Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Precision RNAi using synthetic shRNAmir target sites

ABSTRACT: Precision RNAi using synthetic shRNAmir target sites

PROVIDER: PRJNA904685 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22389900.fastq.gz	Fastqsanger.gz
	SRR22389901.fastq.gz	Fastqsanger.gz
	SRR22389902.fastq.gz	Fastqsanger.gz
	SRR22389903.fastq.gz	Fastqsanger.gz
	SRR22389904.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 60

Similar Datasets

Precision RNAi using synthetic shRNAmir target sites

Project description:Precision RNAi using synthetic shRNAmir target sites

| PRJNA903783 | ENA

Precision RNAi using synthetic shRNAmir target sites

Project description:Loss-of-function genetic tools are widely applied for validating therapeutic targets, but their utility remains limited by incomplete on- and uncontrolled off-target effects. We describe artificial RNA interference (ARTi) based on synthetic, ultra-potent, off-target-free shRNAs that enable efficient, inducible, and reversible suppression of any gene upon introduction of a synthetic target sequence into non-coding transcript regions. ARTi establishes a scalable loss-of-function tool with full control over on- and off-target effects.

2023-07-04 | GSE218617 | GEO

Precision RNAi using synthetic shRNAmir target sites

2023-07-04 | GSE218404 | GEO

Precision RNAi using synthetic shRNAmir target sites.

Project description:Loss-of-function genetic tools are widely applied for validating therapeutic targets, but their utility remains limited by incomplete on- and uncontrolled off-target effects. We describe artificial RNA interference (ARTi) based on synthetic, ultra-potent, off-target-free shRNAs that enable efficient and inducible suppression of any gene upon introduction of a synthetic target sequence into non-coding transcript regions. ARTi establishes a scalable loss-of-function tool with full control over on- and off-target effects.

| S-EPMC10409502 | biostudies-literature

Synthetic lethality-mediated precision oncology via the tumor transcriptome

Project description:Synthetic lethality-mediated precision oncology via the tumor transcriptome

| PRJNA700986 | ENA

Epigenome analysis of dnmt target sites

Project description:Epigenome analysis of dnmt target sites

| PRJNA282482 | ENA

Precision RNA Base Editing in Plant Organelles Using Engineered Synthetic P-type PPR Editing Factors

Project description:RNA editing, particularly cytidine-to-uridine conversions in plant organelles, plays a crucial role in regulating gene expression. While natural PLS-type PPR proteins are specialized in this process, synthetic PPR proteins offer significant potential for targeted RNA editing. In this study, we engineered chimeric editing factors by fusing synthetic P-type PPR guides with the DYW cytidine deaminase domain from a moss mitochondrial editing factor, PPR56. These designer PPR editors (dPPRe) were tested in Escherichia coli and Nicotiana benthamiana chloroplasts and mitochondria, demonstrating efficient and precise de novo RNA editing. Transcriptome-wide analysis of the most efficient chloroplastic dPPRe revealed minimal off-target effects, with only three non-target C sites edited due to sequence similarity with the intended target. This study introduces a novel and precise method for RNA base editing in plant organelles, paving the way for new approaches in gene regulation applicable to plants and potentially other organisms.

2025-04-17 | GSE276199 | GEO

The translational repair pathway is a frequent synthetic lethal target in cancer

Project description:Synthetic lethality exploits the genetic vulnerabilities of cancer cells enabling, a targeted, precision approach to treat cancer. Synthetic lethal discovery approaches have led to clinical successes of PARP inhibitors and the progression of several next-generation therapeutic targets such as WRN, USP1, PKMYT1, POLQ, and PRMT5 into the clinic. To date, however, most discovery efforts in the synthetic lethal space have focused on DNA repair. Here, we show, for the first time in humans, a frequent synthetic lethal interaction between two complexes of the translational repair pathway, PELO/HBS1L and the superkiller (SKI) complex. In distinct genetic contexts, either in 9p21.3 (FOCAD) deleted or MSI-H tumors, we found that phenotypically destabilized SKI complex leads to dependence on the PELO/HBS1L ribosomal rescue complex. We estimate that 20% of all tumors have a destabilized SKI complex. The concomitant loss of PELO in a SKI destabilized tumor drives an unfolded protein stress response, cell cycle arrest, and robust tumor growth inhibition. Furthermore, we demonstrate that the loss of HBS1L phenocopies PELO loss, presenting a second potential therapeutic target within the rescue complex. Our results indicate that PELO/HBS1L represent novel therapeutic targets whose dependence converges upon SKI complex destabilization, a common phenotypic biomarker in diverse genetic contexts and a significant patient population.

2024-10-14 | GSE261804 | GEO

Nm-seq finds thousands of modified 2’-O-methylation sites in mRNA with base precision

Project description:Nm-seq maps 2'-O-methylation sites in human mRNA with base precision The ribose of rna nucleotides can be 2′-O-methylated (nm). despite advances in high-throughput detection, the inert chemical nature of nm still limits sensitivity and precludes mapping in mrna. We leveraged the differential reactivity of 2′-O-methylated and 2′-hydroxylated nucleosides to periodate oxidation to develop nm-seq, a sensitive method for transcriptome-wide mapping of nm with base precision. nm-seq uncovered thousands of nm sites in human mrna with features suggesting functional roles.

2017-05-15 | GSE90164 | GEO

synSTARR-seq with Glucocorticoid Receptor synthetic binding sites in GR18 cell line

Project description:We performed STARR-seq with synthetic libraries (synSTARR-seq) in GR18 cell line (derived from U2OS ATTC:HTB-96, stably transfected with an expression construct for GR), upon glucocorticoid (dexamethasone) or vehicle (ethanol) treatment. The synthetic libraries are variants of the glucocorticoid receptor binding sites (GBS). The "GBS half site" library contains 8 consecutive randomized nucleotides within the core binding sites, while the "Cgt/Sgk library" contains 5 consecutive randomized nucleotides on the flank of the GBS.

2018-10-29 | E-MTAB-6737 | biostudies-arrayexpress

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