Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Modelling of H3K4me3 histone modification data identifies signalling molecules that improve cell maintenance and conversion

ABSTRACT: RNA-seq data from H9 ESC, primary astrocyte and at different time-points (day 7, 14 and 21) during astrocyte differentiation and at conditions with control Matrigel and all ligands predicted by EpiMogrify.

ORGANISM(S): Homo sapiens

PROVIDER: GSE155564 | GEO | 2020/08/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Modelling of H3K4me3 histone modification data identifies signalling molecules that improve cell maintenance and conversion

Project description:Modelling of H3K4me3 histone modification data identifies signalling molecules that improve cell maintenance and conversion

| PRJNA650306 | ENA

Fractionation RNAseq in conjunction with Illumina TRUseq method

Project description:H9 human ESCs (H9 line) were cultured in BMP4 cultured medium on Matrigel-coated plates. Colonies were passaged for maintanence by Gentle Cell Dissociation Reagent

2019-03-20 | E-MTAB-5116 | biostudies-arrayexpress

Mitochondrial reprogramming using dCas9 boosts glia-to-neuron conversion

Project description:Astrocyte-to-neuron conversion has developed into a promising avenue for neuronal replacement therapy. Neurons depend critically on mitochondria function and often die by ferroptosis during the conversion process. Here we examined the extent of adequate mitochondrial reprogramming by morphology and proteome analysis. While mitochondria profoundly changed their morphology during Neurogenin2 (Neurog2) – or Achaete-scute homolog 1 (Ascl1)-mediated astrocyte-to-neuron reprogramming, we found neuron-specific mitochondrial proteins, here identified in a comprehensive proteome analysis of isolated mitochondria from primary neurons and astrocytes, to be only partially and at late stages regulated during the process. To improve this, we used dCas9 technology to induce neuron-specific mitochondrial proteins early during reprogramming. This resulted not only in increased conversion efficiency, but also in faster neuronal generation. Taken together, reprogramming mitochondria in a cell type-specific manner has powerful effects on astrocyte-to-neuron conversion, suggesting mitochondria to be a driving force in this process.

2021-03-29 | PXD014886 | Pride

Signalling molecules in MEFs/FL

Project description:In silico analysis identified signalling molecules related to Wnt (Wnt1, 2, 5a, 5b, 6, 11, 14, Wisp1, 2, sFRP1 and 2, Dkks 2 and 3) and BMP (BMP1, 4, 5) pathways. Many of these tags matched multiple transcripts in GenBank, while other potential molecules could not be detected because the transcripts either lacked an anchoring enzyme site or the site was immediately adjacent to the polyA+ sequence. Keywords: SAGE To identify potential signalling molecules (secreted or cell-cell interacting) implicated in the formation of INPs, we constructed a SAGE library from MEFs

2006-07-27 | E-GEOD-5402 | biostudies-arrayexpress

Discovery of Small Molecules that Target Vascular Endothelial Growth Factor Receptor-2 Signalling Pathway Employing Molecular Modelling Studies.

Project description:Angiogenesis is defined as the formation of new blood vessels and is a key phenomenon manifested in a host of cancers during which tyrosine kinases play a crucial role. Vascular endothelial growth factor receptor-2 (VEGFR-2) is pivotal in cancer angiogenesis, which warrants the urgency of discovering new anti-angiogenic inhibitors that target the signalling pathways. To obtain this objective, a structure-based pharmacophore model was built from the drug target VEGFR-2 (PDB code: 4AG8), complexed with axitinib and was subsequently validated and employed as a 3D query to retrieve the candidate compounds with the key inhibitory features. The model was escalated to molecular docking studies resulting in seven candidate compounds. The molecular docking studies revealed that the seven compounds displayed a higher dock score than the reference-cocrystallised compound. The GROningen MAchine for Chemical Simulations (GROMACS) package guided molecular dynamics (MD) results determined their binding mode and affirmed stable root mean square deviation. Furthermore, these compounds have preserved their key interactions with the residues Glu885, Glu917, Cys919 and Asp1046. The obtained findings deem that the seven compounds could act as novel anti-angiogenic inhibitors and may further assist as the prototype in designing and developing new inhibitors.

