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Homo sapiens

ABSTRACT: ZMYND8 co-localizes with NuRD on target genes and regulates recruitment of GATAD2A/NuRD to sites of DNA damage [RNA-seq]

OTHER RELATED OMICS DATASETS IN: PXD003856GSE79836

PROVIDER: PRJNA317160 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3321927_1.fastq.gz	Fastqsanger.gz
	SRR3321927_2.fastq.gz	Fastqsanger.gz
	SRR3321928_1.fastq.gz	Fastqsanger.gz
	SRR3321928_2.fastq.gz	Fastqsanger.gz
	SRR3321929_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

¬¬ZMYND8 co-localizes with NuRD on target genes and regulates poly-ADP-ribose dependent recruitment of GATAD2A/NuRD to sites of DNA damage

Project description:The NuRD complex is generally thought to repress transcription at both hyper- and hypomethylated regions in the genome. In addition, the complex is involved in the DNA damage response. Here, we show that ZMYND8 bridges NuRD to a number of putative DNA-binding zinc finger proteins. The ZMYND8 MYND domain directly interacts with PPPLΦ motifs in the NuRD subunit GATAD2A. Furthermore, GATAD2A and GATAD2B exclusively form homodimers and they thus define mutually exclusive NuRD subcomplexes. ZMYND8 and MBD3 share a large number of genome-wide binding sites, mostly active promoters and enhancers. Depletion of ZMYND8 does not affect NuRD occupancy genome-wide and expression of NuRD/ZMYND8 target genes in steady-state asynchronous cells. However, ZMYND8 facilitates immediate recruitment of GATAD2A/NuRD to induced sites of DNA damage in a PAR-dependent manner. These results thus show that a specific substoichiometric interaction with a NuRD subunit paralogue provides unique functionality to a distinct NuRD subcomplex.

2016-10-10 | PXD003856 | Pride

ZMYND8 co-localizes with NuRD on target genes and regulates recruitment of GATAD2A/NuRD to sites of DNA damage [RNA-seq]

Project description:The NuRD complex is generally thought to repress transcription at both hyper- and hypomethylated regions in the genome. In addition, the complex is involved in the DNA damage response. Here, we show that ZMYND8 bridges NuRD to a number of putative DNA-binding zinc finger proteins. The ZMYND8 MYND domain directly interacts with PPPL? motifs in the NuRD subunit GATAD2A. Furthermore, GATAD2A and GATAD2B exclusively form homodimers and they thus define mutually exclusive NuRD subcomplexes. ZMYND8 and MBD3 share a large number of genome-wide binding sites, mostly active promoters and enhancers. Depletion of ZMYND8 does not affect NuRD occupancy genome-wide and expression of NuRD/ZMYND8 target genes in steady-state asynchronous cells. However, ZMYND8 facilitates immediate recruitment of GATAD2A/NuRD to induced sites of DNA damage. These results thus show that a specific substoichiometric interaction with a NuRD subunit paralogue provides unique functionality to a distinct NuRD subcomplex.

2016-10-08 | GSE79835 | GEO

ZMYND8 co-localizes with NuRD on target genes and regulates recruitment of GATAD2A/NuRD to sites of DNA damage [ChIP-seq]

Project description:The NuRD complex is generally thought to repress transcription at both hyper- and hypomethylated regions in the genome. In addition, the complex is involved in the DNA damage response. Here, we show that ZMYND8 bridges NuRD to a number of putative DNA-binding zinc finger proteins. The ZMYND8 MYND domain directly interacts with PPPL? motifs in the NuRD subunit GATAD2A. Furthermore, GATAD2A and GATAD2B exclusively form homodimers and they thus define mutually exclusive NuRD subcomplexes. ZMYND8 and MBD3 share a large number of genome-wide binding sites, mostly active promoters and enhancers. Depletion of ZMYND8 does not affect NuRD occupancy genome-wide and expression of NuRD/ZMYND8 target genes in steady-state asynchronous cells. However, ZMYND8 facilitates immediate recruitment of GATAD2A/NuRD to induced sites of DNA damage. These results thus show that a specific substoichiometric interaction with a NuRD subunit paralogue provides unique functionality to a distinct NuRD subcomplex.

