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Mus musculus

ABSTRACT: Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination (RNA-Seq of differentiated NSC after lnc-OPC knockdown)

PROVIDER: PRJNA301058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2927275_1.fastq.gz	Fastqsanger.gz
	SRR2927275_2.fastq.gz	Fastqsanger.gz
	SRR2927276_1.fastq.gz	Fastqsanger.gz
	SRR2927276_2.fastq.gz	Fastqsanger.gz
	SRR2927277_1.fastq.gz	Fastqsanger.gz

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Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination (RNA-Seq of differentiated NSC after lnc-OPC knockdown)

Project description:To quantitative analysis of transcriptome changes caused by lnc-OPC knockdown during OPC differentiation from NSC, lentivirus-based short hairpin RNAs were used to knockdown the lnc-OPC expression in a neural stem cell culture . Subsequently, puromycin-selected NSCs were differentiated to OPC in culture for three days.RNA-Seq was performed on the polyadenylated fraction of RNA isolated from cell samples. DEseq was used for differential gene expression analysis caused by lnc-OPC knockdown. GO functional term enrichment analysis of differential gene expression caused by lnc-OPC knockdown, revealed significant enrichment of âoligodendrocyte developmentâ, âoligodendrocyte differentiationâ, âglia cell developmentâ, and âaxon ensheathmentâ terms that are associated with oligodendrogenesis. mRNA profiles of differentiiated NSC samples after lnc-OPC knockdown by RNA-sequencing.

2015-11-04 | E-GEOD-74647 | biostudies-arrayexpress

Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination (RNA-Seq of differentiated NSC after lnc-OPC knockdown)

Project description:To quantitative analysis of transcriptome changes caused by lnc-OPC knockdown during OPC differentiation from NSC, lentivirus-based short hairpin RNAs were used to knockdown the lnc-OPC expression in a neural stem cell culture . Subsequently, puromycin-selected NSCs were differentiated to OPC in culture for three days.RNA-Seq was performed on the polyadenylated fraction of RNA isolated from cell samples. DEseq was used for differential gene expression analysis caused by lnc-OPC knockdown. GO functional term enrichment analysis of differential gene expression caused by lnc-OPC knockdown, revealed significant enrichment of ‘oligodendrocyte development’, ‘oligodendrocyte differentiation’, ‘glia cell development’, and ‘axon ensheathment’ terms that are associated with oligodendrogenesis.

2015-11-04 | GSE74647 | GEO

Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination

Project description:Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination

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Project description:Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination (RNA-Seq of mouse neural stem cells)

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Project description:Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination (OLIG2 Chromatin immunoprecipitation sequencing (ChIP-Seq) in mouse neural stem cells)

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lnc-EAPV binding proteins in C57BL/6J BMDMs

Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.

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