that Orchestrate the Myeloid and Lymphoid Cell Fates (ChIP-Seq dataset)

Project description:Recent studies have documented genome-wide binding patterns of transcriptional regulators and their associated epigenetic marks in hematopoietic cell lineages. In order to determine how epigenetic marks are established and maintained during developmental progression, we have generated long-term cultures of hematopoietic progenitors by enforcing the expression of the E-protein antagonist Id2. Hematopoietic progenitors that express Id2 are multipotent and readily differentiate upon withdrawal of Id2 expression into committed B lineage cells, thus indicating a causative role for E2A in promoting the B cell fate. Genome-wide analyses revealed that a substantial fraction of lymphoid and myeloid enhancers are pre-marked by H3K4me1 in multipotent progenitors. However, H3K4me1 levels at a subset of enhancers are elevated during developmental progression, resulting in evolving enhancer repertoires that we propose orchestrate the myeloid and B cell fates.

2011-09-01 | GSE30858 | GEO

MLL1 is essential for the senescence-associated secretory phenotype

Project description:This SuperSeries is composed of the SubSeries listed below. Oncogene-induced senescence (OIS) and therapy-induced senescence (TIS), while tumor-suppressive, also promote procarcinogenic effects by activating the DNA damage response (DDR), which in turn induces inflammation. This inflammatory response prominently includes an array of cytokines known as the senescence-associated secretory phenotype (SASP). Previous observations link the transcription-associated methyltransferase and oncoprotein MLL1 to the DDR, leading us to investigate the role of MLL1 in SASP expression. Our findings reveal direct MLL1 epigenetic control over proproliferative cell cycle genes: MLL1 inhibition represses expression of proproliferative cell cycle regulators required for DNA replication and DDR activation, thus disabling SASP expression. Strikingly, however, these effects of MLL1 inhibition on SASP gene expression do not impair OIS and, furthermore, abolish the ability of the SASP to enhance cancer cell proliferation. More broadly, MLL1 inhibition also reduces âSASP-likeâ inflammatory gene expression from cancer cells in vitro and in vivo independently of senescence. Taken together, these data demonstrate that MLL1 inhibition may be a powerful and effective strategy for inducing cancerous growth arrest through the direct epigenetic regulation of proliferation-promoting genes and the avoidance of deleterious OIS- or TIS-related tumor secretomes, which can promote both drug resistance and tumor progression. Previously published samples GSM1135046, GSM1135044, GSM1135047, and GSM1135045 were also studied in this investigation and appear in GSE36641. This did not involve re-sequencing or re-alignment, nor any other deviation from the data protocols in that series. Refer to individual Series

2016-02-22 | E-GEOD-78142 | biostudies-arrayexpress

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