2016-10-08 | GSE79834 | GEO

ZMYND8 co-localizes with NuRD on target genes and regulates recruitment of GATAD2A/NuRD to sites of DNA damage

Project description:ZMYND8 co-localizes with NuRD on target genes and regulates recruitment of GATAD2A/NuRD to sites of DNA damage

| PRJNA317159 | ENA

Homo sapiens

Project description:ZMYND8 co-localizes with NuRD on target genes and regulates recruitment of GATAD2A/NuRD to sites of DNA damage [ChIP-seq]

| PRJNA317161 | ENA

CARM1 hypermethylates the NuRD chromatin remodeling complex to promote cell cycle gene expression and breast cancer development [ChIP-Seq]

Project description:The nucleosome remodeling and deacetylase (NuRD) complex is a large multi-subunit complex that couples ATP-dependent chromatin-remodeling and histone deacetylase activities. Emerging evidence suggested that NuRD are associated with active genes and modulates their expression, but the underlying molecular mechanisms remain ill-defined. Here, we reported that the transcriptional coactivator CARM1 is associated with NuRD through its direct interaction with the GATAD2A/2B subunit, expanding the activities of NuRD to include protein arginine methylation. CARM1 and NuRD co-bind and -activate a large cohort of genes with implications in cell cycle control to facilitate the G1 to S phase transition. This gene activation process requires CARM1 to hypermethylate a key subunit in the NuRD complex, GATAD2A/2B, which is critical for the recruitment of the NuRD complex. The biological significance of this gene activation mechanism is underscored by the high expression of CARM1 and NuRD in breast cancers, and the fact that knockdown CARM1 and NuRD inhibits breast cancer cell growth in vitro and tumorigenesis in vivo. These findings reveal a gene activation program that requires the dual specificity established by CARM1 on chromatin and a key chromatin remodeler.

2024-07-17 | GSE261973 | GEO

CARM1 interacts and hypermethylates the NuRD chromatin remodeling complex to promote gene transcriptional activation and cell cycle progression

Project description:Protein arginine methyltransferase CARM1 has been shown to methylate a large number of non-histone proteins, and play important roles in gene transcriptional activation, cell cycle progress, and tumorigenesis. However, the critical substrates through which CARM1 exerts its functions remain to be fully characterized. Here, we reported that CARM1 directly interacts with the GATAD2A/2B subunit in the nucleosome remodeling and deacetylase (NuRD) complex, expanding the activities of NuRD to include protein arginine methylation. CARM1 and NuRD bind and activate a large cohort of genes with implications in cell cycle control to facilitate the G1 to S phase transition. This gene activation process requires CARM1 to hypermethylate GATAD2A/2B at a cluster of arginines, which is critical for the recruitment of the NuRD complex. The clinical significance of this gene activation mechanism is underscored by the high expression of CARM1 and NuRD in breast cancers, and the fact that knockdown CARM1 and NuRD inhibits breast cancer cell growth in vitro and tumorigenesis in vivo. These findings reveal a gene activation program that requires the dual specificity established by CARM1 on chromatin and a key chromatin remodeler.

2024-07-17 | GSE209909 | GEO

CARM1 interacts and hypermethylates the NuRD chromatin remodeling complex to promote gene transcriptional activation and cell cycle progression

2024-07-17 | GSE208775 | GEO

CARM1 interacts and hypermethylates the NuRD chromatin remodeling complex to promote gene transcriptional activation and cell cycle progression

2024-07-17 | GSE209910 | GEO

Effects of MBD3 depletion on nucleosome occupancy in MCF-7 cells

Project description:We and others have identified that MBD3/NuRD localizes at active promoters and enhancers, suggesting an active role of NuRD at open chromatin region. Because NuRD includes nucleosome remodelers, CHD3 and CHD4, we hypothesized that NuRD regulates nucleosome organization at open chromatin region. To test this idea, we performed micrococcal nuclease digestion followed by massively parallel sequencing (MNase-seq) in MBD3 knockdowned MCF-7 cells. We observed the decrease of nucleosome occupancy at promoters and enhancers in MBD3 knockdowned cells. Our results suggest a regulatory role of MBD3/NuRD at open chromatin region. Mapped nucleosome positioning in control (shLuc) and MBD3 knockdowned MCF-7 cells, in duplicate.

2013-10-31 | E-GEOD-51097 | biostudies-arrayexpress

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