Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The ISR activation confers vulnerability to mitoribosome-targeting antibiotics in melanoma

ABSTRACT: The ISR activation confers vulnerability to mitoribosome-targeting antibiotics in melanoma

PROVIDER: PRJNA737120 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14794200.fastq.gz	Fastqsanger.gz
	SRR14794201.fastq.gz	Fastqsanger.gz
	SRR14794202.fastq.gz	Fastqsanger.gz
	SRR14794203.fastq.gz	Fastqsanger.gz
	SRR14794204.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 88

Similar Datasets

The ISR activation confers vulnerability to mitoribosome-targeting antibiotics in melanoma

Project description:We report the changes in translatome of a commercially available melanoma line upon acquisition of therapy resistance

2021-07-15 | GSE177075 | GEO

Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists

Project description:Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists

| PRJNA506248 | ENA

Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [C790 cells]

Project description:Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [C790 cells]

| PRJNA504897 | ENA

Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [4434 cells]

Project description:Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [4434 cells]

| PRJNA504899 | ENA

Targeting Electron Transport Chain Confers Therapeutic Vulnerability in Castration-Resistant Prostate Cancer

Project description:Most prostate cancer will develop into castration-resistant prostate cancer, which is the most frequent cause of death for prostate cancer patients. Despite novel androgen receptor antagonists have significantly improved clinical outcomes for these patients, some patients still could not benefit from existing treatment regimens. By analyzing the single-cell RNA-sequencing data and bulk-sequencing data, we discovered that oxidative phosphorylation and electron transport chain (ETC) pathway were enhanced in the prostate cancer microenvironment following tumor progression. Meanwhile, high ETC was related to poor clinical outcomes in prostate cancer patients. Both in vitro and in vivo castration-resistant prostate cancer models demonstrated that ETC inhibitor marked suppressed tumor growth and the synergistic antitumor efficacy of the combination of ETC inhibitor and androgen receptor antagonist. Our study indicates that ETC activity is a metabolic vulnerability for advanced prostate cancer and can serve as a novel therapeutic target.

2023-01-15 | GSE206962 | GEO

miRNA profiling in the plasma of patients with in-stent restenosis (ISR)

Project description:Studies of miRNA profiling in the plasma of patients between ISR and non-ISR Venous blood was collected in EDTA in the ward or the cardiac catheterization laboratory before the angiography procedure and heparin administration. Plasma was harvested by centrifugation and stored at -80°C until assayed. Identical volumes of plasma from the 6 patients with ISR and 4 patients with non-ISR were pooled to reach a final volume of 1500µL for each patient. Total RNA was extracted using miRVana isolation kit, dephosphorylated and labeled using miRNA Complete Labeling kit. Scanning was achieved with the illumina iScan System. The result were acquired with the Genome Studio (GenomeStudioV2009.1).

2014-09-02 | E-GEOD-60959 | biostudies-arrayexpress

ISR pathway activation signatures in MEFs: GCN2 and PERK

Project description:In response to different cellular stressors, the ISR kinases, PERK, PKR, HRI and GCN2, activate downstream transcriptional programs. While the core ISR transcription program is well characterized, markers that are specific to each individual ISR kinase activation pathway are not known. To identify markers that are induced by PERK or GCN2, but not the other ISR kinases, we subjected WT, GCN2-/-, and PERK-/- MEFs to amino acid starvation (RPMI 1640 SILAC -Lys -Arg) or Thapsigargin (200nM) treatment for 6 hours to activate the GCN2 and PERK pathways, respectively and performed RNA sequencing.

2022-07-01 | GSE179559 | GEO

A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers

Project description:A deregulated HOX gene axis confers an epigenetic vulnerability in KRAS mutant lung cancers

| PRJNA487264 | ENA

miRNA profiling in the plasma of patients with in-stent restenosis (ISR)

Project description:Studies of miRNA profiling in the plasma of patients between ISR and non-ISR

2014-09-02 | GSE60959 | GEO

ISR activation mediates the behavioral and neurophysiological abnormalities in Down syndrome

Project description:Down syndrome (DS) is the most common genetic cause of intellectual disability and a major biomedical concern. Despite a general consensus that protein homeostasis is essential for normal brain function, little is known about its role in DS. Here, we show that the integrated stress response (ISR)—a conserved signaling network that maintains proteostasis by controlling protein synthesis—is activated in the brains of DS mice and individuals with DS, leading to reduced translation. Genetic and pharmacological suppression of the ISR, either by inhibiting the ISR-initiating double-stranded RNA-activated protein kinase (PKR) or boosting the function of the eIF2•eIF2B complex, which becomes limiting upon ISR activation, de-repressed translation, reversed enhanced inhibitory synaptic transmission, and rescued the deficits in synaptic plasticity and memory in DS mice. Our findings unveil a crucial role for the ISR in DS pathophysiology and suggest tuning of the ISR as a promising therapeutic intervention for DS.

2019-11-02 | GSE138371 | 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