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ABSTRACT: SMS composting

PROVIDER: PRJNA997789 | ENA |

REPOSITORIES: ENA

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Dataset's files

Source:

			Action	DRS
	SRR25393700_subreads.fastq.gz	Fastqsanger.gz
	SRR25393701_subreads.fastq.gz	Fastqsanger.gz
	SRR25393702_subreads.fastq.gz	Fastqsanger.gz
	SRR25393703_subreads.fastq.gz	Fastqsanger.gz
	SRR25393704_subreads.fastq.gz	Fastqsanger.gz

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Investigate the affect of CASZ1b on chromatin accessibility in SMS-CTR cells

Project description:In SMS-CTR cells, the overexpression of CASZ1b in SMS-CTR cells led to a modification of regional chromation accessibility.

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Genome-wide mapping of CASZ1b binding sites and investigate its effect on chromatin status in SMS-CTR cells [CTRtetCASZ1b]

Project description:In SMS-CTR cells, we identified genomewide binding sites of CASZ1b. The overexpression of CASZ1b in SMS-CTR cells led to a regional epigenetic modification.

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Genome-wide mapping of CASZ1 binding sites in differentiated SMS-CTR cells [Trametinib]

Project description:MEK inhibitor trametinib induces SMS-CTR cell differentiation and up-regulates CASZ1 expression. We identified genome-wide binding sites of CASZ1 in differentiated SMS-CTR cells.

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Biomarker Profile for Prediction of Response to SMAC Mimetic Monotherapy in Pediatric Precursor B-Cell Acute Lymphoblastic Leukemia

Project description:SMAC Mimetics (SMs) are currently being evaluated in clinical trials. Biomarkers are urgently needed for prediction of patient response to SMs. This study identified a characteristic gene expression pattern of SM sensitivity suitable for upfront identification of samples with high sensitivity to SMs.

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ChIP-seq analysis of human neuroblastoma cell lines

Project description:The aim of the experiment is to identify genome wide binding sites for the transcription factor MYCN in MYCN non-amplified and MYCN amplified human neuroblastoma cell lines. Datasets are presented for the ChIP-seq analysis in the tetracycline inducible cell line SH-SY5Y-MYCN (SH-SY5Y/6TR(EU)/pTrex-Dest-30/MYCN), derivative of the parental cell line SH-SY5Y; for noninduced cells and for 24 and 48 hours of Tet induction. Analysis for patinet matched MYCN amplified cell lines SMS-KCN and SMS-KCNR is also included.

2016-10-25 | E-MTAB-4100 | biostudies-arrayexpress

Microarray Expression Analysis of SIV infection of Sooty Mangabeys

Project description:Natural SIV infection of sooty mangabeys (SMs) does not progress to disease despite chronic virus replication. In contrast to pathogenic SIV infection of rhesus macaques (RMs), chronic SIV infection of SMs is characterized by low immune activation. To elucidate the mechanisms underlying this phenotype, we longitudinally assessed host gene expression in SIV-infected SMs and RMs. We found that acute SIV infection of SMs is consistently associated with a robust innate immune response, including widespread up-regulation of interferon-stimulated genes (ISGs). Our findings indicate that active immune regulatory mechanisms, rather than intrinsically attenuated innate immune responses, underlie the low immuneactivation of chronically SIV-infected SMs.

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Neuroblastoma cell lines

Project description:Untreated neuroblastoma cell lines SMS-KCN, SMS-KCNR, Kelly, and SH-SY5Y were sequenced on an Illumina GA IIx sequencer.

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Chromatin states and transcription factor binding in SIX1 deficient Rhabdomyosarcoma cells

Project description:Genetic and shRNA-mediated inhibition of SIX1 expression in RMS cells induces myogenic differentiation and impedes RMS tumor growth. To elucidate the mechanism by which SIX1 loss activates a differentiation program, we performed SIX1, MYOD1, and H3K27ac ChIPseq in two SIX1 knockdown SMS-CTR cell lines and one control SMS-CTR cell line to profile changes in transcriptional activity and myogenic transcription factor binding in fusion-negative Rhabdomyosarcoma.

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Gene expression profiling data from sooty mangabeys treated with interferon alpha

Project description:In contrast to pathogenic HIV and SIV infection of humans and macaques, SIV infection of sooty mangabeys (SMs) is typically non-pathogenic despite high virus replication. A key feature of primary SIV infection of SMs is a strong type I interferon (IFN-I) response, characterized by massive up-regulation of interferon-stimulated genes (ISG), followed by rapid resolution during the acute-to-chronic phase transition and establishment of an immune quiescent state that persists throughout the chronic infection. Based on these observations we hypothesized that low levels of IFN-I signaling may be instrumental in preventing chronic immune activation and disease progression in SIV-infected SMs. We used microarrays to characterize gene expression changes induced by IFNalpha treatment. To directly assess the effects of an experimentally-induced augmentation of IFN-I signaling in chronically SIV-infected SMs, we administered recombinant rhesus macaque IFNalpha2-IgFc (rmIFNα2) to eight naturally SIV-infected SMs weekly for 16 weeks and longitudinally monitored viral load, lymphocyte counts, immune activation, SIV-specific CD8+ T-cell responses, and gene expression profile. Administration of rmIFNα2 was bioactive in vivo with gene expression profiling revealing a strong upregulation of numerous ISGs in the blood of treated animals.

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