Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RIP-seq of NAT10 interacted cellular and KSHV transcripts in iSLK-KSHV cells

ABSTRACT: RIP-seq of NAT10 interacted cellular and KSHV transcripts in iSLK-KSHV cells

PROVIDER: PRJNA727481 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14428123_1.fastq.gz	Fastqsanger.gz
	SRR14428123_2.fastq.gz	Fastqsanger.gz
	SRR14428124_1.fastq.gz	Fastqsanger.gz
	SRR14428124_2.fastq.gz	Fastqsanger.gz
	SRR14428125_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

RIP-seq of NAT10 interacted cellular and KSHV transcripts in iSLK-KSHV cells

Project description:Flag-RIP-seq was performed in NAT10-Flag overexpressing iSLK-KSHV cells.

2023-09-27 | GSE173889 | GEO

ac4C-seq of cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV (i.e. iSLK-RGB), iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells

Project description:We used ac4C-seq to detedc cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV, iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells after after doxycycline and sodium butyrate treatment.

2023-09-27 | GSE174161 | GEO

ac4C-seq of cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV (i.e. iSLK-RGB), iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells

Project description:ac4C-seq of cellular and KSHV transcripts in iSLK-Puro, iSLK-KSHV (i.e. iSLK-RGB), iSLK-KSHV (WT), iSLK-KSHV (ΔNAT10) cells

| PRJNA728653 | ENA

Lactylation of NAT10 promotes N4‐acetylcytidine modification on tRNASer-CGA-1-1 to boost oncogenic DNA virus KSHV reactivation

Project description:N4-acetylcytidine (ac4C), a conserved but recently rediscovered RNA modification on tRNAs, rRNAs and mRNAs, is catalyzed by N-acetyltransferase 10 (NAT10). Lysine acylation is a ubiquitous protein modification that controls protein functions. Our latest study demonstrates a NAT10-dependent ac4C modification, which occurs on the polyadenylated nuclear RNA (PAN) encoded by oncogenic DNA virus Kaposi's sarcoma-associated herpesvirus (KSHV), can induce KSHV reactivation from latency and activate inflammasome. However, it remains unclear whether a novel lysine acylation occurs in NAT10 during KSHV reactivation and how this acylation of NAT10 regulates tRNAs ac4C modification. Here, we showed that NAT10 was lactylated by α-tubulin acetyltransferase 1 (ATAT1), as a writer at the critical domain, to exert RNA acetyltransferase function and thus increase the ac4C level of tRNASer-CGA-1-1. Mutagenesis at the ac4C site in tRNASer-CGA-1-1 inhibited its ac4C modifications, translation efficiency of viral lytic genes, and virion production. Mechanistically, KSHV PAN orchestrated NAT10 and ATAT1 to enhance NAT10 lactylation, resulting in tRNASer-CGA-1-1 ac4C modification, eventually boosting KSHV reactivation. Our findings reveal a novel post-translational modification in NAT10, as well as expand the understanding about tRNA-related ac4C modification during KSHV replication, which may be exploited to design therapeutic strategies for KSHV-related diseases.

2024-06-17 | GSE248740 | GEO

ac4C RIP-seq analysis of AGS cells upon NAT10 knockout.

Project description:N4-acetylcytidine (ac4C), a conserved chemical modification in eukaryotic prokaryotes that is catalyzed by the N-acetyltransferase 10 (NAT10) enzyme, plays a crucial role in promoting mRNA stability and translation. However, the biological function and mechanisms of NAT10-mediated ac4C in human cancer were poorly defined. In order to investigate the regulatory mechanism of NAT10 in gastric cancer, we performed ac4C RIP-seq(acRIP-seq) analysis in AGS cells with NAT10 knockout compared with control in two repeats.

2024-07-07 | GSE180494 | GEO

Lactylation of NAT10 promotes N4‐acetylcytidine modification on tRNASer-CGA-1-1 to boost oncogenic DNA virus KSHV reactivation

2024-04-26 | PXD049447 |

RIP-PEN-SHAPE-MaP for 15.5K-interacted RNAs

Project description:RIP-PEN-SHAPE-MaP for 15.5K-interacted RNAs

| PRJNA909819 | ENA

RIP-PEN-SHAPE-MaP for 15.5K-interacted RNAs

Project description:RNA secondary structure is crucial for RNA mentalism, including transcription, splicing, translation, RNA-binding protein interaction as well as turnover. The kink-turn (K-turn) structure motif is is an RNA three-dimensional (3D) structure that exists in all three primary phylogenetic domains and plays vital roles in RNA metabolism. In order to investigate the K-turn secondary structure in vivo, we combined SHAPE-Map and our RIP-PEN-seq to profile the RNA structure of 15.5K-interacted RNAs.

2023-04-10 | GSE220470 | GEO

scRNAseq analysis of lytically and latently infected KSHV-infected iSLK.219 cells with and without caspase inhibitor treatment

Project description:The goal of this analysis was to examine the cell-to-cell variation in Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation and type I interferon response after caspase inhibitor treatment. We profiled the levels of host and viral mRNAs at a single-cell level using the iSLK.219 tissue culture model system (Myoung and Ganem, 2011). We examined gene expression in lytically reactivating cells, lytically reactivating cells treated with caspase inhibitors, and lytically reactivating cells treated with casapse inhibitors and neutralizing antibodies against interferons. (we previously described that caspase inhibitors elicit an interferion response in KSHV-infected cells, Tabtieng et al., 2018). We also examined gene expression in a mixture of latently infected cells and uninfected cells as a control.

2022-09-29 | GSE190558 | GEO

Nuclesome Distribution data for KSHV reactivation

Project description:iSLK.219 cells at 0, 6, 12, 24, and 48 hours post KSHV reactivation. Nucleosome occupancy plays a key role in regulating access to the eukaryotic genomes. Although various chromatin regulatory complexes are known to regulate nucleosome occupancy, the role of DNA sequence in this regulation remains unclear, particularly in mammals. To address this problem, we measured nucleosome distribution at high temporal resolution in human cells at hundreds of genes during the reactivation of KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV). We show that nucleosome redistribution peaks at 24 hours post KSHV reactivation and that the nucleosomal redistributions are widespread and transient. To clarify the role of DNA sequence in these nucleosomal redistributions, we compared the genes with altered nucleosome distribution to a sequence-based computer model and in vitro assembled nucleosomes. We demonstrate that both the predicted model and the assembled nucleosome distributions are concordant with the majority of nucleosome redistributions at 24 hours post KSHV reactivation. We suggest a model in which loci are held in unfavorable chromatin architecture and M-bM-^@M-^\springM-bM-^@M-^] to a transient intermediate state directed by DNA sequence information. We propose that DNA sequence plays a more considerable role in the regulation of nucleosome positions than was previously appreciated. The surprising findings that nucleosome redistributions are widespread, transient, and DNA-directed shift the current perspective regarding regulation of nucleosome distribution in humans. iSLK.219 cells at 0, 6, 12, 24, and 48 hours post KSHV reactivation.

2013-11-19 | E-GEOD-52453 | 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