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XgAriArbu

ABSTRACT: Arianta arbustorum (copse snail)

PROVIDER: PRJEB80335 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR13698326.fastq.gz	Fastqsanger.gz
	ERR13698327.fastq.gz	Fastqsanger.gz
	ERR13702785_1.fastq.gz	Fastqsanger.gz
	ERR13702785_2.fastq.gz	Fastqsanger.gz
	ERR13702786_1.fastq.gz	Fastqsanger.gz

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xgAriArbu

Project description:Arianta arbustorum (copse snail), genomic and transcriptomic data

| PRJEB80334 | ENA

Eristalis arbustorum

Project description:Eristalis arbustorum overview

| PRJNA767155 | ENA

ChIP-seq analysis of SNAIL transcription factor binding sites in RH30 rhabdomyosarcoma cells

Project description:ChIP-seq analysis of SNAIL binding sites in RH30 cells was performed to discover novel SNAIL binding sites in rhabdmyosarcoma cells.

2020-07-15 | GSE152355 | GEO

Genome-wide maps of chromatin state in HeLa cells.

Project description:We report a series of ChIP-Seq results in HeLa cells. Briefly, we performed ChIP-Seq experiments with antibodies specific for Snail, MTA1, and PRMT5 in HeLa cells. We found that Snail, MTA1, and PRMT5 had similar binding motifs. This study gave us a new understanding of the role of Snail in chromatin status and gene transcription.

2019-08-22 | GSE130194 | GEO

Roles of Snail-regulated miRNAs in colon cancer progression

Project description:The transcription factor Snail is known as an EMT regulator to promote cancer metastasis. Identification Snail-regulated miRNAs helps to uncover mechanisms governing CRC metastasis

2013-11-20 | GSE39286 | GEO

ChIP-Seq of Myf5, MyoD, Snai1, HDAC1, HDAC2, E47 and empty vector controls in mouse skeletal myoblasts or myotubes

Project description:In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snail does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells. Genome wide binding sites of various transcription factors and chromatin modifiers in muscle cells

2012-07-04 | E-GEOD-24852 | biostudies-arrayexpress

idEriArbu

Project description:Eristalis arbustorum (plane-faced dronefly)

| PRJEB46302 | ENA

Distinct EMT programs control normal stem cells and cancer stem cells of mammary tissue

Project description:Cancer stem cells (CSCs) are proposed to be responsible for metastatic dissemination and clinical relapse in a variety of cancers. Analogies between CSCs and normal tissue stem cells (SC) has led to the notion that CSCs often co-opt the normal SC program of their tissue-of-origin. The cell-biological program termed epithelial-mesenchymal transition (EMT) has been found to encourage entrance of normal and neoplastic mammary cells into the corresponding SC states. Using genetically engineered knock-in reporter mouse lines, we demonstrate that in the murine mammary lineage, the paralogous EMT-inducing transcription factors Snail and Slug, are selectively exploited by CSCs and normal SCs respectively. Slug, when expressed at physiological levels, only activates a partial EMT program and is dispensable in CSCs. In contrast, Snail drives a far more complete transition into the mesenchymal state and controls both tumor-initiation and metastatic dissemination. Consistent with their functional distinctions, Snail controls far more target genes than Slug, and their distinct functions are determined by their divergent N-terminal domains. Our findings underscore fundamental distinctions between the SC program operating in normal and neoplastic SCs, and hint for potential avenues of selective therapeutic elimination of breast CSCs. We sought to understand differential ability to activate the EMT program in breast cancer cells by transcription factors Snail and Slug. Hence, we mapped genome-wide Snail and Slug binding sites in murine MMTV-PyMT breast cancer cell lines that express high level of Snail or high level of Slug respectively. Specifically, we performed Snail ChIP seq in the mesenchymal pBl.3G cells, and Slug ChIP-seq in the epithelial pBl.1G cells.

2015-09-02 | E-GEOD-61198 | biostudies-arrayexpress

Snail-dependent epithelial splicing regulatory protein 1 (ESRP1) silencing drives malignant transformation of human pulmonary epithelial cells [miRNA]

Project description:The significance of epithelial-to-mesenchymal transition (EMT)-inducing transcription factors in the onset of non-small cell lung cancer has not been resolved. Here, we report increased Snail expression in pulmonary premalignant lesions relative to histologically normal-appearing pulmonary epithelium. Utilizing immortalized human pulmonary epithelial cells and isogenic derivatives, we document Snail-dependent anchorage-independent growth of the epithelial cells in vitro, as well as transformation, primary tumor growth, and metastatic behavior in vivo. Epithelial splicing regulatory protein 1 (ESRP1) tumor suppressor silencing was a requirement for Snail-driven transformation in vivo, and we identified ESRP1 loss in Snail-expressing pulmonary premalignant lesions in situ. Snail drives these and other carcinogenic signaling programs in an ALDH+CD44+CD24- pulmonary stem cell subset in which ESRP1 and stemness-repressing micro-RNAs are inhibited.

2017-12-16 | GSE108136 | GEO

MicroRNA response to Snail overexpression in lung cancer cell lines

Project description:Analysis of four lung cancer cell lines transfected with a vector expressing the transcriptional repressor Snail versus a vector control. Aberrant Snail expression is known to induce an EMT program in lung cancers.

2013-07-17 | GSE48922 | GEO

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