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Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [ATAC-seq]

ABSTRACT: Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [ATAC-seq]

PROVIDER: PRJNA945901 | ENA |

REPOSITORIES: ENA

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Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [RNA-seq]

Project description:Microglia are the tissue resident macrophages of the central nervous system (CNS). Dysregulation of inflammatory processes in the CNS is associated with aging, and neurodegenerative diseases, where microglia acquire a sensitized, or primed, phenotype, which is characterized by an increased inflammatory phenotype and an exaggerated reactivity to immune challenges. Transcriptomic profiling of microglia in different neurodegenerative disease and aging mouse models identified a common, primed, gene expression signature. However, the transcriptional mechanisms that mediate microglia priming still remains unclear. In DNA repair deficient (Ercc1Δ/ko) mice, microglia acquire a profound primed phenotype and by integrating RNA-seq and ATAC-seq data of Ercc1Δ/ko microglia, we identified transcription factors IRF7, IRF9 and SMAD3 as possible core regulators of microglia priming. Our data suggest that increased IRF7/IRF9 activity and decreased SMAD3 activity might be important for microglia to acquire a primed gene signature. This study provides insight in the transcriptomic regulation of primed microglia, which are implicated in aging and neurodegenerative diseases.

2024-12-31 | GSE227606 | GEO

Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [ATAC-seq]

2024-12-31 | GSE227605 | GEO

Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice

Project description:Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice

| PRJNA945895 | ENA

Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [RNA-seq]

Project description:Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice [RNA-seq]

| PRJNA945900 | ENA

Transcriptional regulation of microglia priming by IRF7, IRF9 and SMAD3 in accelerated aging mice

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

2024-12-31 | GSE227607 | GEO

Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

Project description:To investigate the role of the IRF family in the regulation of interferon stimulated genes, we conducted CRISPR/Cas9 mediated genome editing of Irf3, Irf7 or Irf9 in sgScd2 Th1 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of control, sgScd2, sgScd2/sgIrf3, sgScd2/sgIrf7 or sgScd2/sgIrf9 Th1 cells.

2022-08-03 | GSE200636 | GEO

Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

Project description:Effect of deletion of Irf3, Irf7 or Irf9 on gene expression in sgScd2 Th1 cells.

| PRJNA825571 | ENA

ChIP-seq for IRF7

Project description:We performed ChiP-Seq for IRF7 in GM-CSF induced bone-marrow cells. IRF7 ChIP-Seq in myeloid cells

2014-12-03 | E-GEOD-62697 | biostudies-arrayexpress

Deficiency of Tlr7 and Irf7 increases the severity of COVID-19 through the reduced interferon production

Project description:Toll-like receptor 7 (Tlr7) deficiency-accelerated severe COVID-19 is associated with reduced production of interferons (IFNs). However, the underlying mechanisms remain elusive. Here, we demonstrate that the deficiency of Tlr7 and Irf7 globally and/or in immune cells in mice increases the severity of COVID-19 via impaired IFN activation in both immune and/or non-immune cells, leading to increased lung viral loads. These effects are associated with reduced IFN alpha and gamma production. The deficiency of Tlr7 in the infected mice tends to cause the reduced production and nuclear translocation of Interferon regulatory factor 7 (IRF7), indicative of reduced IRF7 activation. Despite higher amounts of lung viral antigen, Tlr7 or Irf7 deficiency resulted in substantially reduced production of antibodies against SARS-CoV-2, thereby delaying the viral clearance. These results highlight the importance of the activation of TLR7 and IRF7, leading to IFN production on the development of innate and adaptive immunity against COVID-19.

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ChIPseq Smad3-JMJD3

Project description:ChIPseq Smad3-JMJD3

| PRJEB2739 | ENA