Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide gene expression prolifing post GNL3 knockdown in human neural progenitor cells

ABSTRACT: We used two siRNAs to knock down GNL3 in human neural progenitor cells which were derived from normal human induced pluripotent stem cells (ATCC, ACS-1011). GNL3 knockdown experiments were done in three biological replicates. Total RNA was extracted from GNL3 knockdown and control groups for RNA sequencing (Illumina Hiseq2000, paired-end 100 bp). Genes that affected by both siRNAs were considered differentially expressed genes between GNL3 knockdown and control groups (adjusted P value < 0.05). Using Gene Ontology and KEGG pathway analysis, we found that those differentially exrepssed genes were mainly related to immune response, response to cytokine, cell cycle, and p53 signaling pathway.

ORGANISM(S): Homo sapiens

PROVIDER: GSE150945 | GEO | 2020/05/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

High throughput sequencing of small RNAs from Drosophila cells infected with a panel of viruses

2013-01-01 | GSE43031 | GEO

GNL3/nucleostemin links DNA replication homeostasis and replication forks stability

Project description:The regulation of replication forks stalling and replication origins firing must be tightly coordinated to prevents genomic instability. Here we show that GNL3/nucleostemin, a GTP-binding protein able to shuttle between the nucleolus and the nucleoplasm, limits replicative stress by limiting replication origins firing. GNL3 is in proximity of nascent DNA and its depletion reduces forks speed but increases forks density and replication origins firing. When subjected to exogenous replicative stress, cells impaired for GNL3 exhibits MRN-dependent resection and RPA phosphorylation. Strikingly, inhibition of origin firing using CDC7 inhibitor decreased resection in absence of GNL3 but not in absence of BRCA1, suggesting that GNL3 does not protect nascent strand directly from resection. Consistent with this, overexpression of GNL3 leads to an increased resection in response to replicative stress and enhanced origin firing efficiency. These data indicate that the probability of origins firing is tightly regulated by GNL3 to limit replicative stress. Finally, we show that ORC2 and GNL3 interacts together in the nucleolus. We propose a model where GNL3 level is crucial to determine the correct amount of ORC2 on chromatin by sequestrating it in the nucleolus thanks to the capacity of GNL3 to shuttle between nucleoplasm and nucleolus.

2023-07-01 | GSE180865 | GEO

Knockdown of human TCF4 affects multiple signaling pathways involved in cell survival, epithelial-to-mesenchymal transition and neuronal differentiation

Project description:TCF4 is an important neurodevelopmental transcription factor associated with schizophrenia and Pitt-Hopkins syndrome. In this study, we used genome-wide expression profiling to determine the effects of acute TCF4 knockdown on gene expression in SH-SY5Y neuroblastoma cells. Pathway and enrichment analysis on the differentially expressed genes in TCF4-knockdown cells identified an over-representation of genes involved in TGF-β signaling, epithelial-to-mesenchymal transition (EMT) and apoptosis. Among the most significantly differentially expressed genes were the EMT regulators SNAI2 and DEC1 and the proneural genes NEUROG2 and ASCL1. Altered expression of several mental retardation genes such as UBE3A (AS), ZEB2 (MWS) and MEF2C was also found in TCF4-depleted cells. These data suggest that TCF4 regulates a number of convergent signaling pathways involved in cell differentiation and survival in addition to a subset of clinically important mental retardation genes. To identify TCF4-mediated gene expression changes in SH-SY5Y cells, experiments were conducted with two control (mock and GAPDH KD) and two TCF4 knockdown (KD1 and KD2) groups. Two non-overlapping siRNAs against TCF4 were designed and transfected over a 72h period to induce global knockdown of TCF4 transcripts. In parallel, cells were mock transfected (mock; transfection reagent only) and transfected with an unrelated siRNA against GAPDH (GAPDH KD) in order to control for background gene expression changes due to transfection, presence of dsRNA and activation of the cellular silencing machinery. After transfection, RNA was extracted from all cells, converted to cDNA and labelled for microarray hybridization. Each of the four treatment groups (mock, GAPDH KD, KD1 and KD2) contained three biological replicates which were processed at the same time using the Toray microarray platform.

