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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq of human embryonic stem cells H1 ESC cells and the differentiated NPC cells with FOXK1/2 and SIN3A knock down and the control condition.

ABSTRACT: In order to investigate the genome-wide binding profile of the forkhead transcription factor FOXK2 in human embryonic stem cells (ESCs) and downstream cell types, we generated the RNA-seq data with FOXK1/2 and SIN3A siRNA in H1 ESC cells and FOXK1/2 siRNA in the differentiated NPC cells.

INSTRUMENT(S): Illumina HiSeq 3000

ORGANISM(S): Homo sapiens

SUBMITTER: Yaoyong Li

PROVIDER: E-MTAB-9639 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The forkhead transcription factor FOXK2 premarks lineage-specific genes in human embryonic stem cells for activation during differentiation.

Ji Zongling Z Li Yaoyong Y Liu Sean X SX Sharrocks Andrew D AD

Nucleic acids research 20210201 3

Enhancers play important roles in controlling gene expression in a choreographed spatial and temporal manner during development. However, it is unclear how these regulatory regions are established during differentiation. Here we investigated the genome-wide binding profile of the forkhead transcription factor FOXK2 in human embryonic stem cells (ESCs) and downstream cell types. This transcription factor is bound to thousands of regulatory regions in human ESCs, and binding at many sites is maint ...[more]

PMID: 33434264

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Epigenetic and transcriptional regulation of starvation-induced atrophy and autophagy programs by Foxk1 and Sin3A

Project description:Autophagy is the primary catabolic process triggered in response to starvation. Although autophagic regulation within the cytosolic compartment is well established, it is becoming clear that nuclear events also regulate the induction or repression of autophagy. Nevertheless, a thorough understanding of the mechanisms by which sequence-specific transcription factors modulate expression of genes required for autophagy is lacking. Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts. Interestingly, Foxk1/2 serve to counter-balance another forkhead transcription factor, Foxo3, which induces an overlapping set of autophagic and atrophic targets in muscle. Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes. Remarkably, mTOR promotes the transcriptional activity of Foxk1 by facilitating nuclear entry to specifically limit basal levels of autophagy in nutrient-rich conditions. Our study highlights an ancient, conserved mechanism whereby nutritional status is interpreted by mTOR to restrict autophagy by repressing essential autophagy genes via Foxk-Sin3-mediated transcriptional control. Examination of (1) chromatin binding of Foxk1 and Sin3A in non-starved myoblasts and (2) gene expression profiling upon either starvation or siRNA-mediated depletion of Foxk1 relative to a non-starved control.

2014-11-17 | E-GEOD-56932 | biostudies-arrayexpress

ChIP-seq of FOXK2 in human embryonic stem cells H1 ESC, and the differentiated mesendoderm cells and and NPC cells

Project description:In order to investigate the genome-wide binding profile of the forkhead transcription factor FOXK2 in human embryonic stem cells (ESCs) and downstream cell types, we generated the ChIP-seq data of FOXK2 in H1 ESC cells and two differentiated types of cells, mesendoderm cells and NPC cells.

2020-12-21 | E-MTAB-9630 | biostudies-arrayexpress

Epigenetic and transcriptional regulation of starvation-induced atrophy and autophagy programs by Foxk1 and Sin3A

2014-11-17 | GSE56932 | GEO

Gene regulated by mutant ASXL1 KO and FOXK1/FOXK2 KO in K562 cell line

Project description:Gene regulated by mutant ASXL1 KO and FOXK1/FOXK2 KO in K562 cell line

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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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FoxK1/2 – New Components in Insulin Regulation of Cellular and Mitochondrial Metabolism

Project description:A major target of insulin signaling is the FoxO family of Forkhead transcription factors, which translocate from the nucleus to the cytoplasm following insulin-stimulated phosphorylation. Here we show that the Forkhead transcription factors FoxK1 and FoxK2 are also downstream targets of insulin action, but that following insulin stimulation, they translocate from the cytoplasm to nucleus, reciprocal to the translocation of FoxO1. FoxK1/FoxK2 translocation to the nucleus is dependent on the Akt-mTOR pathway, while its localization to the cytoplasm in the basal state is dependent on GSK3. Knockdown of FoxK1 and FoxK2 in liver cells results in upregulation of genes related to apoptosis and down-regulation of genes involved in cell cycle and lipid metabolism. This is associated with decreased cell proliferation and altered mitochondrial fatty acid metabolism. Thus, FoxK1/K2 are reciprocally regulated to FoxO1 following insulin stimulation and play a novel role in the control of apoptosis, metabolism and mitochondrial function.

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SIN3A-regulated LIF-responsive genes in MCF7 cells

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2012-08-01 | E-GEOD-35696 | biostudies-arrayexpress

SIN3A Acetylation Complex - Fam60a defines a variant Sin3a-Hdac complex in embryonic stem cells required for self-renewal

Project description:Sin3a is the central scaffold protein of the prototypical Hdac1/2 chromatin repressor complex, crucially required during early embryonic development for the growth of pluripotent cells of the inner cell mass. Here, we explore the endogenous composition of the Sin3a-Hdac complex in pluripotent embryonic stem (ES) and differentiated cells. To do this, we established an endogenous double immunoprecipitation strategy coupled with quantitative mass spectrometry (ENDIP-MS) allowing us to define the precise composition of the Sin3a complex in multiple cell types. We identify the Fam60a subunit as a key defining feature of a variant Sin3a complex present in ES cells, but not in differentiated cells. Fam60a co-occupies H3K4me3 positive promoters with Sin3a and is essential to maintain it on chromatin. Consistent with this, Fam60a depletion phenocopies the loss of Sin3a, leading to decreased proliferation, an extended G1-phase and the deregulation of genes associated with differentiation. Taken together, our data characterise Fam60a as an essential core subunit of a variant Sin3a complex in ES cells required to promote rapid proliferation and to prevent unscheduled differentiation.

2017-05-19 | PXD005464 | Pride

Genome-wide maps of chromatin state in LbetaT2 cells or in the pituitary tissues of wild-type and Foxk2 knockout mice.

Project description:First, we report a series of ChIP-seq results in LbetaT2 cells. Briefly, we performed ChIP-seq experiments with antibodies specific for Foxk2, Sin3a, Tet1 and Uhrf1 in LbetaT2 cells. We found that a total of 343 different promoters including Nab2 that are co-targeted by Foxk2, Sin3a, Tet1 and Uhrf1. Next, hMeDIP-seq and ChIP-seq experiments with antibodies specific for 5hmC and H3K18ub in the pituitary tissues of wild-type and Foxk2 knockout mice were performed. The results showed that compared to the wild-type mice, knockout of Foxk2 reduced the enrichment of 5hmC and H3K18ub on the Foxk2 target gene.This study revealed a critical switch control of FOXK2 for GnRH pulse frequency-dependent LH production and gave us a new understanding of the role of Foxk2 in chromatin status and gene transcription.

2020-05-01 | GSE130615 | GEO

Analysis of gene expression in Idasanutlin-arrested SIN3A and SIN3B depleated cells

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