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Histone deacetylase 3 contributes to the anti-viral innate immunity of macrophages through interacting with FOXK1 to regulate STAT1/2 transcription [RNA-seq]

ABSTRACT: Histone deacetylase 3 contributes to the anti-viral innate immunity of macrophages through interacting with FOXK1 to regulate STAT1/2 transcription [RNA-seq]

PROVIDER: PRJNA787588 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17182614_1.fastq.gz	Fastqsanger.gz
	SRR17182614_2.fastq.gz	Fastqsanger.gz
	SRR17182615_1.fastq.gz	Fastqsanger.gz
	SRR17182615_2.fastq.gz	Fastqsanger.gz
	SRR17182616_1.fastq.gz	Fastqsanger.gz

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Histone deacetylase 3 contributes to the anti-viral innate immunity of macrophages through interacting with FOXK1 to regulate STAT1/2 transcription [RNA-seq]

Project description:It is well known that IFNα/β activates the JAK/STAT signaling pathway and suppresses viral replication through induction of interferon stimulated genes (ISGs). Here we reported that knockout of HDAC3 from macrophages resulted in decreased expression of STAT1 and STAT2, leading to a defective anti-viral immunity in cells and mice. Further studies showed that HDAC3 interacted with a conserved transcription factor Forkhead Box K1 (FOXK1), co-localized with FOXK1 at the promoter of STAT1 and STAT2, and was required for protecting FOXK1 from lysosomal system mediated degradation. Constantly, FOXK1 deficient macrophages also showed low STAT1 and STAT2 expression with defective response to virus. Thus, our studies uncovered the biological importance of HDAC3 on regulating antiviral immunity of macrophages through interaction with FOXK1 to regulate the expression of STAT1 and STAT2.

2022-05-12 | GSE190577 | GEO

Histone deacetylase 3 contributes to the anti-viral innate immunity of macrophages through interacting with FOXK1 to regulate STAT1 and STAT2

Project description:Histone deacetylase 3 contributes to the anti-viral innate immunity of macrophages through interacting with FOXK1 to regulate STAT1 and STAT2

| PRJNA787584 | ENA

Histone deacetylase 3 and FOXK1 formed a transcriptional complex involved in regulating the expression of STAT1 and STAT2 [ChIP-seq]

2022-05-12 | GSE190578 | GEO

Histone deacetylase 3 and FOXK1 formed a transcriptional complex involved in regulating the expression of STAT1 and STAT2 [ChIP-seq]

Project description:Histone deacetylase 3 and FOXK1 formed a transcriptional complex involved in regulating the expression of STAT1 and STAT2 [ChIP-seq]

| PRJNA787587 | ENA

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.

2020-06-26 | GSE151029 | GEO

Histone deacetylase 3 contributes to the anti-viral innate immunity of macrophages through interacting with FOXK1 to regulate STAT1 and STAT2

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

2022-05-12 | GSE190579 | GEO

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

Project description:D3, D5 and D10 EBs from iHA-Foxk1 and Foxk1 KO cells were harvested for RNA and submitted for sequencing to understand the transcriptional profile of these cells during differentiation in the presence and absence of FOXK1

2023-05-08 | GSE202562 | GEO

Gene expression alterations by the mTORC1-FOXK1 pathway

Project description:C-C chemokine ligand 2 (CCL2) plays pivotal roles in tumor formation, progression, and metastasis. Although CCL2 expression has been found to be dependent on the nuclear factor (NF)–κB signaling pathway, the regulation of CCL2 production in tumor cells has remained unclear. We have identified a noncanonical pathway for regulation of CCL2 production that is mediated by mammalian target of rapamycin complex 1 (mTORC1) but independent of NF-κB. Multiple phosphoproteomics approaches identified the transcription factor forkhead box K1 (FOXK1) as a downstream target of mTORC1. Activation of mTORC1 induces dephosphorylation of FOXK1 resulting in transactivation of the CCL2 gene. Inhibition of the mTORC1-FOXK1 axis attenuated insulin-induced CCL2 production as well as the accumulation of tumor-associated monocytes-macrophages and tumor progression in mice. Our results suggest that FOXK1 directly links mTORC1 signaling and CCL2 expression in a manner independent of NF-κB, and that CCL2 produced by this pathway contributes to tumor progression.

2017-11-28 | GSE67810 | 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

2023-05-08 | GSE202517 | GEO

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

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