2013-08-20 | E-GEOD-48367 | biostudies-arrayexpress

High throughput sequencing of small RNAs from Drosophila cells infected with a panel of viruses

Project description:We report the cloning and sequencing of both endogenous small RNAs and virus-derived siRNAs produced by the antiviral RNAi pathway in Drosophila. We find that a diverse panel of viruses are targeted by the RNAi pathway in Drosophila to produce abundant virus-derived siRNAs, and these siRNAs map to various locations within the viral genomes. Knockdown of various RNAi and miRNA pathway components alters the levels of these viral small RNAs. Drosophila DL1 cells were treated with dsRNA for 3 days to deplete factors involved in the antiviral RNAi pathway and miRNA pathway, then were challenged with one of four viruses for 4 days. Total RNA was collected, and the small RNA populations from 15-29 nt were cloned and sequenced.

2013-01-01 | E-GEOD-43031 | biostudies-arrayexpress

GNL3 ChIP-seq

Project description:GNL3 ChIP-seq

| PRJNA786539 | ENA

mRNA-Seq identifies the differentially expressed mRNA in negative control and METTL3 knockdown HULEC-5a

Project description:To identify the molecular mechanism by which METTL3 regulates endothelial barrier function, we performed RNA-seq and MeRIP-seq in HULEC-5a cells with stable METTL3 knockdown and control cells. The RNA-seq results revealed that 437 transcripts were significantly downregulated (fold change <0.5) after METTL3 knockdown. The MeRIP-seq results revealed that the m6A peaks in 1011 transcripts were decreased in abundance (fold change >1.2). Intriguingly, 55 transcripts overlapped in the RNA-seq and MeRIP-seq data

2022-05-20 | GSE200649 | GEO

MeRIP-Seq (m6A-Seq) identifies the mRNA m6A modification target in negative control and METTL3 knockdwon HULEC-5a

2022-05-20 | GSE200648 | GEO

CRISPR RNA-seq from K562 (ENCSR455VFL)

Project description:RNA-seq on K562 cells treated with a CRISPR gRNA against GNL3. (GNL3-BGKcLV08) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2021-06-15 | GSE177305 | GEO

Microarray expression profiling of C. elegans N2 L4 control (RNAi) vs. nhr-25 (RNAi) and N2 (Wt) vs. acs-3 (ft5) mutants

Project description:Acyl-coA synthases (ACSs) produce fatty acyl-CoAs that are used in metabolic and signaling pathways. Metazoans have a large number of ACS genes with differing expression patterns and substrate preferences, but the physiological roles of most ACS genes are unknown. Here, we focused on the C. elegans acyl CoA synthase, ACS-3, which is known to regulate fat uptake and de novo fat synthesis through the conserved nuclear hormone receptor, nhr-25. We performed microarray analysis of acs-3 mutants to elucidate the acs-3-regulated transcription program. This analysis revealed an enrichment among differentially regulated genes of those involved in lipid metabolism, pathogen and wounding responses, and sterol binding genes, among others. As the immunity genes were the most represented gene class, we performed pathogen sensitivity assays to test the phenotypic consequences of this immune gene regulation. Interestingly, acs-3 mutants were hypersensitive to the fungal pathogen D. coniospora, but only mildly sensitive to the bacterial pathogen P. aeruginosa. acs-3 mutation suppressed nhr-25 mutant sensitivity to P. aeruginosa, yet surprisingly microarray analysis of nhr-25(RNAi) animals revealed significant overlap with the acs-3 mutant transcriptome, with an enrichment of pathogen response genes. The upregulation of pathogen response genes in acs-3(ft5) mutants and following nhr-25 reduction-of-function (rf) does not appear to be due to a constitutive osmotic response or defective cuticle barrier, two potential explanations for the acs-3(ft5) and nhr-25(rf) expression of innate immunity genes in the absence of pathogen exposure. Together, these data indicate that ACS-3 promotes resistance to the fungal pathogen, D. coniospora and regulates innate immunity genes through an unknown mechanism. Potential roles for ACS-3 in innate immunity are discussed.

2014-03-21 | GSE48605 | GEO

CRISPR RNA-seq from HepG2 (ENCSR940FIN)

Project description:RNA-seq on HepG2 cells treated with a CRISPR gRNA against GNL3. (GNL3-BGHcLV05-E) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2021-06-15 | GSE177899 | 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