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RNA-seq identification of herpes simplex virus type 1 transcription in Neuro-2a cells overexpressing FOXK1 and FOXF1

ABSTRACT: We used inducible Neuro-2a cell lines with stable expression of FOXK1 and FOXF1. The cells were induced to express FOX protein under doxycycline for 36 hours and then infected with HSV-1 for five hours. The cells were collected and cleaved, and total RNA was extracted for RNAseq analysis

ORGANISM(S): Mus musculus

PROVIDER: GSE286127 | GEO | 2025/01/31

REPOSITORIES: GEO

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

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Identification of the binding DNA of FOXF1 by ChIP in Neuro-2a cells

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RNA-seq identification of herpes simplex virus type 1 transcription in Neuro-2a cells overexpressing ONECUT2

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

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Identification of herpes simplex virus 1 and host targets of miR-138 by comparative PAR-CLIP in Neuro-2a and 293T cells

Project description:This is a part of the study that shows that a host microRNA, miR-138, represses herpes simplex virus 1 (HSV-1) gene expression through both viral and host targets. These PAR-CLIP analyses identified viral and host targets of miR-138 in Neuro-2a (mouse neuroblastoma) and 293T (human embryonic kidney) cells. We constructed two cell lines derived from Neuro-2a cells, one overexpressing miR-138 (N2A138) and one antagonizing miR-138 (N2Aanti138). We also constructed two cell lines derived from 293T cells, one overexpressing miR-138 (293T138) and one control cells (293Tcontrol). Uninfected N2A138 and N2Aanti138 were compared by PAR-CLIP for host targets in Neuro-2A cells. 293T138 and 293Tcontrol cells infected for 4 and 8 hours were compared by PAR-CLIP for HSV-1 targets in 293T cells. 293T138 and 293Tcontrol cells infected for 4 hours were also compared for host targets in 293T cells.

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Comparative transcriptomic analysis of WT, FOXK1/2 KO, DKO cells and FOXK1 KO cells with reconstitution of several FOXK1 mutants

Project description:The goal of this study was to apply Next Generation Sequencing analyses to identify genes and pathways regulated by the FOXK1 and FOXK2 transcription factor in HeLa cells and to see whether reconstitution of FOXK1 WT and mutants can rescue the altered gene regulation in FOXK1 KO cells. Gene Ontology (GO) analysis did not uncover any dysregulated DNA damage–related pathways upon FOXKs KO. We found that cells reconstituted with any of the three FOXK1 mutants could largely rescue dysregulated gene expression in FOXK1 KO cells, similar to cells reconstituted with WT FOXK1. These suggesting that FOXK1's role in DNA damage response is not by direct transcriptional regulation of DNA damage related pathways and all the three FOXK1 mutants could not affect transcription.

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2023-05-08 | GSE202562 | GEO

ATAC-seq datasets from differentiating iHA-Foxk1 and Foxk1 KO mESCs in mesodermal conditions

Project description:50k cells from D3, D5 and D10 EBs from iHA-Foxk1 and Foxk1 KO cells were harvested for ATAC-seq and submitted for sequencing to understand the chromatin dynamics of these cells during differentiation in the presence and absence of FOXK1

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O-GlcNAcylation of FOXK1 orchestrates the E2F pathway

Project description:Gene transcription is a highly regulated process, and deregulation of transcription factors activity underlie numerous pathologies including cancer. FOXK1 and FOXK2 (FOXK1/2) transcription factors have recently emerged as important regulators of cell metabolism, autophagy and cell differentiation. While FOXK1/2 possesses many overlapping functions in normal biology, their specific functions as well as deregulation of their transcriptional activity in cancer is less clear and often contradictory. FOXK1, but less FOXK2, is known to have oncogenic properties as higher expression levels of FOXK1 has been observed in several cancers and is correlated with tumor progression, invasion, and metastasis. However, the molecular mechanism by which FOXK1 exert its oncogenic properties in caner remains unknown. Here we show that elevated expression of FOXK1, but not FOXK2, in normal human fibroblasts promotes transcription of E2F target genes associated with increased proliferation and delayed senescence entry. Fibroblasts overexpressing FOXK1 are also more prone to cellular transformation with minimal oncogenic combinations, suggesting important oncogenic proprieties of FOXK1. Mechanistically, we found that FOXK1, but not FOXK2, is specifically modified by O-GlcNAcylation. FOXK1 O-GlcNAcylation is modulated during the cell cycle and its highest levels coincides with the G1/S phase transition. Moreover, FOXK1 O-GlcNAcylation is increased following cell transformation and loss of this modification leads to decreased FOXK1 ability to promote cellular transformation and tumor growth. Cells overexpressing FOXK1 O-GlcNAcylation-defective mutants have lower E2F1 expression, cell proliferation, and tumour growth. Our results define a distinct role of FOXK1 via O-GlcNAcylation in controlling the cell cycle through the orchestration of the E2F pathway.

2024-06-10 | PXD050014 | Pride

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.

2008-09-04 | E-GEOD-11112 | biostudies-arrayexpress

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