Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation

ABSTRACT: PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation

PROVIDER: PRJNA1046501 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR26988323.fastq.gz	Fastqsanger.gz
	SRR26988324.fastq.gz	Fastqsanger.gz
	SRR26988325_1.fastq.gz	Fastqsanger.gz
	SRR26988325_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 52

Similar Datasets

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [iCLIP]

Project description:PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [iCLIP]

| PRJNA1046504 | ENA

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [Polysome profiling]

Project description:PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [Polysome profiling]

| PRJNA1231450 | ENA

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [CUT&RUN]

Project description:PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [CUT&RUN]

| PRJNA1231449 | ENA

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [RNA-seq]

Project description:PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [RNA-seq]

| PRJNA1046505 | ENA

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [iCLIP]

Project description:Pseudouridine (Y) is the most widespread RNA modification type on cellular RNAs and is dynamically catalyzed by a family of Y synthases (PUSes) in response to pathophysiological cues. PUS10 has been previously shown to regulate miRNA biogenesis in addition to modifying tRNAs, however its role in adapting gene expression to stress remains elusive. Here, we establish a novel role for PUS10 as a regulator of LTR retrotransposon-driven inflammatory response. Using Pus10 KO mice, we demonstrate that Pus10 depletion leads to upregulation of interferon-stimulated genes (ISGs) and increased resistance to viral infection in vitro and in vivo. Mechanistically, PUS10 regulates a subset of 5’-derived tRNA (tdR) fragment, 5’ tdR Gly-GCC, that via targeting specific LTR retroelements modulates RNA-DNA hybrids accumulation and cGAS/STING/IRF3 pathway. Importantly, reduced PUS10 activity correlate with chronic autoimmune conditions, pinpointing PUS10 as a potential contributor to human immune regulation.

2025-06-13 | GSE248956 | GEO

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [small RNA-seq]

Project description:PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [small RNA-seq]

| PRJNA1046506 | ENA

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [CUT&RUN]

2025-06-13 | GSE291044 | GEO

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [Polysome profiling]

2025-06-13 | GSE291043 | GEO

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation [small RNA-seq]

2025-06-13 | GSE248958 | GEO

PUS10-induced tRNA fragmentation impacts retrotransposon-driven inflammation

Project description:Pseudouridine synthases (PUSs) catalyze the isomerization of uridine (U)-to-pseudouridine (Ψ) and have emerging roles in development and disease. How PUSs adapt gene expression under stress remains mostly unexplored. We identify an unconventional role for the Ψ “writer” PUS10 impacting intracellular innate immunity. Using Pus10 knock-out mice, we uncover cell-intrinsic upregulation of interferon (IFN) signalling, conferring resistance to inflammation in vivo. Pus10 loss alters tRNA-derived small RNAs (tdRs) abundance, perturbing translation and endogenous retroelements expression. We found one of the differentially expressed tDRs is derived from tRNA glycine (tDR Gly). To delinate the tDR Gly interactome, we employed an optimized pull-down strategy using PUS10 KO cells followed by data-independent acquisition-based quantitative mass spectrometry analysis.

2025-05-27 | PXD061235 | 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