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PolyA site sequencing (PAS-seq) analysis of Hela cells treated with NC ASO or snoRD50a ASOs

ABSTRACT: polyA site sequencing (PAS-seq) analysis of Hela cells treated with NC ASO or snoRD50a ASOs

PROVIDER: PRJEB19851 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1869551.fastq.gz	Fastqsanger.gz
	ERR1869552.fastq.gz	Fastqsanger.gz
	ERR1869553.fastq.gz	Fastqsanger.gz
	ERR1869554.fastq.gz	Fastqsanger.gz
	ERR1869555.fastq.gz	Fastqsanger.gz

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polyA site sequencing (PAS-seq) analysis of Hela cells treated with NC ASO or snoRD50a ASOs

Project description:Our RNA-seq experiment (E-MTAB-5383) and subsequent in vitro analysis suggested that snoRD50a is a trans-acting RNA that can function in mRNA 3' processing. To test this hypothesis at transcriptomic level, we performed PAS-seq experiments to compare the polyA+ transcripts profile between negative control ASO (nc ASO) and snoRD50a ASO treated Hela cells, ASO (antisense oligonucletode) technique is a commonly used technique to deplete nuclear RNAs. snoRD50a ASO is used to deplete endogenous snoRD50a. See related experiments: E-MTAB-5383; E-MTAB-5384.

2017-05-31 | E-MTAB-5389 | biostudies-arrayexpress

PolyA site sequencing (PAS-seq) analysis of Hela cells treated with NC ASO or snoRD50a ASOs

Project description:Our RNA-seq experiment and subsequent in vitro analysis suggested that snoRD50a is a trans-acting RNA that can function in mRNA 3' processing. To test this hypothesis at transcriptomic level, we performed PAS-seq experiments to compare the polyA+ transcripts profile between negative control ASO (nc ASO) and snoRD50a ASO treated Hela cells

2017-07-01 | GSE98219 | GEO

Fip1 iCLIP-seq in Hela cells without treatment or treated with negative control anti-sense oligos (ASO) or snoRD50a ASO to study how snoRD50a affects Fip1/RNA interaction in mRNA 3' processing

Project description:We aimed to discover trans-acting RNA molecules involved in mRNA 3 processing. We reasoned that, if there exist such functional RNAs, they must directly associate with the key machinery responsible for mRNA 3 processing. Therefore, it would be of great value to comprehensively identify RNAs interacting with pre-mRNA 3 processing complex. To this goal, we took advantage of previously well-characterized system combined with high-throughput sequencing to investigate the target RNAs at the transcriptomic level. Fip1 protein is an essential mRNA 3' processing factor. Our in vitro data suggested that snoRD50a affects Fip1/RNA interaction in SV40 late (SVL) polyA site 3' processing. To determine whether snoRD50a influences Fip1/RNA interaction at transcriptomic level in vitro, we performed Fip1 iCLIP-seq experiments in Hela cells transfected with control NC ASO (negative control anti-sense DNA) or snoRD50a ASO.

2017-06-01 | E-MTAB-5384 | biostudies-arrayexpress

HTS-Seq analysis of Hela cells treated with NC ASO or snoRD50a ASOs

Project description:HTS-Seq analysis of Hela cells treated with NC ASO or snoRD50a ASOs

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Project description:PolyA site sequencing (PAS-seq) analysis of Hela cells treated with NC ASO or snoRD50a ASOs

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Fip1 iCLIP-seq in Hela cells without treatment or treated with NC ASO, snoRD50a ASO

Project description:Fip1 iCLIP-seq in Hela cells without treatment or treated with NC ASO, snoRD50a ASO

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Fip1 iCLIP-seq in Hela cells without treatment or treated with NC ASO, snoRD50a ASO

Project description:We aimed to compare the Fip1/RNA interaction at transcriptomic level upon snoRD50a knockdown. To this goal, we utilized Fip1 iCLIP-seq protocol in both control and snoRD50a KD hela cells.

2017-07-01 | GSE98220 | GEO

Expression analysis of mice hepatic NMuLi cells treated LNA gapmer ASO containing nucleobase modification

Project description:Antisense oligonucleotide (ASO) has the potential to induce hybridization-dependent effects by inadvertent binding of ASOs to RNA with sequences similar to that of the target RNA. In the present study, we examined the effects of the nucleobase derivatives introduced into the gapmer ASOs on gene expression. We performed microarray analysis using NMuLi cells (mouse liver-derived cells) treated with LNA gapmer ASO containing nucleobase modification.

2022-07-12 | GSE197166 | GEO

PolyA Sequencing of K562 Cells

Project description:RNA chemical structure analysis using icSHAPE and icLASER reveals hexameric sequences that have structure differences inside and outside of cells. One such sequence that had higher in-cell reactivity was the sites of polyadenylation or PAS sequence within the 3’-UTRs. We aimed to understand this difference as we postulated it could be utilized to predict transcriptome-wide polyadenylation. To obtain direct positions with high polyadenylation sequence signal, we generated the first polyadenylation sequencing data (PAS-seq) for K562 cells. PAS-seq uses polyA tail priming to identify the sites of polyA tail selection directly. Inspection of PAS reads demonstrated clear buildup of read depth at the 3’-end of transcripts and we obtained sites of high PAS read depth and low PAS read depth.

2021-08-04 | GSE145400 | GEO

Targeted ASO-mediated Atp1a2 knockdown in astrocytes reduces SOD1 aggregation and accelerates disease onset in mutant SOD1 mice

Project description:Astrocyte-specific ion pump α2-Na+/K+-ATPase plays a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS). Here, we test the effect of Atp1a2 mRNA-specific antisense oligonucleotides (ASOs) to induce α2-Na+/K+-ATPase knockdown in the widely used ALS animal model, SOD1*G93A mice. Two ASOs led to efficient Atp1a2 knockdown and significantly reduced SOD1 aggregation in vivo. Although Atp1a2 ASO-treated mice displayed no off-target or systemic toxicity, the ASO-treated mice exhibited an accelerated disease onset and shorter lifespan than control mice. Transcriptomics studies reveal downregulation of genes involved in oxidative response, metabolic pathways, trans-synaptic signaling, and upregulation of genes involved in glutamate receptor signaling and complement activation, suggesting a potential role for these molecular pathways in de-coupling SOD1 aggregation from survival in Atp1a2 ASO-treated mice. Together, these results reveal a role for α2-Na+/K+-ATPase in SOD1 aggregation and highlight the critical effect of temporal modulation of genetically validated therapeutic targets in neurodegenerative diseases.

2023-11-30 | GSE196843 | GEO

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