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Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver

ABSTRACT: Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver

PROVIDER: PRJNA809743 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18117726.fastq.gz	Fastqsanger.gz
	SRR18117727.fastq.gz	Fastqsanger.gz
	SRR18117728.fastq.gz	Fastqsanger.gz
	SRR18117729.fastq.gz	Fastqsanger.gz
	SRR18116330.fastq.gz	Fastqsanger.gz

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Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver (ChIP-seq)

Project description:The goal of this study was to apply next-generation sequencing (NGS) analyses to identify genes and pathways regulated by the Foxk1 transcription factor in the liver and to see the effects of liver-specific Foxk1 deficiency in the diet-induced non-alcoholic steatohepatitis (NASH) model. Transcriptome and ChIP-seq analysis revealed that liver Foxk1 promotes the pathogenesis of NASH by regulating the expression of a series of molecules involved in hepatic lipid metabolism in an mTORC1-dependent manner.

2022-03-01 | GSE197324 | GEO

Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver (RNA-seq)

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Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver (ChIP-seq)

Project description:Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver (ChIP-seq)

| PRJNA809748 | ENA

Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver (RNA-seq)

Project description:Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver (RNA-seq)

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Next-generation sequencing reveals the regulatory mechanism of transcription factor Foxk1 in the liver

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

2022-03-01 | GSE197326 | GEO

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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Comparative transcriptomic analysis of 3T3-L1 adipocytes with modulated level of Foxk1 and Foxk2 transcription factor

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 3T3-L1 adipocytes. We found, that series of enzymes involved in metabolism of lipids and carbohydrates, as well as cell migration, proliferation and adhesion are regulated in response to this transcription factor, thereby providing important insight into biological role of Foxk1 and Foxk2 for cells survival and metabolism.

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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.

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

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