Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Treatment of MM cells with non-targeting (NT) or ILF2 targeting oligonucleotide antisenses (ASOs)

ABSTRACT: Treatment of MM cells with non-targeting (NT) or ILF2 targeting oligonucleotide antisenses (ASOs)

PROVIDER: PRJNA793865 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17413218_1.fastq.gz	Fastqsanger.gz
	SRR17413218_2.fastq.gz	Fastqsanger.gz
	SRR17413219_1.fastq.gz	Fastqsanger.gz
	SRR17413219_2.fastq.gz	Fastqsanger.gz
	SRR17413220_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Treatment of MM cells with non-targeting (NT) or ILF2 targeting oligonucleotide antisenses (ASOs)

Project description:To gain insights into the molecular mechanisms by which myeloma cells overcome ILF2 ASO-induced DNA damage activation, we performed bulk RNA sequencing (RNA-seq) analysis of ASO-treated KMS11 and JJN3 cells at early (1 week) and late (3 weeks) treatment time points.

2023-11-28 | GSE192944 | GEO

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

G-rich motifs within phosphorothioate-based antisense oligonucleotides (ASOs) drive activation of FXN expression through indirect effects

Project description:Evaluation of the effect of 3 ASOs targeting FXN on mRNA levels

2022-10-28 | GSE205526 | GEO

Microarray of NFAT1-shRNA (KD) vs Non-targeting shRNA (NT) metastatic melanoma cell line

Project description:The metastatic melanoma cell line A375SM was stably transduced with NFAT 1 shRNA utilizing the pSIH-HI- 5 copGFP lentiviral vector. A non-targeting (NT) shRNA construct with no known homology to any human gene was was created and transduced into A375SM cells as a control. These two sets of cells were then subjected to microarray profiling using the Human OneArray microarray (version HOA 6.1, GEO Platform GPL19137) from Phalanx Biotech Group. NFAT shRNA A375SM cells vs. NT-shRNA A375SM cells were subjected to microarray analysis. 3 biological replicates for each cell type were used.

2016-01-06 | E-GEOD-76541 | biostudies-arrayexpress

Antisense oligonucleotide-mediated inclusion of the TRA2β ultraconserved poison exon induces the expression of a lncRNA with anti-tumor effects

Project description:Dysregulated expression of oncogenic splicing factors (SFs) occurs in human tumors in part through alterations in splicing of poison exons (PE), highly conserved exons that trigger RNA degradation. TRA2β is one such SF that undergoes PE suppression in tumor cells. Therefore, manipulation of TRA2β-PE can be a promising therapeutic strategy for cancer. Here, we demonstrate that low TRA2β-PE inclusion correlates with decreased patient survival across multiple tumor types. TRA2β-PE-targeting antisense oligonucleotides (ASOs) induce anti-cancer phenotypes and widespread transcriptomic alterations in cell culture models by causing both TRA2β protein knockdown and upregulation of TRA2β-PE-containing transcripts, which act as long-noncoding RNAs (lncRNAs) to sequester nuclear proteins. Finally, we demonstrate efficacy of TRA2β-PE-targeting ASOs in preclinical 3D organoid and in vivo patient-derived xenograft models. Together, this demonstrates that oncogenic SFs can be drugged using PE-targeting ASOs and elucidates a mechanism by which the TRA2β-PE acts both as a regulator of TRA2β protein expression and as a lncRNA that controls cancer cell growth.

2024-12-20 | PXD042941 | Pride

Expression analysis of Huh-7 cells treated with LNA gapmer targeting glucocorticoid receptor (GR) RNA

Project description:Antisense oligonucleotide (ASO) has the potential to induce off-target effects due by inadvertent binding of ASOs to unintended RNAs that have a sequence similar to the target RNA. In the present study, we focused on the effects of oligonucleotide extension of gapmer ASOs on off-target effects. We performed microarray analysis using Huh-7 cells (human liver-derived cells) treated with a 14-mer LNA gapmer ASO and the extended 18-mer derivatives with the same core 14-mer region.

2021-12-15 | GSE188684 | GEO

Beauveria bassiana strain:NT | isolate:sp | breed:NT | cultivar:NT

Project description:Beauveria bassiana strain:NT | isolate:sp | breed:NT | cultivar:NT Transcriptome or Gene expression

| PRJNA450457 | ENA

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

Oligonucleotide-based arrayCGH

Project description:Oligonucleotide-based arrayCGH

| PRJNA92921 | ENA

Off target expression data from iPSC derived microglia treated with APOE/TREM2 ASOs for 24h/48h. The iPSC cells are from a wild type donor (BIONi10C).

Project description:Microglia play important roles in maintaining brain homeostasis and neurodegeneration. The discovery of genetic variants in genes predominately or exclusively expressed in myeloid cells, factors for Alzheimer’s disease (AD) highlights the importance of microglial biology in the brain. such as Apolipoprotein E (APOE) and triggering receptor expressed on myeloid cells 2 (TREM2), as the strongest risk factors for Alzheimer’s disease (AD) highlights the importance of microglial biology in the brain. The sequence, structure and function of several microglial proteins are poorly conserved across species, which has hampered the development of strategies aiming to modulate the expression of specific microglial genes. One way to target APOE and TREM2 is to modulate their expression using antisense oligonucleotides (ASOs). In this study, we identified selective and potent ASOs for human APOE and TREM2. We proved their efficacy in human iPSC microglia in vitro, as well as their pharmacological activity in vivo in a xenografted microglia model. We demonstrate ASOs targeting human microglia can modify their transcriptional profile and their response to amyloid-b plaques in vivo in a model of AD. This study is the first proof-of-concept that human microglial can be modulated using ASOs in a dose-dependent manner to manipulate microglia phenotypes in vivo. Since ASOs can have off-target effects, besides the expected decrease of APOE and TREM2 mRNA, this microarray was performed to determine the off-target profiles of the ASOs. iPSC derived microglia were treated with the ASOs with 1.25uM and 20uM dosages, and the compounds were incubated either 24hours or 48hours.

2024-04-24 | GSE243243 | GEO

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