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Genome-wide map of MAZ transcription factor in primary human erythroid cells

ABSTRACT: Genome-wide map of MAZ transcription factor in primary human erythroid cells

PROVIDER: PRJNA579097 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10334727_1.fastq.gz	Fastqsanger.gz
	SRR10334727_2.fastq.gz	Fastqsanger.gz
	SRR10334728_1.fastq.gz	Fastqsanger.gz
	SRR10334728_2.fastq.gz	Fastqsanger.gz
	SRR10334729_1.fastq.gz	Fastqsanger.gz

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Genome-wide map of MAZ transcription factor in primary human erythroid cells

Project description:We report the distribution of binding sites of Myc-associated zinc finger (MAZ) transcription factor in primary human erythroid cells

2021-06-30 | GSE139281 | GEO

MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter

Project description:Most E2F-binding sites repress transcription through the recruitment of Retinoblasoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.

2017-10-04 | PXD006857 | Pride

CRISPR and biochemical screens Identify MAZ as a co-factor in CTCF-mediated insulation at Hox Clusters

Project description:In this experiment, we sought to identify how the distribution of MAZ change in WT, MAZ HoxA(Δ5|6), and MAZ HoxD(Δ4|8) cells during differentiation of mouse embryonic stem cells (ESCs) into cervical motor neurons (MNs)

2022-02-06 | GSE190991 | GEO

Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and gamma-globin expression in erythroid cells primary adult human erythroid progenitor cells

Project description:Recombinant erythroid Kruppel-like factor fused to GATA1 up-regulates delta- and gamma-globin expression in erythroid cells primary adult human erythroid progenitor cells

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KLF1/EKLF regulatory networks in primary erythroid cells

Project description:KLF1 (EKLF) regulates a diverse suite of genes to direct erythroid cell differentiation from bi-potent progenitors. To determine the local cis-regulatory contexts and transcription factor networks in which KLF1 operates, we performed KLF1 ChIP-seq in the mouse. We found at least 945 sites in the genome of E14.5 fetal liver erythroid cells which are occupied by endogenous KLF1. Many of these recovered sites reside in erythroid gene promoters such as β-globin, but the majority are distant to any known gene. Our data suggests KLF1 directly regulates most aspects of terminal erythroid differentiation including production of α and β-globin protein chains, heme biosynthesis, co-ordination of proliferation and anti-apoptotic pathways, and construction of the red cell membrane and cytoskeleton by functioning primarily as a transcriptional activator. Additionally, we suggest new mechanisms for KLF1 co-operation with other transcription factors, in particular the erythroid transcription factor GATA1, to maintain homeostasis in the erythroid compartment. Examination of KLF1 occupancy in primary erythroid cells. KLF1-ChIP and input samples were run on AB SOLiD Systems 2.0 and 3.0. The genomic alignment files (*sorted.txt) and peak file (*bed) contain the combined System 2.0 and 3.0 data.

2010-04-08 | E-GEOD-20478 | biostudies-arrayexpress

CRISPR and biochemical screens identify MAZ as a co-factor in CTCF-mediated insulation at Hox clusters [MAZ KO]

Project description:In this experiment, we sought to analyze how transcriptome of WT and MAZ knock-out (KO) cells change during differentiation of mouse embryonic stem cells (ESCs) into cervical motor neurons (MNs)

2022-02-06 | GSE157137 | GEO

CRISPR and biochemical screens identify MAZ as a co-factor in CTCF-mediated insulation at Hox clusters [MAZ KO]

Project description:CRISPR and biochemical screens identify MAZ as a co-factor in CTCF-mediated insulation at Hox clusters [MAZ KO]

| PRJNA660249 | ENA

Expression analysis of ZBP-89 deficient human primary erythroid progenitors

Project description:The molecular mechanisms underlying erythroid-specific gene regulation remain incompletely understood. Closely spaced binding sites for GATA, NF-E2/maf and CACCC interacting transcription factors play functionally important roles in globin and other erythroid-specific gene expression. We and others recently identified the CACCC-binding transcription factor ZBP-89 as a novel GATA-1 and NF-E2/mafK interacting partner. Here, we examined the role of ZBP-89 in human globin gene regulation and erythroid maturation using a primary CD34+ cell ex vivo differentiation system. We show that ZBP-89 protein levels rise dramatically during human erythroid differentiation, and that ZBP-89 occupies key cis-regulatory elements within the globin and other erythroid gene loci. ZBP-89 binding correlates strongly with RNA Pol II occupancy, active histone marks, and high-level gene expression. ZBP-89 physically associates with the histone acetyltransferases (HATs) p300 and Gcn5/Trrap, and occupies common sites with Gcn5 within the human globin loci. Lentiviral shRNA knockdown of ZBP-89 results in reduced Gcn5 occupancy, decreased acetylated histone 3 levels, lower globin and erythroid-specific gene expression, and impaired erythroid maturation. Addition of the HDAC inhibitor valproic acid partially reverses the reduced globin gene expression. These findings reveal an activating role for ZBP-89 in human globin gene regulation and erythroid differentiation. Keywords: Human primary erythroid progenitors Expression data of human erythroid progenitors transduced with lentivirus expressing short hairpins against ZBP-89 and control empty vector

2011-08-01 | E-GEOD-31092 | biostudies-arrayexpress

CRISPR and biochemical screens identify MAZ as a co-factor in CTCF-mediated insulation at Hox clusters [MAZ motif deletion RNA-seq]

Project description:In this experiment, we sought to analyze how transcriptome of WT and Maz HoxA(Δ5|6) cells change during differentiation of mouse embryonic stem cells (ESCs) into cervical motor neurons (MNs)

2022-02-06 | GSE157138 | GEO

Expression analysis of ZBP-89 deficient human primary erythroid progenitors

2011-08-02 | GSE31092 | GEO