Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Endothelial-specific mitochondiral complex III KO leads to lung endothelial cell gene deregulation.

ABSTRACT: Endothelial-specific mitochondiral complex III KO leads to lung endothelial cell gene deregulation.

PROVIDER: PRJNA498407 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8109841.fastq.gz	Fastqsanger.gz
	SRR8109842.fastq.gz	Fastqsanger.gz
	SRR8109843.fastq.gz	Fastqsanger.gz
	SRR8109844.fastq.gz	Fastqsanger.gz
	SRR8109845.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Endothelial-specific mitochondiral complex III KO leads to lung endothelial cell gene deregulation.

Project description:Endothelial cells (ECs) require glycolysis for proliferation and migration during angiogenesis; however, the necessity for the mitochondrial respiratory chain during angiogenesis is not known. Here we report that inhibition of respiratory chain complex III impairs proliferation, but not migration of ECs in vitro by decreasing the NAD+/NADH ratio. To determine whether mitochondrial respiration is necessary for angiogenesis in vivo, we conditionally ablate a subunit of the respiratory chain complex III (QPC) in ECs. Loss of QPC decreases respiration, resulting in diminished EC proliferation, and impairment in retinal and tumor angiogenesis. Loss of QPC does not decrease genes associated with anabolism or nucleotides levels in ECs, but diminishes amino acid levels. Our findings indicate that mitochondrial respiration is necessary for angiogenesis, and that the primary role of mitochondria in ECs is to serve as biosynthetic organelles for cell proliferation.

2018-10-26 | GSE121770 | GEO

Epidermal overexpression of ∆NLef1 leads to deregulation of epidermal stem cell fate

Project description:Epidermal overexpression of ∆NLef1 leads to deregulation of epidermal stem cell fate

| PRJNA484336 | ENA

Identification of endothelial derived factors that promote metastasis III

Project description:Identification of endothelial derived factors that promote metastasis III

| PRJNA606757 | ENA

RNA-seq of CCBE1 KO and WT murine hearts

Project description:CCBE1 is a secreted extracellular matrix protein expressed by epicardial cells but its role during epicardial development was still unknown.Using a Ccbe1 knockout (KO) mouse model, we observed that loss of CCBE1 leads to congenital heart defects including thinner and hyper-trabeculated ventricular myocardium. In addition, Ccbe1 mutant hearts displayed reduced proliferation of cardiomyocyte and epicardial cells. RNA-seq data of CCBE1 KO and WT murine hearts indicated deregulation of genes associated with development and morphogenesis including the epithelial-to-mesenchymal transition.

2022-10-23 | E-MTAB-12217 | biostudies-arrayexpress

Prostate cancer resistance leads to a global deregulation of translation factors and unconventional translation

Project description:Prostate cancer resistance leads to a global deregulation of translation factors and unconventional translation

| PRJNA742424 | ENA

Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders

Project description:Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders. Human fetal neurons were chosen to examine the impact of HIV-1 Vpr protein on gene expression

2012-12-07 | E-GEOD-42424 | biostudies-arrayexpress

Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders.

Project description:Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders. Using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Vpr) on the expression of miRNAs and mRNAs.

2013-02-12 | E-GEOD-44266 | biostudies-arrayexpress

Aortic macrophages and endothelial cells of apoE KO mice aortas after plaque regression induced apoE adenoviral transfer

Project description:Aortic macrophages and endothelial cells of apoE KO mice were sorted and analyzed by microarray 2 weeks after regression was induced by adenoviral transfer of apoE. Aortic macrophages (CD45+ F4/80+ CD11b+) and endothelial cells (CD45- CD31+) were sorted from apoE KO mice and the RNA extracted and hybridized to Affymetrix Mouse Gene 1.0 ST array. We pooled aortas from 5 mice for each sort.

2015-01-01 | E-GEOD-42691 | biostudies-arrayexpress

Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders.

2013-02-12 | GSE44266 | GEO

Endothelial Sirtuin1 Suppresses Whole-body Insulin Sensitivity by Modulating the Secretome

Project description:Sirtuin1 (Sirt1) in skeletal muscle (SK) and fat protects against metabolic damage by stimulating insulin sensitivity. Here we report that mice with selective deletion of endothelial Sirt1 (E-Sirt1-KO) paradoxically exhibit heightened whole-body insulin sensitivity. Akt phosphorylation, glucose uptake, and glycolysis are boosted in SK and brown adipose tissue (BAT) of E-Sirt1-KO mice. E-Sirt1-KO mice have higher energy expenditure and are partially protected from high-fat diet-induced insulin resistance. Enhanced insulin sensitivity and peripheral tissue Akt phosphorylation in E-Sirt1-KO mice is transferrable to wild-type mice via the systemic circulation after surgical parabiosis. Silencing of Sirt1 in endothelial cells upregulates transcription of the F-actin-binding protein thymosin beta-4 (Tβ4), whose secretion activates Akt in skeletal myotubes. Sirt1 downregulation stimulates endothelial Tβ4 transcription through inhibition of autophagy and upregulation of nuclear factor-kappa B signaling. Thus, unlike Sirt1 in skeletal muscle and fat, endothelial Sirt1 curtails whole-body insulin sensitivity by inhibiting expression of secreted Tβ4

2021-12-02 | ST002204 | MetabolomicsWorkbench

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