Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis induced by EV-A71 infection

ABSTRACT: Transcriptome analysis induced by EV-A71 infection

PROVIDER: PRJNA637599 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis induced by EV-A71 infection

Project description:In this study, we aimed to adopt the transcriptome sequencing technology to obtain the different changes of transcriptome profiles after infecting with EV-A71 in human neuroblastoma cell line SH-SY5Y. And then, through systematic bioinformatics analysis, we hope to find useful clues for the pathogenesis of HFMD.

2023-06-05 | GSE151893 | GEO

Role of Rab11 in Enterovirus A71 (EV-A71) infection

Project description:A siRNA screening using a commercially available membrane trafficking library identified Rab11 as a pro-viral host factor in motor neuron NSC34 cell line infected with EV-A71, a major causative agent of Hand, Foot and Mouth Disease (HFMD). This project aims at deciphering the role of Rab11 during EV-A71 infection by using various molecular virology and cell biology approaches. We also identified Rab11 interacting partners during EV-A71 infection by pulldown and mass spectrometry.

2024-06-28 | PXD043870 | Pride

Transcriptome analysis induced by CTN, CV-A16, CVS and EV-A71 infection

Project description:Transcriptome analysis induced by CTN, CV-A16, CVS and EV-A71 infection

| PRJNA637593 | ENA

Temporal Proteomic and Phosphoproteomic Analysis of EV-A71-infected Human Cells

Project description:We performed time-resolved quantification of the whole proteome and phosphoproteome changes of rhabdomyosarcoma cells (RD) upon EV-A71 infection at 0 hpi, 1 hpi, 2 hpi, 4 hpi, 8 hpi, and 12 hpi based on 6-plex TMT labeling method. This project contains all LC-MS/MS raw files.

2022-07-23 | MSV000089954 | MassIVE

Temporal Proteomic and Phosphoproteomic Analysis of EV-A71-infected Human Cells

2022-07-23 | MSV000089953 | MassIVE

Transcriptome of human neuroblastoma SH-SY5Y cells in response to 2B protein of enterovirus-A71

Project description:Non-structural 2B protein of enterovirus-A71 has reported involving in intracellular Ca2+ manipulation and altering cellular homeostasis such as inducing cell death in human SH-SY5Y cells. The aim of the study is to profile transcriptomic signature of human neuroblastoma SH-SY5Y cells altered by EV-A71 2B protein using RNA-sequencing analysis. We generated mRNA expression profiles of SH-SY5Y cells transfected with EV-A71 2B protein fused with mCherry and FLAG tag protein (2BmCherry) and mCherry as well as parental SH-SY5Y cells. We find that 7 genes including CCL2, RELB, IL32, PLAT, PTGES, PHLDA1, and TNFRSF9 are uniquely overexpressed in 2BmCherry comparing to mCherry. Moreover, there were 333 upregulated and 333 downregulated genes showed significant different expression level in 2BmCherry transcriptome in comparison with SHSY5Y transcriptome but not in mCherry vs SHSY5Y comparison. Functional analysis showed that EV-A71 2B upregulated genes involved Ca2+-related signaling pathways participating gene expression, immune response, apoptosis, and long-term potentiation (synaptic adaptation) of neuron in the transfected SH-SY5Y cells.

2021-12-23 | GSE191270 | GEO

Inhibition of viral suppressor of RNAi proteins by designer peptides protects from enteroviral infection in vivo

Project description:RNA interference (RNAi) is an antiviral immunity conserved in diverse eukaryotes including mammals, while viruses encodes viral suppressors of RNAi (VSRs) as countermeasures. However, the physiological impact of RNAi on viral infection in mammals has not been fully assessed, and it also remains unknown whether antiviral RNAi can be therapeutically exploited. Here, we show that peptides designed to target enterovirus A71 (EV-A71)-encoded protein 3A, a well-characterized VSR, triggered an effective antiviral response. These VSR-targeting peptides, particularly ER-DRI, abrogated the VSR function of 3A, which enabled EV-A71-derived siRNA production and unlocked RNAi response that potently inhibited EV-A71 infection in mammals. ER-DRI treatment elicited a strong in vivo antiviral RNAi response that protected mice against lethal EV-A71 challenge. It also potently inhibited another enterovirus, Coxsackievirus-A16, dependently of RNAi. Our findings demonstrate that antiviral RNAi does have a physiologically important impact in mammals and targeting VSRs is a promising strategy for antiviral therapies.

2021-07-31 | GSE179496 | GEO

Transcriptome analysis induced by CTN, CV-A16, CVS and EV-A71 infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-08-24 | GSE151894 | GEO

Effects of Monocyte/Macrophages on the Severity of Hand, Foot, and Mouth Disease Patients due to Enterovirus

Project description:To elucidate alterations in immune cells during enterovirus 71 (EV-A71) infection and explore potential interaction mechanisms.Single-cell sequencing technology was used to sequence peripheral blood monocytes (PBMCs) obtained from a severe hand, foot and mouth disease (HFMD) patient due to EV-A71 and a healthy control.

2024-06-20 | GSE269965 | GEO

Enterovirus 3A protein disrupts endoplasmic reticulum homeostasis through interaction with GBF1

Project description:Enterovirus A71 (EV-A71) is a single-stranded, positive sense RNA virus causing endoplasmic reticulum stress to induce or modulate downstream signaling pathways known as the unfolded protein responses (UPR). The 3A protein of EV-A71 was identified as a major regulator of the UPR caused by infection with EV-A71. To identify the molecular pathways for the 3A protein to regulate the UPR, we performed RNA sequencing (RNA-seq) with RD cells expressing the 3A protein. Wild type or defective mutant of 3A protein that carried alanine substitutions of Ile8 or Ile10 (3A-I8A or -I10A) was expressed in the cells. The RNA-seq with cells expressing either WT or mutant 3A was performed.

2024-06-16 | GSE268418 | 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