Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

13 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CRISPR screen to identify regulators of neuronal differentiation

ABSTRACT: To search for factors regulating neuronal differentiation, we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid human ESCs. The regulators were identified by the quantification of depletion of their mutant clones within a pooled loss-of-function library upon neuronal differentiation.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Homo sapiens

SUBMITTER: Shay Kinreich

PROVIDER: E-MTAB-11944 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

CRISPR screen for the identification of host factors for ZIKA virus infection

Project description:To search for host factors regulating Zika virus infection, we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid human ESCs. The regulators were identified by the quantification of enrichment of their mutant clones within a pooled loss-of-function library upon Zika virus infection.

2023-05-31 | E-MTAB-11945 | biostudies-arrayexpress

CRISPR screen of human embryonic stem cell line h-pES10 for the identification of host factors for SARS-COV-2 infection

Project description:To search for host factors regulating SARS-COV-2 infection, we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid human ESCs. The regulators were identified by the quantification of enrichment of their mutant clones within a pooled loss-of-function library upon SARS-COV-2 infection.

2023-08-09 | E-MTAB-12505 | biostudies-arrayexpress

Identifying regulators of parental imprinting by CRISPR/Cas9 screening in haploid human embryonic stem cells

Project description:To search for factors regulating paternally imprinted genes (PEGs), we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid parthenogenetic ESCs. This by staining a pooled CRISPR library with a PEG10 antibody and next FACS-sorted for cells that presented de-novo PEG10 expression.

2021-10-21 | E-MTAB-11014 | biostudies-arrayexpress

Reduced representation bisulfite sequencing (RRBS) of haploid, diploid and triploid hESCs

Project description:To test the differences in genome-wide DNA methylation signatures of haploid, diploid and triploid hESCs, we extracted genomic DNA from these cells and performed RRBS.

2023-05-04 | E-MTAB-11478 | biostudies-arrayexpress

RRBS of hESCs harboring imprinting-related genetic perturbations

Project description:To search for factors regulating paternally imprinted genes (PEGs), we performed a genome-wide CRISPR/Cas9 screen in haploid hpESCs, and further analyzed the molecular phenotype upon perturbation of candidate PEGs regulators.

2021-10-21 | E-MTAB-11015 | biostudies-arrayexpress

CRISPR-Cas9 RBM10 synthetic lethality screen

Project description:Genome-wide CRISPR-Cas9 knockout screen using TKOv1 sgRNA library was performed in isogenic RBM10-proficient and RBM10-deficient HCC827 cells.

2023-03-04 | E-MTAB-12724 | biostudies-arrayexpress

Genome-wide CRISPR-Cas9 screen in isogenic parental and RBM10-KO HCC827 cells

Project description:Genome-wide CRISPR-Cas9 knockout screen using TKOv1 sgRNA library performed in isogenic RBM10-proficient and RBM10-deficient HCC827 cells.

2024-03-01 | E-MTAB-13626 | biostudies-arrayexpress

A CRISPR/Cas9-mediated screen identifies regulators of early plasma cell differentiation

Project description:The differentiation of B cells into antibody-secreting cells depends on cell division-coupled, epigenetic and other cellular processes that are incompletely understood. We have developed a CRISPR/Cas9-based screen that models an early stage of T cell-dependent plasma cell differentiation and measures B cell survival or proliferation versus the formation of CD138+ plasmablasts. Here, we refined and extended this screen to more than 500 candidate genes that are highly expressed in plasma cells. Among known genes whose deletion preferentially affected plasmablast formation were the transcriptional regulators Prdm1, Irf4 and Pou2af1, and the Ern1 gene encoding the ER stress sensor IRE1a. Moreover, we newly identified several genes involved in NF-kB or p38 signaling (Pim2, Nfkbia, Mapk14), vesicle trafficking (Arf4, Preb) and epigenetic regulators that form part of the NuRD complexes (Hdac1, Mta2, Mbd2). Defective plasmablast formation caused by Ern1 deletion could not be rescued by spliced XBP1 (XBP1s), a transcription factor dependent on and downstream of IRE1a, suggesting that in early plasma cell differentiation IRE1a acts independently of XBP1s. The deletion of ARF4, a small GTPase required for ER-to-Golgi transport, impaired plasmablast formation by blocking antibody secretion. Plasmablast formation after Hdac1 deletion was consistently reduced by about 50%, while deletion of the closely related Hdac2 gene had no effect. Hdac1 knock-out led to strongly perturbed protein expression of antagonistic transcription factors that specify plasma cell versus B cell identity (by decreasing IRF4 and BLIMP1 and increasing BACH2 and PAX5). Taken together, our results highlight specific and non-redundant roles for Ern1, Arf4 and Hdac1 in the early steps of plasma cell differentiation.

2022-12-22 | PXD038201 | Pride

Identify proinsulin regulators using CRISPR screen and mouse genetics [CRISPR screen]

Project description:Proinsulin is the precursor of insulin in pancreatic beta cells. Altered proinsulin and proinsulin to insulin ratio mark beta cell dysfunction, predictuing disease progression into type 1 and type 2 diabetes. Of essential role for beta cell function, knowledge about proinsulin production and its role in disease are currently very limited. Using genome wide CRISPR screen, we identified 84 proinsulin regulators including classical protein convertases Pcsk1 and Cpe, and novel factors like Pdia6. Among the list 29 proinsulin regulators were trajectory genes involved in disease progression in obesity and type 2 diabetes in humans. In vivo mouse genetics study revealed unique genetic architecture and quantitative trait loci (QTLs) modulating plasma proinsulin levels. Integrative analyzing and mapping of the QTL signals directly pinpointed to proinsulin regulators identified from the CRISPR screen, which in return greatly improved resolution of the mouse genetic study. 4 out of 5 overlapped genes can be individually validated. Knocking down the leading hits Pdia6 leads to decreased proinsulin content and remarkable loss of proinsulin granules in beta cells. Consequently, proinsulin secretion was greatly decreased. Mechanistically, protein translation rate was greatly impaired after knocking down Pdia6. Our study demonstrated the power of combining in vitro functional genomics with in vivo mouse genetics study to identify proinsulin regulatory network in pancreatic beta cells.

2023-11-15 | GSE245845 | GEO

CRISPR screen for NMD regulators

Project description:Nonsense-mediated decay (NMD) is a pathway that degrades messenger RNAs containing premature termination codons. Here, a genome-wide screen for NMD factors uncovered an unexpected mechanism that broadly governs 3ʹ untranslated region (UTR)-directed regulation. The screen revealed that NMD requires lysosomal acidification, which allows transferrin-mediated iron uptake, which in turn is necessary for iron-sulfur (Fe-S) cluster biogenesis. This pathway converges on the Fe-S cluster-containing ribosome recycling factor ABCE1, whose impaired function results in the movement of ribosomes into 3ʹ UTRs where they displace exon junction complexes, thereby abrogating NMD. Importantly, these effects extend beyond NMD substrates, with ABCE1 activity required to maintain the accessibility of 3ʹ UTRs to diverse regulators, including microRNAs and RNA binding proteins. Due to the sensitivity of the Fe-S cluster of ABCE1 to iron availability and reactive oxygen species, these findings reveal an unanticipated vulnerability of 3ʹ UTR-directed regulation to lysosomal dysfunction, iron deficiency, and oxidative stress.

2020-07-14 | GSE144162 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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