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

Autophagy and alternative NF-kappaB inhibition by RNAi against RELB, ATG5 or ULK1 in A549 human cancer cells

ABSTRACT: In order to understand the contribution of autophagy and alternative NF-kappaB signalling to transcriptional output in A549 lung cancer cells, RNAi was used to knockdown the expression of core autophagy genes (ATG5, ULK1) or the key subunit of alternative NF-kappaB RELB. Seven samples were prepared for each biological replicate; two sequence independent non-targeting control siRNAs were transfected as a negative control. Three sequence independent siRNAs targeting the core autophagy machinery were transfected (ATG5 si, ATG5 si(2), ULK1 si). N.B. ATG5 si(2) only partially ablates Atg5 protein expression whereas ATG si has greater efficacy. Two sequence independent siRNAs targeting RELB were transfected (RELB si, RELB si(2) ). Three independent biological replicates of all conditions were obtained, by performance of the experiment on different days.

ORGANISM(S): Homo sapiens

SUBMITTER: Simon Wilkinson

PROVIDER: E-GEOD-73158 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Autophagy and alternative NF-kappaB inhibition by RNAi against RELB, ATG5 or ULK1 in A549 human cancer cells

Project description:In order to understand the contribution of autophagy and alternative NF-kappaB signalling to transcriptional output in A549 lung cancer cells, RNAi was used to knockdown the expression of core autophagy genes (ATG5, ULK1) or the key subunit of alternative NF-kappaB RELB.

2015-09-18 | GSE73158 | GEO

Gene expression profile of human trabecular meshwork cells with silenced expression of autophagy genes Atg5 and Atg7

Project description:In order to investigate the effects of downregulated autophagy in TM cells, we conducted gene expression analysis in human TM cells deficient in autophagy. For this, three independent strains of primary human TM cells were transfected with a cocktail of siRNAs to specifically silence the expression of the autophagy genes Atg5 and Atg7 (siAtg5/7). A scrambled siRNA (siNC) was used as control.

2019-10-01 | GSE122652 | GEO

Homo sapiens

Project description:Autophagy and alternative NF-kappaB inhibition by RNAi against RELB, ATG5 or ULK1 in A549 human cancer cells

| PRJNA296066 | ENA

Gene expression profile of human trabecular meshwork cells with silenced expression of autophagy genes Atg5 and Atg7 subjected to cyclic mechanical stretch

Project description:In order to investigate the effects of downregulated autophagy in TM cells response to mechanical stretch, we conducted gene expression analysis in human TM cells deficient in autophagy and subjected to cyclic mechanical stretch. For this, three independent strains of primary human TM cells were transfected with a cocktail of siRNAs to specifically silence the expression of the autophagy genes Atg5 and Atg7 (siAtg5/7), and subjected to cyclic mechanical stress (15% elongation, 1 cycle/sec, 24h).

2021-04-14 | GSE159793 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of lack of autophagy on sorted mouse lung ILC2 Transcriptomes

Project description:Atg5, a key gene of the autophagy can affect ILC2 effector functions ex vivo. Increased ILC2 activation leads to the development of airway hyperreactivity and lung inflammation. Targeting Atg5 (autophagy) may therefore represent a novel therapeutic target to treat asthma.

2020-02-27 | GSE139573 | GEO

Mass spectrometry proteomics reveals proteins that function in mTOR regulated selective autophagy

Project description:We used proteomic profiling to identify proteins in the mTOR-autophagy axis. Mouse cell lines lacking individual autophagy genes (Atg5 or Ulk1/Ulk2) were treated with an mTOR inhibitor to induce autophagy and cultured in media with either glucose or galactose. Mass spectrometry proteome profiling revealed an elevation of both known autophagy proteins and candidates for new autophagy components.

