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ZEB2 orchestrates a transcriptional program to safeguard the integrity of human CD4+ Th1 EM cells

ABSTRACT: ZEB2 orchestrates a transcriptional program to safeguard the integrity of human CD4+ Th1 EM cells

PROVIDER: PRJNA1072732 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27848243_1.fastq.gz	Fastqsanger.gz
	SRR27848243_2.fastq.gz	Fastqsanger.gz
	SRR27848244_1.fastq.gz	Fastqsanger.gz
	SRR27848244_2.fastq.gz	Fastqsanger.gz
	SRR27848245_1.fastq.gz	Fastqsanger.gz

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ZEB2 orchestrates a transcriptional program to safeguard the integrity of human CD4+ Th1 EM cells

Project description:CD4+ Th1 cells migrate to sites of inflammation, where they are indispensable for eliminating intracellular pathogens. The lineage defining transcription factor T-bet establishes the Th1 transcriptional programme, directing IFNG to drive effector responses and inducing subordinate transcription factors to shape their phenotype. Aberrant Th1 cell activity drives the pathogenesis of multiple autoimmune diseases, but the detailed mechanisms by which Th1 cells maintain or lose their integrity remain largely uncharacterised. Using immunogenomics and high resolution immune phenotyping in human CD4+ cells, we discovered that the transcription factor ZEB2 is lineage restricted to Th1EM cells. Detailed molecular validation using CRISPR/Cas9 deletion of ZEB2, whole genome transcriptomics and pathway mapping has revealed that ZEB2 is a signalling hub for multiple pathways, stabilising the integrity and function of human CD4+ Th1EM cells. Furthermore, our disease linked pathway mapping suggests that ZEB2 is implicated in the control of Th1-mediated autoimmune disease.

2024-08-31 | GSE254977 | GEO

MLL-fusion-driven leukemia requires SETD2 to safeguard genomic integrity

Project description:MLL-fusion-driven leukemia requires SETD2 to safeguard genomic integrity

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Nf2 orchestrates β-arrestin2-biased PTH1R signaling to safeguard skeletal integrity

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Blood vessel-resident macrophages safeguard blood and vessel integrity in zebrafish

Project description:Blood vessel-resident macrophages safeguard blood and vessel integrity in zebrafish

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ZEB2 protects the heart from ischemic damage

Project description:infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin 4 (TMSB4) and Prothymosin (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.

2021-03-23 | PXD022212 | Pride

ZNF512B protects critical regulatory regions to safeguard long term genomic integrity. [screening]

Project description:ZNF512B protects critical regulatory regions to safeguard long term genomic integrity. [screening]

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Blood-resident macrophages safeguard blood and vessel integrity

Project description:Macrophages are essential in immune defence, tissue development, and disease onset and progression. Their function is in part dictated by their microenvironment and origin. Tissue-resident macrophages originate from yolk sac progenitors, persisting in adult organs and tissues mainly through self-renewal. Although ubiquitously present throughout the body, no dedicated macrophage population is known to function within the vast network of blood vessels, despite the importance of maintaining a healthy vascular and blood system. Here, we identified a distinctive population of macrophages residing within blood vessels, which we termed blood-resident macrophages (bMΦ). bMΦ actively survey the blood to eliminate foreign particles and unfit cells, and act as the first responders to endothelial damage. bMΦ emerge directly from the main axial vessels of zebrafish embryos though an atypical endothelial-to-macrophage transition (EMacT), independent of Runx1 and Csf1r, both essential for hematopoietic stem cell and myeloid cell production, respectively. Our data thus unveil the existence of a specialized population of macrophages that function within the confinement of the vasculature to safeguard blood from foreign threats and maintain blood vessel integrity. These discoveries not only expand our understanding of immune surveillance mechanisms but also offer potential avenues for the treatment of bloodborne diseases and vascular injuries.

2026-03-11 | PXD052344 | Pride

Zeb2 is Essential for Bergmann Glial Development and Cerebellar Organization

Project description:Cerebellar circuitry is critical for balance and motor control among a wide array of functions and largely consists of granule and Purkinje neurons. Bergmann glia in the cerebellum form distinct morphological structures that facilitate granule neuron migration during development and that maintain the cerebellar organization and functional integrity. At present, molecular control of the formation and morphogenesis of Bergmann glia remains obscure. In this study, we found that Zeb2 (a.k.a. Sip1 or Zfhx1b), a Mowat-Wilson syndrome-associated transcriptional regulator, is highly restricted to Bergmann glia and is essential for their development and maturation. The mice with Zeb2 ablation in the cerebellar neural progenitor exhibit dysgenesis of cerebellar cortical lamination and locomotion defects. Deletion of Zeb2 markedly reduced Bergmann glial proliferation, differentiation and the establishment of the normal radial scaffold, disrupting migration of granule cell progenitors from external to internal granular layers. Transcriptome profiling indicated that Zeb2 regulates multiple pathways including FGF and Notch signaling as well as axonal guidance cues including Netrin G2 and Gdf10 to control Bergmann glial development. Our data reveal that Zeb2 acts as a transcriptional integrator of diverse signaling pathways to regulate the formation and morphogenesis of Bergmann glia ensuring maintenance of cerebellar integrity, suggesting that Zeb2 dysfunction in Bergmann glia might contribute to motor deficits in Mowat-Wilson syndrome.

2018-06-25 | GSE84098 | GEO

ZNF512B protects critical regulatory regions to safeguard long term genomic integrity. [CUT&RUN]

Project description:ZNF512B protects critical regulatory regions to safeguard long term genomic integrity. [CUT&RUN]

| PRJNA849011 | ENA

ZNF512B protects critical regulatory regions to safeguard long term genomic integrity. [scRNA-Seq]

Project description:ZNF512B protects critical regulatory regions to safeguard long term genomic integrity. [scRNA-Seq]

| PRJNA849028 | ENA