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ATAC-seq analysis to investigate the role of FOXF1/2 in senescent cells.

ABSTRACT: ATAC-seq analysis revealed that the FOXF1/2 depletion decreased chromatin accessibility at enhancers of pro-inflammatory SASP genes

ORGANISM(S): Homo sapiens

PROVIDER: GSE291619 | GEO | 2026/03/31

REPOSITORIES: GEO

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CUT&RUN analysis to investigate the role of FOXF1/2 in senescent cells.

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RNA-seq analyses of FOXF1/2- and p300/CBP-depleted senescent IMR-90 cells

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Effects of the FOXF1 on herpes simplex virus 1 and host chromatin accessibility in Neuro-2a cells

Project description:This is a part of the study that shows that a host gene,FOXF1, promote herpes simplex virus 1 (HSV-1) genome accessibility. These ATAC analyses viral and host genome accessibility in Neuro-2a cells. Neuro-2a cells were transfected with pFOXF1 and pcDNA plasmids for 42 hours then infected with herpes simple virus1 for 3 hours.

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Multiome (GEX + ATAC) profile at single cell level of Foxf1 positive endothelial cells and mesenchymal cells from mouse lung at E18.5

Project description:Foxf1 is enriched and differentially expressed in lung cells derived from mesoderm. We used single cell RNA sequencing (snRNAseq + snATAC) to analyze the dynamic transcriptional regulation in various lung cell types. The single cell analysis show the cell specific regulation of Foxf1 by distal enhancers that contribute to the molecular pathology of ACDMPV.

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H3K27Ac ChIP-seq to investigate the role of ACLY pathway in senescent cells.

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Foxf1 enchances pulmonary inflammation and mastocytosis

Project description:The Forkhead Box f1 (Foxf1) transcriptional factor (previously known as HFH-8 or Freac-1) is expressed in endothelial and smooth muscle cells in the embryonic and adult lung. To assess effects of Foxf1 during lung injury, we used CCl4 injury model. Foxf1+/- mice developed severe airway obstruction and bronchial edema, associated with increased numbers of pulmonary mast cells and increased mast cell degranulation following injury. Pulmonary inflammation in Foxf1+/- mice was associated with diminished expression of Foxf1, increased mast cell tryptase and increased expression of CXCL12, the latter being essential for mast cell migration and chemotaxis. Foxf1 haploinsufficiency caused pulmonary mastocytosis and enhanced pulmonary inflammation following chemically-induced lung injury, indicating an important role for Foxf1 in the pathogenesis of pulmonary inflammatory responses. Keywords: Influence of genetic modification on the pulmonary inflamation Foxf1+/- mice in which the Foxf1 allele was disrupted by an in-frame insertion of a nuclear localizing -galactosidase (-Gal) gene were bred for ten generations into the Black Swiss mouse genetic background. Carbon tetrachloride (CCl4; Sigma, St Louis, MO) was dissolved in mineral oil at a 1:20 ratio v/v and a single intraperitoneal (i.p.) injection of CCl4 (0.5 l of CCl4/ 1g of body weight) was administered to male Foxf1+/- mice or their wild type (WT) littermates as described.

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Foxf1 enchances pulmonary inflammation and mastocytosis

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Mouse embryonic lung FOXF1 ChIP-seq analysis

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Foxf1+/- mouse lung gene expression analysis

Project description:Analysis of genes dysregulated due to haploinsufficiency of Foxf1 in postnatal day 0.5 mouse lungs Total RNA obtained from six Foxf1+/- mouse lungs compared to six wildtype littermate mouse lungs

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