Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

ABSTRACT: Small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

PROVIDER: PRJEB26666 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2572830.fastq.gz	Fastqsanger.gz
	ERR2572831.fastq.gz	Fastqsanger.gz
	ERR2572832.fastq.gz	Fastqsanger.gz
	ERR2572833.fastq.gz	Fastqsanger.gz
	ERR2572834.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

Preliminary small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

Project description:Preliminary small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

| PRJEB26664 | ENA

Small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

Project description:Proliferation of tumor cells transfected with ASO-1537S is inhibited compared to controls. The aim of the experiment is to determine changes in microRNA expression profiles with treatment, compared to controls, using 3 biological replicates for each condicition.

2023-06-02 | E-MTAB-6768 | biostudies-arrayexpress

Preliminary small RNAseq of human breast cancer cell line MDA-MB-231 transfected with antisense oligonucleotide 1537S (ASO-1537S), compared to control oligonucleotide (ASO-C) and untreated cells

2023-06-02 | E-MTAB-6762 | biostudies-arrayexpress

Heart RNA-seq of therapeutic RBM20 antisense oligonucleotide (ASO) treatment in a mouse model of heart failure with preserved ejection fraction (HFpEF)

Project description:We report the heart RNA-sequencing of control animals and animals of a mouse model of heart failure treated or not with RBM20 antisense oligonucleotide. This study aims to investigate the therapeutic effect of antisense oligonucleotide (ASO)-mediated downregulation of the cardiac splice factor RBM20 in a mouse model of heart failure with preserved ejection fraction. 8-week old wild type and titin N2B KO mice with increased wall stiffness were subcutaneously injected with 50 mg/kg/week RBM20 ASO for 8 weeks. RNA from 4 left ventricles per group were isolated using TRIzol followed by a clean-up with the QIAGEN RNA micro kit. The cDNA libraries were generated using the Illumina TruSeq Stranded mRNA LT Sample Prep Kit and 2x150 paired end sequenced on HiSeq4000. The RNA-Sequencing analysis confirms that RBM20 ASO treatment increased the expression of compliant titin isoforms and improved impaired ventricular filling and cardiac function. RNA-seq confirmed RBM20 dependent isoform changes of known targets such as Titin, Ldb3, Camk2d, and Ank3, and served as a sensitive indicator of potential side effects, largely limited to genes related to the immune response.

2021-12-06 | E-MTAB-9361 | biostudies-arrayexpress

Antisense oligonucleotide activity in tumour cells is influenced by intracellular LBPA distribution and 6 extracellular vesicles recycling

Project description:Next generation modified antisense oligonucleotides (ASOs) are commercially approved new therapeutic modalities, yet poor productive uptake and endosomal entrapment in tumour cells limit their broad application. We compared intracellular traffic of anti KRAS antisense oligonucleotide (AZD4785) in good and poor productive uptake tumour cells, PC9 and LK2 respectively. We found that the majority of AZD4785 is rapidly delivered to CD63+ late endosomes (LE) in both cell lines. Importantly, lysobisphosphatidic acid (LBPA) that triggers ASO LE escape is presented in CD63+ LE in PC9 but not in LK2 cells. Moreover, both cells recycle AZD4785 in the extracellular vesicles (EVs) however AZD4785 quantification by advanced mass spectrometry and proteomic analysis revealed that LK2 recycles more AZD4785 and RNA-binding proteins. Finally, stimulating LBPA intracellular production or blocking EV recycling enhanced AZD4785 activity in LK2 but not in PC9 cells thus offering novel strategy to possibly enhance ASO potency in poor productive uptake tumour cells.

2021-11-10 | PXD027804 | Pride

Antisense oligonucleotide therapy for calmodulinopathy

Project description:Calmodulinopathies are rare inherited arrhythmia syndromes caused by dominant gain of function variants in one of three genes, CALM1, CALM2, and CALM3, which each encode the identical calmodulin (CaM) protein. We hypothesized that antisense oligonucleotide (ASO)-mediated depletion of an affected calmodulin gene would ameliorate disease manifestations, while the other two calmodulin genes would preserve CaM level and function. Here we tested this hypothesis using human induced pluripotent stem cell-derived cardiomyocyte (iPSC-CM) and mouse models of CALM1 pathogenic variants. Human CALM1F142L/+ iPSC-CMs exhibited prolonged action potentials, modeling congenital long QT syndrome. CALM1-depleting ASOs did not alter CaM protein level and normalized repolarization of CALM1F142L/+ iPSC-CMs. Similarly, an ASO targeting murine Calm1 depleted Calm1 transcript without affecting CaM protein level. This ASO alleviated drug-induced arrhythmia in CalmN98S/+ mice without causing observable toxicity. These results provide proof-of-concept that ASOs targeting individual calmodulin genes are potentially effective and safe therapies for calmodulinopathies.

2024-06-13 | GSE245945 | GEO

Antisense oligonucleotide therapy for calmodulinopathy

Project description:Antisense oligonucleotide therapy for calmodulinopathy

| PRJNA1030420 | ENA

The transcriptome profile after antisense L1 ASO treatment [ssRNA-Seq]

Project description:We performed RNA-seq assay in Scramble ASO and antisense Mus1_L1 ASO treated AML12 cells to reveal the trscriptiome associated with MATR3 protein. The libraries were constructed by ribosome-depleted and strand-specific kits.

2023-06-28 | GSE228646 | GEO

Microarray analysis of in vivo inhibition of mir-122 with an antisense oligonucleotide.

Project description:Current understanding of microRNA (miRNA) biology is limited, and antisense oligonucleotide (ASO) inhibition of miRs is a powerful technique for their functionalization. To uncover the role of the liver-specific miR-122 in the adult liver, we inhibited it in vivo using a 2’-O-methoxyethyl phosphorothioate ASO. This microrarray experiment was used to identify changes in mRNA levels due to the inhibition of miR-122 that accompanied phenotypic observations of reduced cholesterol and triglycerides, increased fatty acid oxidation, and decreased fatty acid and cholesterol synthesis rates observed in hepatocytes. Keywords: single treatment vs. control

2006-03-01 | GSE3603 | GEO

Profiling the interactome of oligonucleotide drugs by proximity biotinylation

Project description:Drug-ID applies proximity biotinylation to identify drug-protein interactions inside living cells. The covalent conjugation of a drug molecule with a biotin ligase enables targeted biotinylation of the drug-bound proteome and its identification by SILAC-MS/MS. We investigate the interactome of two well-known small molecule drugs, JQ1 and SAHA, and applied it for the identification of the interactome of RNaseH-recruiting antisense oligonucleotides (ASO). Drug-ID allows to de novo profile the drug-protein interactome under native conditions, directly inside living cells and at the pharmacologically effective concentration of the drug using minimal amount of input material. We apply the technology to study the dose-dependent aggregation of ASOs and the effect of different wing chemistries (LNA, Fluoro, MOE) and ASO lengths on the ASO-protein interactome. Finally, we demonstrate the detection of stress-induced interactome changes (Actinomycin D treatment) in living cells. Particularly broadly applicable in the field of oligonucleotide therapeutics is the in situ variant of the approach, which uses a recombinant biotin ligase and does not require genetic manipulation of the target cell.

2024-01-09 | PXD045992 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data