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The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [MeDIP-Seq]

ABSTRACT: The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [MeDIP-Seq]

PROVIDER: PRJNA888375 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21845249.fastq.gz	Fastqsanger.gz
	SRR21845250.fastq.gz	Fastqsanger.gz
	SRR21845251.fastq.gz	Fastqsanger.gz
	SRR21845252.fastq.gz	Fastqsanger.gz

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Similar Datasets

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [MeDIP-Seq]

Project description:The objectives of this study are to understand the regulatory roles of MAZ in biological processes using the NGS-deriveed ChIP-seq, DNA-MEDIP-seq and RNA-seq data in HAP1 control cells and MAZ knockout cells. Our comparative analysis of these data generated from the HAP1 control and MAZ KO cells shows that MAZ is required for recruiting STAT1 to its target sites by reshaping epigenetic landscape in the human genome, thereby mediating antiviral response cells. MEDIP-seq was performed using the MagMeDIP-seq Package from Diagenode in HAP1 control and HAP1 MAZ knockout cells following manufacturer's instructions.

2024-04-04 | GSE215082 | GEO

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [ChIP-Seq]

Project description:The objectives of this study are to understand the regulatory roles of MAZ in biological processes using the NGS-deriveed ChIP-seq, DNA-MEDIP-seq and RNA-seq data in HAP1 control cells and MAZ knockout cells. Our comparative analysis of these data generated from the HAP1 control and MAZ KO cells shows that MAZ is required for recruiting STAT1 to its target sites by reshaping epigenetic landscape in the human genome, thereby mediating antiviral response cells. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for STAT1 and H3K4me3, H3K27Ac in HAP1 cells.

2024-03-25 | GSE215081 | GEO

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [RNA-Seq]

2024-04-04 | GSE215080 | GEO

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome

Project description:The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome

| PRJNA888372 | ENA

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [ChIP-Seq]

Project description:The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [ChIP-Seq]

| PRJNA888373 | ENA

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [RNA-Seq]

Project description:The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome [RNA-Seq]

| PRJNA888374 | ENA

The Myc-Associated Zinc Finger Protein (MAZ) controls STAT1-mediated antiviral response by reshaping epigenome

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

2024-03-25 | GSE215083 | GEO

The Myc-Associated Zinc Finger Protein (MAZ) Works Both Independently and Together with CTCF to Control Cohesin Positioning and Genome Organization

Project description:Purpose: The objectives of this study are to evaluate the roles of MAZ in cellular processes using the NGS-deriveed ChIP-seq, RNA-seq and Hi-C profiles in K562 wild type and siRNA MAZ knockdown cells Methods: ChIP-Seq and Hi-C profiles of K562 wild-type (WT) and siRNA MAZ knockdown cells were generated by deep sequencing in duplicate or triplicate using Illumina GAIIx. The ChIP-seq sequence reads were analyzed with Burrows–Wheeler Aligner (BWA) followed by MACS software; The Hi-C sequence reads were analyzed with Juicer and HiC-Pro software. Results: Comparative analysis of the ChIP-seq, RNA-seq and Hi-C data between K562 wild type and siRNA MAZ knockdown cells indicates that 1.MAZ colocalizes with CTCF in the genome, and helps stabilize CTCF binding; 2. MAZ is able to arrest the cohesin complex independently of CTCF and contributes additively to cohesin localization when it is associated with CTCF; 3. MAZ, similarly to CTCF, acts as an insulator protein to block interaction between promoter and enhancer ; 4. MAZ can pause the elongating form of RNA Pol II; and 5. MAZ helps control local chromatin organization and some aspects of TAD structure. Conclusions: Our study represents the first detailed analysis of retinal transcriptomes, with biologic replicates, generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

2021-01-01 | GSE143937 | GEO

Members of an array of zinc finger proteins specify distinct Hox chromatin boundaries [ChIP-Seq2]

Project description:In this experiment, we sought to identify how the distribution of CTCF, MAZ, and RAD21 change in CTCF-degron (no auxin), CTCF-degron (auxin), CTCF-degron MAZ KO (no auxin), and CTCF-degron MAZ KO (auxin) backgrounds in mouse embryonic stem cells (ESCs).

2024-08-21 | GSE230481 | GEO

Global transcriptions upon MAZ knockdown HUDEP-2 cells

Project description:Hemoglobinopathies, such as sickle cell disease and β-thalassemia, are common genetic disorders remaining significant global health challenges due to their associated morbidity and mortality. Increasing fetal hemoglobin (HbF) levels has emerged as a promising therapeutic strategy for these disorders. In this study, we report MAZ as a repressor of γ-globin expression in human erythroid cells. Depletion of MAZ in HUDEP-2 and patient-derived β-thalassemia cells leads to significant inductions both of γ-globin mRNA and protein levels, resulting in increased HbF percentages and HbF+ erythroid cells. We demonstrate that MAZ occupies at the MYB promoter. MAZ depletion reduced MYB and BCL11A levels. Restoration of MYB re-silenced the γ-globin levels in MAZ depleted cells. Our findings uncover the MAZ-MYB axis in γ-globin regulation, highlighting MAZ as a potential target to enhance HbF levels in patients with hemoglobin disorders.

2025-11-01 | GSE281501 | GEO

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