Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-43714

ABSTRACT: Microarray to find ATF5 dependent genes in response to proteasome inhibition

OTHER RELATED OMICS DATASETS IN: PRJNA187148PRJNA187149PRJNA187146

PROVIDER: E-GEOD-43714 | ExpressionAtlas | 2015-07-10

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-43714-analysis-methods.tsv	Tabular
	E-GEOD-43714-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-43714-configuration.xml	Xml
	E-GEOD-43714-percentile-ranks.tsv	Tabular
	E-GEOD-43714.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 89

Similar Datasets

Mus musculus

Project description:Microarray to find ATF5 dependent genes in response to proteasome inhibition

| PRJNA187149 | ENA

Mus musculus

Project description:Microarray to find CHOP dependent genes in response to proteasome inhibition

| PRJNA187148 | ENA

Project description:Microarray to find CHOP/ATF5 dependent genes in response to proteasome inhibition

| PRJNA187146 | ENA

E-GEOD-43713

Project description:Microarray to find CHOP dependent genes in response to proteasome inhibition

2015-07-10 | E-GEOD-43713 | ExpressionAtlas

Transcription profiling of human hepatocytes treated with doxorubicin and Trovafloxacin, super-series of E-GEOD-11940 and E-GEOD-11941

Project description:This SuperSeries is composed of the following subset Series:; GSE11940: Topoisomerase II inhibition involves characteristic chromosomal expression patterns: Doxorubicin study; GSE11941: Topoisomerase II inhibition involves characteristic chromosomal expression patterns: Trovafloxacin study Experiment Overall Design: Refer to individual Series

2008-10-26 | E-GEOD-11942 | biostudies-arrayexpress

Homo sapiens

Project description:CFTR dependent response

| PRJNA91655 | ENA

Whole Genome Sequencing to Discover Familial Myeloma Risk Genes

Project description:<p>We identified germline <a href="https://www.ncbi.nlm.nih.gov/gene/?term=23028">KDM1A</a> truncating mutations in patients with multiple myeloma (MM), and loss of heterozygosity (LOH) in tumors. KDM1A mutation burden is higher in sporadic MM patients than in controls, and mRNA levels are lower in MM compared with normal plasma cells. KDM1A pharmacological inhibition in vitro promotes myeloma cell proliferation, and in mice promotes plasma cell expansion, enhanced secondary immune response to T cell dependent antigens, and upregulation of MYC oncogene transcriptional targets. Our findings provide important new insights into the role of KDM1A to suppress B cell malignancies.</p>

| phs001819 | dbGaP

Oryza sativa

Project description:OsNPR1-dependent rice genes

| PRJNA115047 | ENA

ULK1 as a novel therapeutic target to enhance immune checkpoint therapies against melanoma

Project description:Immune checkpoint inhibitors (ICIs) have transformed the treatment of melanoma. However, the majority of patients have primary or acquired resistance to ICIs, limiting durable responses and patient survival. Interferon-gamma (IFNg) signaling and the expression of IFNg-stimulated genes correlate with either response or resistance to ICIs, in a context-dependent manner. While IFNg-inducible immunostimulatory genes are required for response to ICIs, chronic IFNg signaling induces the expression of immunosuppressive genes, promoting resistance to these therapies. Here, we show that high levels of ULK1 correlate with poor survival in melanoma patients and overexpression of ULK1 in melanoma cells enhances IFNg-induced expression of immunosuppressive genes, with minimal effects on the expression of immunostimulatory genes. In contrast, genetic or pharmacological inhibition of ULK1 reduces expression of IFNg-induced immunosuppressive genes. ULK1 binds IRF1 in the nuclear compartment of melanoma cells, controlling its binding to the PD-L1 promoter region. Additionally, pharmacological inhibition of ULK1 in combination with anti-PD-1 therapy further reduces melanoma tumor growth and enhances anti-tumor immune responses in vivo. Our data suggest that targeting ULK1 represses IFNg-dependent immunosuppression. These findings support the combination of ULK1 drug-targeted inhibition with ICIs for the treatment of melanoma patients to improve response rates and patient outcomes.

2023-02-02 | PXD035347 | Pride

Inhibition of Hedgehog Signaling Pathway Impairs Cancer Cell Growth via Promotion of Autophagy

Project description:Analysis of gene expression levels in response to inhibition of Hh signaling in ovarian and glioma cancer cells using a cDNA microarray technique. Microarray analyses revealed that differentially expressed genes (DEGs) in human cancer cells are enriched in the senescence and autophagy pathways in response to the inhibition of Hh signaling. Further investigations showed that inhibition of Hh signaling induced autophagy..

2014-06-15 | GSE54936 | 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