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SOX7 ChIP-seq in HUVECs

ABSTRACT: SOX7 ChIP-seq in HUVECs

PROVIDER: PRJEB12816 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1279120.fastq.gz	Fastqsanger.gz
	ERR1279117.fastq.gz	Fastqsanger.gz
	ERR1279118.fastq.gz	Fastqsanger.gz
	ERR1279119.fastq.gz	Fastqsanger.gz

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SOX7 ChIP-seq in HUVECs

Project description:We investigated SOX7 binding events on the chromatin under basal conditions in human umbilical vein endothelial cells, upon overexpression of human SOX7-mCherry and immunoprecipitating mCherry. Cells overexpressing only the mCherry tag were used as negative control condition, and peaks called here were substracted from the SOX7-mCherry peaks.

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Sox18 ChIP-seq in HUVECs

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Project description:To find out the target of transcription factor Sox7 and Sox17, DNA microarray analysis was performed with RNA from Sox7 and Sox17 knockdown HUVECs.

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Sox7 regulates lineage decisions in cardiovascular progenitor cells

Project description:Specification of the mesodermal lineages requires a complex set of morphogenetic events orchestrated by interconnected signaling pathways and gene regulatory networks. The transcription factor Sox7 has critical functions in differentiation of multiple mesodermal lineages, including cardiac, endothelial, and hematopoietic. Using a doxycycline-inducible mouse embryonic stem cell (mESC) line, we have previously shown that expression of Sox7 in cardiovascular progenitor cells promotes expansion of endothelial progenitor cells. Here, we show that the ability of Sox7 to promote endothelial cell fate occurs at the expense of the cardiac lineage. Using ChIP-Seq coupled with ATAC-Seq we identify downstream target genes of Sox7 in cardiovascular progenitor cells and, by integrating these data with transcriptomic analyses, we define Sox7-dependent gene programs specific to cardiac and endothelial progenitor cells. Further, we demonstrate a protein-protein interaction between SOX7 and GATA4 and provide evidence that Sox7 interferes with the transcriptional activity of Gata4 on cardiac genes. In addition, we show Sox7 modulates WNT and BMP signaling during cardiovascular differentiation. Our data represent the first genome-wide analysis of Sox7 function and reveal a critical role for Sox7 in regulating signaling pathways that affect cardiovascular progenitor cell differentiation.

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ChIP-Seq on SOX7-V5 tagged mouse embryos at E9.5 and E10.5

Project description:We intended to identify the potential binding targets of SOX7 in mouse during development (E9.5-E10.5)

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Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha

Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.

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ChIP-Seq on SOX7-V5 tagged mouse embryos at E9.5 and E10.5

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Project description:H3K27Ac is one of the expressed enhancer markers in endothelial cells, but its genomic localization is unknown. This time, we established a new antibody for H3K27ac, and performed ChIP-seq to identify H3K27ac binding site in whole genome manner under hypoxia. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with or without hypoxia (1%O2) for 24hours, then H3K27ac binding regions were identified. Normoxia was used as a control condition. HUVECs were used within the first 6 passages.

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