Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

ABSTRACT: Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

PROVIDER: PRJNA715228 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13991131_1.fastq.gz	Fastqsanger.gz
	SRR13991131_2.fastq.gz	Fastqsanger.gz
	SRR13991132_1.fastq.gz	Fastqsanger.gz
	SRR13991132_2.fastq.gz	Fastqsanger.gz
	SRR13991133_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

| PRJNA715232 | ENA

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [RNA-seq]

Project description:Explore the potential downstream signaling pathways that inhibit TGEV replication after knocking out TMEM41B by RNA-seq analysis.

2021-11-19 | GSE169095 | GEO

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [Focused cell]

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [Focused cell]

| PRJNA715218 | ENA

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [RNA-seq]

Project description:Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [RNA-seq]

| PRJNA715205 | ENA

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication

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

2021-11-19 | GSE169113 | GEO

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [PigGeCKO]

Project description:We use the a porcine genome-scale CRISPR/Cas9 knockout (PigGeCKO) library (Zhao et al., 2020) to identify key host factors facilitating TGEV infection in porcine cells.

2021-11-19 | GSE169111 | GEO

Genome-scale CRISPR screen identifies TMEM41B as a critical host factor required for coronavirus replication [Focused cell]

Project description:We use the Focused-library to identify key host factors facilitating TGEV infection in porcine cells.

2021-11-19 | GSE169108 | GEO

CRISPR screens identify candidate host factors for SARS and MERS coronavirus infection

Project description:Severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) are zoonotic pathogens that can cause severe respiratory disease in humans. Identification of the host factors that are necessary for viral infection and virus-induced cell death is critical to our understanding of the viral life cycle and can potentially aid the development of new treatment options. Here, we report CRISPR screen results of both SARS-CoV and MERS-CoV infections in derivatives of the human hepatoma cell line Huh7. Our screens identified the known entry receptors ACE2 for SARS-CoV and DPP4 for MERS-CoV. Additionally, the SARS-CoV screen uncovered several components of the NF-κB signaling pathway (CARD10, BCL10, MALT1, MAP3K7, IKBKG), while the MERS-CoV screen revealed the polypyrimidine tract-binding protein PTBP1, the ER scramblase TMEM41B, furin protease and several transcriptional and chromatin regulators as candidate factors for viral replication and/or virus-induced cell death. Together, we present several known and unknown coronavirus host factors that are of interest for further investigation.

2024-01-08 | GSE252396 | GEO

Genome-scale CRISPR screen identifies TMEM41B as a multi-function host factor required for coronavirus replication.

Project description:Emerging coronaviruses (CoVs) pose a severe threat to human and animal health worldwide. To identify host factors required for CoV infection, we used α-CoV transmissible gastroenteritis virus (TGEV) as a model for genome-scale CRISPR knockout (KO) screening. Transmembrane protein 41B (TMEM41B) was found to be a bona fide host factor involved in infection by CoV and three additional virus families. We found that TMEM41B is critical for the internalization and early-stage replication of TGEV. Notably, our results also showed that cells lacking TMEM41B are unable to form the double-membrane vesicles necessary for TGEV replication, indicating that TMEM41B contributes to the formation of CoV replication organelles. Lastly, our data from a mouse infection model showed that the KO of this factor can strongly inhibit viral infection and delay the progression of a CoV disease. Our study revealed that targeting TMEM41B is a highly promising approach for the development of broad-spectrum anti-viral therapeutics.

| S-EPMC8675922 | biostudies-literature

TMEM41B is an endoplasmic reticulum Ca2+ release channel maintaining naive T cell quiescence and responsiveness

Project description:In mammalian cells, endoplasmic reticulum (ER) passively releases Ca2+ under steady state, but channels involved remain elusive. Here, we report that TMEM41B, an ER-resident membrane protein critical for autophagy, lipid metabolism, and viral infection, functions as an ER Ca2+ release channel. Biochemically, purified recombinant TMEM41B forms a concentration-dependent Ca2+ channel in single-channel electrophysiology assays. Cellularly, TMEM41B deficiency causes ER Ca2+ overload, while overexpression of TMEM41B depletes ER Ca2+. Immunologically, ER Ca2+ overload leads to upregulation of IL-2 and IL-7 receptors in naive T cells, which in turn increases basal signaling of JAK-STAT, AKT-mTOR, and MAPK pathways. This dysregulation drives TMEM41B-deficient naive T cells into a metabolically activated yet immunologically naive state. ER Ca2+ overload also downregulates CD5, lowering the activation threshold of TMEM41B-deficient T cells and leading to heightened T cell responses during infections. In summary, we identify TMEM41B as a concentration-dependent ER Ca2+ release channel, revealing an unexpected role of ER Ca2+ in naive T cell quiescence and responsiveness.

2025-03-01 | GSE285373 | 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