2020-01-23 | PXD014990 | Pride

National University of Singapore MEF

Project description:miRNA expression of 6h EBSS treatment induced autophagy in Atg5 WT and KO mouse embryonic fibroblasts (MEF) were examined. For the 1st comparison, the control group is Atg5 WT MEF without EBSS treatment, the experiment group is Atg5 KO MEF without EBSS treatment; For the 2nd comparison, the control group is Atg5 WT MEF without EBSS treatment, the experiment group is Atg5 WT MEF with 6h EBSS treatment; For the 3rd comparison, the control group is Atg5 WT MEF with 6h EBSS treatment, the experiment group is Atg5 KO MEF with 6h EBSS treatment.The PIQORTM Analyzer were used for the analysis.

2011-11-21 | E-MTAB-880 | biostudies-arrayexpress

Identification Atg5-related microRNAs involved in the regulation of tumor formation

Project description:Autophagy plays an important role in physiology and tumorigenesis. We and others have demonstrated that Ha-ras overexpression induces autophagy in NIH3T3 cells. Autophagic machinery is regulated by a family of autophagy associated genes (Atg). The inducible Ha-ras oncogene was introduced into mouse embryo fibroblast Atg5 wild type [MEF-Atg5(+/+)] and Atg5 knock-out [MEF-Atg5(-/-)] cells and the stable cell lines MR and M5R were established, respectively. Our results showed that M5R cell induced larger tumor formation compared with MR cells while these two cell lines were subcutaneously injected into SCID mice under Ha-ras overexpression conditions. It indicates that Atg5 is involved in the suppression of Ras-related tumor formation. MicroRNA (miRNA), approximately 22 nucleotide of non-coding RNA, regulates transcription and translation of the target genes and is involved in cell differentiation and tumorigenesis. A miRNA microarray (932 probes) screening was conducted to identify the autophagy-tumorigenesis-related miRNAs. Among the significant genes, miR-224 was highly expressed in autophagy deficient cell and it induced tumors. Overexpression miR-224 enhanced the activity of migration and invasion in vitro and tumor formation in vivo. In conclusion, this is the first report to demonstrate that autophagy suppresses tumor formation through down-regulation of microRNA in this case miR-224. MR and M5R cell lines were treated with IPTG for 48 hr. In addition, these cell lines were subcutaneously injected into mice to induce tumor formation. The RNA samples were extracted from above cell lines and tumors. In this research, BEL/ITRI 15K V1.0 miRNA microarray chips were used to evaluate the miRNA expression profile.

2012-06-25 | E-GEOD-38911 | biostudies-arrayexpress

RNA-sequencing of differentiated mouse skeletal muscle cells following the depletion of EYA3

Project description:Mouse skeletal muscle cells were subjected to treatment with siRNAs targeting EYA3 or a non-targeting siRNA (si-Ctrl). Differential gene expression analysis was performed on the resulting data.

2023-10-06 | GSE212436 | GEO

Estrogen Receptor β Activation Inhibits Colitis by Promoting the NLRP6-Mediated Autophagy

Project description:Estrogen receptor β (ERβ) and NOD-, LRR- and pyrin domain-containing 6 (NLRP6) are highly expressed in intestinal tissues and reduce intestinal inflammation, but their underlying mechanisms are unclear. We found that ERβ and NLRP6 levels were reduced in patients with inflammatory bowel disease (IBD), and that deletion of ERβ or NLRP6 was exacerbated colitis in mouse models. We discovered that ERβ exerted its anti-inflammatory activity by inducing NLRP6-mediated autophagy. Specifically, ERβ directly regulated NLRP6 gene expression and NLRP6 inflammasome activation through genomic and non-genomic effects. NLRP6 directly interacted with multiple autophagy-related proteins (including ULK1, BECN1, ATG5-ATG12-ATG16L1 complex, p62, and PHB2). Autophagy stimulation suppresses the inflammatory response by eliminating excess ERβ, NLRP6, ASC, Casp-1, IL-1β, TNF-α and damaged mitochondria. These findings indicate that ERβ-NLRP6-autophagy forms a negative feedback loop to maintain intestinal epithelial cell homeostasis and facilitate tissue repair.

2023-06-05 | GSE151864 | 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