Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-PROT-45

ABSTRACT: Region and cell-type resolved quantitative proteomic map of the human heart.

TISSUE(S): Mitral Valve, Right Atrium, Pulmonary Valve, Pulmonary Artery, Atrial Septum, Left Atrium, Right Ventricle, Pulmonary Vein, Tricuspid Valve, Ventricular Septum, Aorta, Inferior Vena Cava, Left Ventricle, Aortic Valve

PROVIDER: E-PROT-45 | ExpressionAtlas | 2022-01-07

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-PROT-12-analysis-methods.tsv	Tabular
	E-PROT-45-analysis-methods.tsv	Tabular
	E-PROT-45-configuration.xml	Xml
	E-PROT-45-factors.xml	Xml
	E-PROT-45-zoomifications-log.tsv	Tabular

Items per page:

1 - 5 of 12

Similar Datasets

E-PROT-11

Project description:Initial quantitative proteomic map of 28 mouse tissues using the SILAC mouse

2021-11-09 | E-PROT-11 | ExpressionAtlas

RBM20 orchestrates cardiac pre-mRNA

Project description:The RNA-binding protein RBM20 has been implicated in dilated cardiomyopathy (DCM), a major cause of chronic heart failure. To determine how RBM20 regulates alternative splicing, we combined transcriptome-wide CLIP-seq, RNA-seq, and quantitative proteomics in cell culture, rat, and human hearts. Our analyses revealed a distinct RBM20 RNA-recognition element in predominantly intronic binding sites and linked repression of exon splicing with RBM20-binding near 3prime- and 5prime-splice sites. Our proteomic data show RBM20 interaction with U1- and U2-snRNPs and suggests splicing repression through spliceosome stalling at complex A. Among direct RBM20 targets are several genes involved in DCM as well as new genes not previously associated with the disease process. In human failing hearts, we demonstrate that reduced expression levels of RBM20 affect alternative splicing of several direct targets, indicating that differences in RBM20 gene expression may affect cardiac function. These findings reveal a new mechanism to understand the pathogenesis of human heart failure. The provided data files for RNA-seq contain information for reads that map to human RBM20 only.

2014-11-11 | E-MTAB-2572 | biostudies-arrayexpress

E-PROT-7

Project description:Cell type-resolved quantitative proteomics of mouse liver

2022-01-14 | E-PROT-7 | ExpressionAtlas

E-PROT-27

Project description:Systems-wide quantitative proteomic study of breast cancer tumours

2021-05-25 | E-PROT-27 | ExpressionAtlas

HeLa mRNA interactome

Project description:Pull-down of poly(A)-mRNA cross linked proteins using two cross-linking methods (conventional cross-linking and PAR-cross-linking) to identify all mRNA-binding proteins (GO:0003729). The provided data is quantitative proteomic data for comparison of cross-linking and control samples.

2012-08-14 | E-MTAB-869 | biostudies-arrayexpress

E-PROT-62

Project description:Quantitative proteomics of human heart samples collected in vivo reveal the remodeled protein landscape of dilated left atrium without atrial fibrillation.

2022-01-10 | E-PROT-62 | ExpressionAtlas

Reanalysis of Pandey lab's draft of the human proteome

Project description:The availability of human genome sequence has transformed biomedical research over the past decade. However, an equivalent map for the human proteome with direct measurements of proteins and peptides was lacking. To this end, Akhilesh Pandey's lab reported a draft map of the human proteome based on high resolution Fourier transform mass spectrometry-based proteomics technology, which included an in-depth proteomic profiling of 30 histologically normal human samples including 17 adult tissues, 7 fetal tissues and 6 purified primary hematopoietic cells ( http://dx.doi.org/10.1038/nature13302 ). The profiling resulted in identification of proteins encoded by greater than 17,000 genes accounting for ~84% of the total annotated protein-coding genes in humans. This large human proteome catalog (available as an interactive web-based resource at http://www.humanproteomemap.org) complements available human genome and transcriptome data to accelerate biomedical research in health and disease. Pandey's lab and collaborators request that those considering use of this primary dataset for commercial purposes contact pandey@jhmi.edu. The full details of this study can be found in the PRIDE database: www.ebi.ac.uk/pride/archive/projects/PXD000561/. This ArrayExpress entry represents a top level summary of the metadata only which formed the basis of the reanalysis performed by Joyti Choudhary's team ( jc4@sanger.ac.uk ), results of which are presented in the Expression Atlas at EMBL-EBI : http://www.ebi.ac.uk/gxa/experiments/E-PROT-1.

2015-03-10 | E-PROT-1 | biostudies-arrayexpress

The transcriptomic and proteomic map of human primary cells

Project description:The transcriptomic and proteomic map of human primary cells

| PRJNA787705 | ENA

Identification of an effective early signaling signature during neo-vasculogenesis in vivo by ex vivo proteomic profiling

Project description:Therapeutic neo-vasculogenesis in vivo can be achieved by the co-transplantation of human endothelial colony-forming progenitor cells (ECFCs) with mesenchymal stem/progenitor cells (MSPCs).The underlying mechanism is not completely understood thus hampering the development of novel stem cell therapies.We hypothesized that proteomic profiling could be used to retrieve the in vivo signaling signature during the initial phase of human neo-vasculogenesis. ECFCs and MSPCs were therefore either transplanted alone or co-transplanted subcutaneously into immune deficient mice. Early cell signaling, occurring within the first 24 hours in vivo, was analyzed using antibody microarray proteomic profiling.Vessel formation and persistence were verified in parallel transplants for up to 24 weeks. Proteomic analysis revealed significant alteration of regulatory components including caspases, calcium/calmodulin-dependent protein kinase, DNA protein kinase,human ErbB2 receptor-tyrosine kinase as well as mitogen-activated protein kinases.Therapeutic candidate caspase-4 was selected from array results for targeting vascular network formation in vitro as well as modulating therapeutic vasculogenesis in vivo. As a proof-of-principle, caspase-4 and general caspase-blocking led to diminished endothelial network formation in vitro and significantly decreased vasculogenesis in vivo. Proteomic profiling ex vivo thus unraveled a signaling signature which can be targeted to modulate neo-vasculogenesis in vivo.

2013-04-09 | GSE45896 | GEO

Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors

Project description:The aging of pancreatic beta-cells may undermine their ability to compensate for insulin resistance, leading to the development of type 2 diabetes (T2D). Aging beta-cells acquire markers of cellular senescence and develop a senescence-associated secretory phenotype (SASP) that can lead to senescence and dysfunction of neighboring cells through paracrine actions, contributing to beta-cell failure. Herein, we defined the beta-cell SASP signature based on unbiased proteomic analysis of conditioned media of cells obtained from human senescent beta-cells. These experiments revealed that the beta-cell SASP is enriched for factors associated with inflammation, cellular stress response, and extracellular matrix remodeling across species.

2021-03-18 | GSE162521 | 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