Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

ABSTRACT: Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

PROVIDER: PRJNA1127522 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Chromatin distribution alterations of histone modifacations and PRC2 complex caused by Rack7 deletion in primary astrocyte [ChIP-Seq]

Project description:Dysregulation of epigenetic mechanisms play crucial roles in brain development and disease. Emerging evidence suggests that RACK7, an epigenetic reader protein, may play a role in brain development, but in vivo exploration of RACK7 in neural development and the underlying mechanisms are still lacking. Here, we established a conditional knock-out Rack7 mouse model and show that Rack7-deficient mice exhibit overt developmental defects. Multicomplex immunofluorescence staining (mIF) of cell-type specific markers indicates that the developmental defects are associated with compromised astrocyte development. Mechanistically, we surprisingly found RACK7 interacts with PRC2 complex, which acts as the histone H3K27 methyltransferase. Our results suggest RACK7 binding with PRC2 complex helps to establish the proper genomic location of histone H3K27me3 modification. Deletion of Rack7 in astrocyte leads to a remarkable decrease of H3K27me3 chromatin enrichment. genome-wide?. Functionally, we found RACK7 works together with H3K27me3 to prevent overactivation of Wnt signaling pathway and other astrocyte differentiation genes. Collectively, our study provides new insights into the cellular and molecular mechanisms underlying brain development regulated by RACK7.

2025-05-30 | GSE270581 | GEO

Effects of deletion Rack7 on gene expression in primary astrocyte during mouse postnatal development [RNA-Seq]

2025-05-30 | GSE270582 | GEO

RACK7 ChIP-seq in pediatric glioblastomas cell lines.

Project description:We identified that RACK7 recognizes the histone H3.3G34R mutaion in vitro. In order to determine the interaction between RACK7 and H3.3G34R mutaion in cells, we used three pediatric glioblastoma (pGBM) cell lines. SJ-HGGx6c(R6) and SJ-HGGx42c(R42) have heterozygous G34R mutation, while SJ-HGGx39c(WT39) has wildtype H3F3A, which encodes H3.3, and we also corrected H3.3G34R in R6 and R42 cells to wildtype H3.3 by CRISPR/Cas9 mediated knock-in. Finally, we performed RACK7 ChIP-seq in these cell lines to explore the function of RACK7 and H3.3G34R mutation.

2020-08-10 | GSE138060 | GEO

Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (ChIP-Seq Ring1b)

Project description:to understand the genome wide alterations in PRC2-mediated K27me3 and PRC1 distribution caused by oncohistone K27M mutation or novel PRC2 inhibitor – EZHIP

2019-04-08 | GSE124741 | GEO

Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (ChIP-Seq H2K27me3)

Project description:to understand the genome wide alterations in PRC2-mediated K27me3 and PRC1 distribution caused by oncohistone K27M mutation or novel PRC2 inhibitor – EZHIP

2019-04-08 | GSE124740 | GEO

Ependymoma associated protein EZHIP inhibits PRC2 through a H3 K27M like mechanism (ChIP-Seq CBX2)

Project description:to understand the genome wide alterations in PRC2-mediated K27me3 and PRC1 distribution caused by oncohistone K27M mutation or novel PRC2 inhibitor – EZHIP

2019-04-08 | GSE124739 | GEO

Effects of deletion Rack7 on gene expression in primary astrocyte during mouse postnatal development [RNA-Seq]

Project description:Effects of deletion Rack7 on gene expression in primary astrocyte during mouse postnatal development [RNA-Seq]

| PRJNA1127524 | ENA

A Surveillance System of Active Enhancers by a RACK7-histone Demethylase Complex (ChIP-Seq I)

Project description:Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer âbrakeâ to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis. ChIP-seq data of RACK7, KDM5C and histone modifications in parental and RACK7-KO ZR-75-30 cells.

2016-04-07 | E-GEOD-71323 | biostudies-arrayexpress

A Surveillance System of Active Enhancers by a RACK7-histone Demethylase Complex (ChIP-Seq II)

2016-04-07 | E-GEOD-76637 | biostudies-arrayexpress

A Surveillance System of Active Enhancers by a RACK7-histone Demethylase Complex (RNA-Seq I)

2016-04-07 | E-GEOD-71325 | biostudies-arrayexpress