| S-EPMC6468367 | biostudies-literature

Signalling molecules in MEFs/FL

2006-07-27 | GSE5402 | GEO

DNA microarrays of Wilson's disease patient-specific induced pluripotent stem cells

Project description:Wilson’s disease (WD) is a relevant human genetic disease caused by mutations in the ATP7B gene, whose product is a liver enzyme responsible for copper export into bile and blood. Interestingly, the spectrum of ATP7B mutations is vast and can influence clinical presentation (a variable spectrum of hepatic and neural manifestations), though the reason for this is not well understood. Here we describe the successful generation of iPSCs from a Chinese patient with Wilson’s disease that bears the R778L Chinese hotspot mutation in the ATP7B gene. Global gene expression profiling with DNA microarrays showed that WD iPSCs cluster together with human ESCs (H9) compared to donor fibroblasts. WD patient fibroblasts were isolated and expanded from a dermal biopsy of a middle age Chinese Han male, WD iPSCs were generated by overexpression of human Oct4/Sox2/Klf4/c-Myc in WD fibroblasts and expanded on Matrigel with mTESR1 culture medium. For DNA microarray analysis, WD fibroblasts (passage 5), 3 cell lines of WD iPSCs growing on Matrigel (passage 8) and human ES H9 growing on Matrigel (passage 40) were treated with Trizol, followed by RNA extraction and hybridization.

2010-12-01 | E-GEOD-24997 | biostudies-arrayexpress

Ex vivo modelling of pancreatic cancer recapitulates in vivo extracellular matrix signatures and drug responses

Project description:The ex vivo modelling of pancreatic ductal adenocarcinoma (PDAC) using patient-derived cells is a promising tool to predict treatment responses. Matrigel-based organoid and organotypic approaches are limited by their undefined molecular composition, hindering the recapitulation of the tumour’s characteristic desmoplasia, which is known to promote drug resistance. To overcome these limitations, we used self-assembling peptide amphiphiles (PAs) gelled in a minimal extracellular matrix to model the pancreatic tumour microenvironment and to establish 3D multicellular cultures of patient-derived PDAC cells, pancreatic stellate cells and macrophages. Matrisome analysis of 3D cultures demonstrated consistent ECM protein deposition, which was highly reminiscent of the corresponding primary PDAC tissues. The proteomic data obtained was also compared to the corresponding patient-derived xenografts (PDX) in nude mice and Matrigel-based cultures. Characterisation of the chemosensitivity of the cultures revealed realistic treatment responses by PDAC cells in PA hydrogels based on the responses of their corresponding PDX tumours. Histological, transcriptional and functional techniques confirmed these similarities, which were not observed in Matrigel-based cultures. These findings demonstrate the biomimetic nature of PA hydrogels, which enable cultured cells to recreate the PDAC matrisome ex vivo and to respond to chemotherapeutic agents in a predictive manner.

2021-07-06 | PXD013254 | Pride

Transcriptional changes and microRNA expression profiles during NeuroD1-mediated astrocyte-to-neuron conversion

Project description:To reveal the molecular mechanisms underlying astrocyte-to-neuron reprogramming, we performed RNA-seq analysis on human astrocyte cultures (HA1800) during NeuroD1(ND1)-mediated neuronal reprogramming.

2023-07-10 | GSE214749 | GEO

Mitochondrial metabolites: undercover signalling molecules.

Project description:Mitochondria are one of most characterized metabolic hubs of the cell. Here, crucial biochemical reactions occur and most of the cellular adenosine triphosphate (ATP) is produced. In addition, mitochondria act as signalling platforms and communicate with the rest of the cell by modulating calcium fluxes, by producing free radicals, and by releasing bioactive proteins. It is emerging that mitochondrial metabolites can also act as second messengers and can elicit profound (epi)genetic changes. This review describes the many signalling functions of mitochondrial metabolites under normal and stress conditions, focusing on metabolites of the tricarboxylic acid cycle. We provide a new framework for understanding the role of mitochondrial metabolism in cellular pathophysiology.

| S-EPMC5311903 | biostudies-literature

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