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CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

ABSTRACT: CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

PROVIDER: PRJNA485962 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7692121.fastq.gz	Fastqsanger.gz
	SRR7692122.fastq.gz	Fastqsanger.gz
	SRR7692123.fastq.gz	Fastqsanger.gz
	SRR7692124.fastq.gz	Fastqsanger.gz

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CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (mRNA)

Project description:Purpose: The purpose is to systemically identify RNA expression changes after lnc-Dpf3 knockdown in CCR7-stimulated mDCs Methods: We profiled RNA seq in mDCs transfected with si-Lnc-Dpf3 or si-NC and stimulated with or without CCR7 ligand CCL19 and CCL21. Results: CCR7 stimulation induced profound RNA expression changes in mDCs, and a set of genes were differentially expressed in lnc-Dpf3-knockdown DC

2020-05-25 | GSE118531 | GEO

CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (lncRNA)

Project description:CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (lncRNA)

| PRJNA485961 | ENA

CCR7L-inducible lnc-Dpf3 restrains dendritic cell migration by inhibiting HIF1α-mediated glycolysis (lncRNA)

Project description:Purpose: The purpose is to systemically identify long non-coding RNAs (lncRNAs) in CCR7 Ligands-stimulated mDCs Methods: We profiled lncRNA seq in mDCs stimulated with or without CCR7 ligand CCL19 and CCL21. Results: CCR7 stimulation induced profound lncRNAs expression in mDCs

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Project description:An experiment was performed to analyze the effect of knockdown of dpf3 during zebrafish embryogenesis.Morpholino against dpf3 and control morpholino were injected into eggs and eggs were kept under standard conditions for 72 hours. Embroys were harvested, total RNA was extracted and used for microarray analysis.

2008-08-01 | E-TABM-354 | biostudies-arrayexpress

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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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