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Genome-wide maps of FOXO1 binding sites in human endothelial cells

ABSTRACT: Genome-wide maps of FOXO1 binding sites in human endothelial cells

PROVIDER: PRJNA528316 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8758300.fastq.gz	Fastqsanger.gz
	SRR8758301.fastq.gz	Fastqsanger.gz
	SRR8758302.fastq.gz	Fastqsanger.gz
	SRR8758303.fastq.gz	Fastqsanger.gz
	SRR8758304.fastq.gz	Fastqsanger.gz

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Genome-wide maps of FOXO1 binding sites in human endothelial cells

Project description:ChIP-Seq profiling of human umbilical vein endothelial cells (HUVECs) overexpressing constitutively active FOXO1 to identify FOXO1 DNA binding sites and to assess changes in the histone modifications H3K4me3 and H3K27ac.

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aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA binding ability

Project description:Strict regulation of proliferation is vital for development, whereas unregulated cell proliferation is a fundamental characteristic of cancer. The polarity protein atypical protein kinase C lambda/iota (aPKC lambda) is associated with cell proliferation through unknown mechanisms. In endothelial cells, suppression of aPKC lambda impairs proliferation despite hyperactivated mitogenic signaling. Here we show that aPKC lambda phosphorylates the DNA binding domain of forkhead box O1 (FoxO1) transcription factor, a gatekeeper of endothelial growth. Although mitogenic signaling excludes FoxO1 from the nucleus, consequently increasing c-Myc abundance and proliferation, aPKC lambda controls c-Myc expression via FoxO1/miR-34c signaling without affecting its localization. We find this pathway is strongly activated in the malignant vascular sarcoma, angiosarcoma, and aPKC inhibition reduces c-Myc expression and proliferation of angiosarcoma cells. Moreover, FoxO1 phosphorylation at Ser218 and aPKC expression correlates with poor patient prognosis. Our findings may provide a new therapeutic strategy for treatment of malignant cancers, like angiosarcoma.

2019-11-12 | PXD011595 | Pride

Genome Wide Mapping of Foxo1 Binding-sites in Murine T Lymphocytes

Project description:The Forkhead box O (Foxo) family of transcription factors has a critical role in controlling the development, differentiation, and function of T cells. However, the direct target genes of Foxo transcription factors in T cells have not been well characterized. In this study, we focused on mapping the genome wide Foxo1-binding sites in naïve CD4+ T cells, CD4+ T cells, and Foxp3+ regulatory T (Treg) cells. By using chromatin immunoprecipitation coupled with deep sequencing (ChIP-Seq), we identified Foxo1 binding sites that were shared among or specific to the three T cell populations. Here we describe the experiments, quality controls, as well as the deep sequencing data. Part of the data analysis has been published by Ouyang W et al. in Nature 2012 (1) and Kim MV et al. in Immunity 2013 (2), and the associated data set were uploaded to NCBI Gene Expression Omnibus. ChIP DNAs were prepared from T cells isolated from C57BL/6 mice using Foxo1 antibody and T cells isolated from Foxo1tag/tagbirA mice using Streptavin-coated beads. ChIP-seq libraries were prepared following a standard protocol.

2014-08-19 | E-GEOD-60470 | biostudies-arrayexpress

Mapping of WT FOXO1 and M1L FOXO1 binding sites in SUDHL4 cells

Project description:Mapping of WT FOXO1 and M1L FOXO1 binding sites in SUDHL4 cells

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Genome-wide maps of YAP, TAZ and TEAD1 binding sites in human endothelial cells

Project description:Genome-wide maps of YAP, TAZ and TEAD1 binding sites in human endothelial cells

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Genome Wide Mapping of Foxo1 Binding-sites in Murine T Lymphocytes

2014-08-19 | GSE60470 | GEO

Genome-wide maps of YAP, TAZ and TEAD1 binding sites in human endothelial cells

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Project description:Analysis of transcriptional changes upon silencing of endothelial VEGF. Because transcription factor Foxo1 levels increase under VEGF silencing, we hypothesized that Foxo1 transcriptional activity would be apparent in a whole-genome microarray. Double-silencing of VEGF+Foxo1 was also performed to determine which transcriptional changes are Foxo1-dependent in a VEGF-deficient background.

2015-12-31 | E-MTAB-2515 | biostudies-arrayexpress

Trasncripional regulation by overexpression of constitutively active FOXO1 (CA-FOXO1) in human endothelial cells

Project description:To identify genes regulated by FOXO1, we performed RNA-seq analysis of human unbilical vein endothelial cells (HUVECs) overexpressing CA-FOXO1 by adenovirus. CA-FOXO1 is constructed by mutating three amino-acids phosphorylated by Akt, T24, S256, and S319, and is constitutively localized in the nucleus compared to wild-type FOXO1.

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