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Regulation of influenza A virus infection by Lnc-PINK1-2:5

ABSTRACT: A549 cells were transduced with a lentivirus expressing lnc-PINK1-2:5 at a MOI of 200 for 48 h. The cells were then infected with PR/8 at a MOI of 0.01 for 48 h. RNA-seq was done on the RNA samples from three vector control and three lnc-PINK1-2:5-overexpressing cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179747 | GEO | 2021/07/13

REPOSITORIES: GEO

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Regulation of influenza A virus infection by Lnc-PINK1-2:5

Project description:Regulation of influenza A virus infection by Lnc-PINK1-2:5

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Project description:In previous study we found that Lnc-URIDS increased in diabetic dermal fibroblast and delayed wound healing.To further verify the roles of lnc-URIDS in fibroblast during wound heaing, A lnc-URIDS shRNA lentivirus and a control lentivirus were transfected into rat dermal fibroblast respectively (three independent replicates for each group) for 48h. Then, differential expressed genes between Control fibroblast and Lnc-URIDS knockdown fibroblast were detected by using microarray expression profiling though Agilent rat 4 x 44K gene expression microarrays (Agilent Technologies, Santa Clara, CA) .

2022-09-24 | GSE214034 | GEO

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

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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Transcriptional profile of pink1 mutant flies

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Project description:Loss of function in the PTEN-induced kinase 1 gene (Pink1) causes an early-onset, autosomal recessive form of PD. The translational Pink1-/- rat shows cranial sensorimotor deficits including: declines in ultrasonic vocalization, negative impacts on social vocal function, and alterations to thyroarytenoid muscle structure. The aim of this study was to identify differentially expressed genes using RNA-sequencing and bioinformatic analysis of the thyroarytenoid muscle of male Pink1-/- rats compared to wildtype controls. To construct gene co-expression networks and gene modules, a WGCNA was used to identify biological networks of interest including where Pink1 was a central node with interconnecting genes. Data are congruent with previous findings demonstrating changes to thyroarytenoid muscle structure. These data are consistent with the hypothesis that differences in peripheral biology may influence the early pathogenesis of vocalizations at the level of the thyroarytenoid muscle.

2020-05-27 | GSE151209 | GEO

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Project description:To investigate the PINK1 regulates mitochondrial function, we performed the gene expression data for two independent libraries for Pink1-/- and Pink1+/+ mice, at two different time points, 4 and 24 months.

2023-05-16 | GSE217775 | GEO

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