Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide CRISPR screening identifies SEC31A as a regulator of alpha cell survival

ABSTRACT: Genome-wide CRISPR screening identifies SEC31A as a regulator of alpha cell survival

PROVIDER: PRJNA917308 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22950320_1.fastq.gz	Fastqsanger.gz
	SRR22950320_2.fastq.gz	Fastqsanger.gz
	SRR22950321_1.fastq.gz	Fastqsanger.gz
	SRR22950321_2.fastq.gz	Fastqsanger.gz
	SRR22950322_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 30

Similar Datasets

Genome-wide CRISPR screening identifies SEC31A as a regulator of alpha cell survival

Project description:Impairment of the glucagon response to hypoglycemia is among the severe clinical consequences in patients with type 1 or advanced type 2 diabetes. However, an incomplete understanding of the stress-response mechanism(s) in alpha cells has limited the insights into the pathophysiology underlying the dysregulated glucagon response and precluded the development of therapeutics. In this study, we undertook an unbiased, genome-wide screening by transducing alpha cells with a CRISPR lentiviral library to identify potential proteins that regulate stress resistance in alpha cells. We identified SEC31A, a gene responsible for the ER-Golgi transportation system, as a critical mediator of cell survival in response to stress. To provide clinical relevance to these findings, we performed transcriptome analysis using pseudoislets generated from sorted and re-aggregated human alpha cells with a knockdown of SEC31A. Our study offers insights into the regulatory mechanism(s) underlying ER stress resistance in pancreatic alpha cells with implications for treating hypoglycemia in T1D and advanced T2D

2023-12-23 | GSE222009 | GEO

Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation

Project description:Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation

| PRJNA681195 | ENA

Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [CRISPR screening]

Project description:Genome-Scale CRISPR Knockout Screening Identifies BACH1 as a Key Regulator of Aflatoxin B1-Induced Oxidative Damage [CRISPR screening]

| PRJNA819546 | ENA

Epigenetic-focused CRISPR/Cas9 screen identifies ASH2L as a regulator of glioblastoma cell survival

Project description:Epigenetic-focused CRISPR/Cas9 screen identifies ASH2L as a regulator of glioblastoma cell survival

| PRJNA832577 | ENA

Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [Amplicon-seq]

Project description:Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [Amplicon-seq]

| PRJNA681912 | ENA

Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [RNA-seq]

Project description:Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [RNA-seq]

| PRJNA681200 | ENA

CRISPR-Cas9 Screening Identifies UBE3C as a Top Negative Regulator of THEMIS Protein Expression

Project description:CRISPR-Cas9 Screening Identifies UBE3C as a Top Negative Regulator of THEMIS Protein Expression

| PRJNA1430406 | ENA

CRISPR Screening in Glioblastoma

Project description:This is an in vitro genome-wide CRISPR/cas9 screen in human glioblastoma stem cells, screening for genes essential for survival of these cells. These cells express cas9 and have been transfected with a guide RNA library causing gene knockouts. We will analyse the sequencing data for depletion of guide RNAs. In this particular study, we will do RNA sequencing to correlate CRISPR with expression levels in specific cancer cell subpopulations. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2016-03-22 | E-ERAD-448 | biostudies-arrayexpress

Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [m6A-RIP-seq]

Project description:Pooled CRISPR Screening Identifies m6A as a Positive Regulator of Macrophage Activation [m6A-RIP-seq]

| PRJNA681201 | ENA

Epigenetic-focused CRISPR/Cas9 screen identifies ASH2L as a regulator of glioblastoma cell survival

Project description:Glioblastoma is the most common and aggressive primary brain tumor with dismal prognosis, highlighting an urgent need for novel treatment strategies. In this study, we investigated epigenetic regulators of glioblastoma cell survival through CRISPR/Cas9 based genetic ablation screens using our customized sgRNA library EpiDoKOL, which targets critical functional domains of chromatin modifiers. Screens conducted in multiple cell lines revealed ASH2L, a histone lysine methyltransferase complex subunit, as a major regulator of glioblastoma cell viability. ASH2L depletion led to cell cycle arrest and apoptosis. RNA sequencing and Cut&Run sequencing together identified a set of cell cycle regulatory genes, such as TRA2B, BARD1, KIF20B, ARID4A, SMARCC1 that were downregulated upon ASH2L depletion. Mass spectrometry analysis demonstrated the interaction partners of ASH2L in glioblastoma cell lines as COMPASS family members including SETD1A, SETD1B, MLL1 and MLL2, however glioblastoma cells had differential dependency to COMPASS members for survival. The growth of ASH2L-depleted glioblastoma cells was markedly slower than controls in orthotopic in vivo models. TCGA analysis showed high ASH2L expression in glioblastoma compared to low grade gliomas and immunohistochemical analysis revealed significant ASH2L expression in glioblastoma tissues, attesting to its clinical relevance. Therefore, high throughput, robust and affordable screens with focused libraries, such as EpiDoKOL, holds great promise to enable rapid discovery of novel epigenetic regulators of cancer cell survival, such as ASH2L. Together, we suggest that targeting ASH2L could serve as a new therapeutic opportunity for glioblastoma.

2023-11-13 | GSE201657 | 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