Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (RNA-Seq BGI)

ABSTRACT: Through genome-wide profiling of chromatin dynamics, we revealed a profound increase of global chromatin accessibility and a switch from H3K9me3 to H3K9ac on cis-regulatory DNA elements of cyst-associated genes during cystogenesis. In an integrated epigenomic and transcriptomic analysis, we identified a transcription factor network associated with dynamic shifts in chromatin states. Functionally, we showed that inhibition of H3K9ac acetyltransferase or H3K9me3 demethylase restored chromatin states and gene expression program to slow cyst growth in PLD mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE202008 | GEO | 2023/01/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (ChIP-Seq)

Project description:Through genome-wide profiling of chromatin dynamics, we revealed a profound increase of global chromatin accessibility and a switch from H3K9me3 to H3K9ac on cis-regulatory DNA elements of cyst-associated genes during cystogenesis. In an integrated epigenomic and transcriptomic analysis, we identified a transcription factor network associated with dynamic shifts in chromatin states. Functionally, we showed that inhibition of H3K9ac acetyltransferase or H3K9me3 demethylase restored chromatin states and gene expression program to slow cyst growth in PLD mice.

2023-01-27 | GSE202007 | GEO

Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (ATAC-Seq)

2023-01-27 | GSE202006 | GEO

Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (RNA-Seq female)

2023-07-18 | GSE237568 | GEO

Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (ChIP-Seq female)

2023-07-18 | GSE237567 | GEO

Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (ATAC-Seq female)

2023-07-18 | GSE237566 | GEO

Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (RNA-Seq Illumina)

2023-01-27 | GSE202009 | GEO

Quantitative Proteomic Study Unmasks Fibrinogen Pathway in Polycystic Liver Disease

Project description:(1) Background: Polycystic liver disease (PLD) is a heterogeneous group of congenital disorders characterized by bile duct dilatation and cyst development derived from cholangiocytes. Nevertheless, the cystogenesis mechanism is currently unknown and the PLD treatment is limited to liver transplantation. Novel and efficient therapeutic approaches are th6us needed. In this context, the present work has a principal aim to find novel molecular pathways, as well as new therapeutic targets, involved in the hepatic cystogenesis process. (2) Methods: Quantitative proteomics based on SWATH–MS technology were performed comparing hepatic proteomes of Wild Type and mutant/polycystic livers in a polycystic kidney disease (PKD) murine model (Pkd1cond/cond;Tam-Cre−/+). (3) Results: We identified several proteins altered in abundance, with twofold cut-off up-regulation or down-regulation and an adjusted p-value significantly related to hepatic cystogenesis. Then, we performed enrichment and a protein–protein analysis identifying a cluster focused on hepatic fibrinogens. Finally, we validated a selection of targets by RT-qPCR, Western blotting and immunohistochemistry, finding a high correlation with quantitative proteomics data and validating the fibrinogen complex. (4) Conclusions: This work identified a novel molecular pathway in cystic liver disease, highlighting the fibrinogen complex as a possible new therapeutic target for PLD.

2022-04-04 | PXD031253 | Pride

Confirmation of the gene expression pattern in Mxi1-deficient mouse

Project description:For final aim to completes network map between gene that is concerned in cystogenesis, verifies meaning genes connected with cyst formation analyzing gene pattern in Mxi1 KO mouse that have phenotype of polycystic kidney disease. Monitoring meaning genes through microarray analysis, and confirm the function of these genes. Also, find pathway including meaning genes and new pathway related with PKD. Completes network map concerned in cystogenesis through integrates knowing pathway and predicting pathway. Develope diagnostic of cyst disease and cure target through such completed network map, and wish to clear new role of cyst formation connection gene through in vivo model and examine closely control system of cyst formation mechanism. Keywords: Cystogenesis Use 1 mouse at each experiment and control. Indirect labeling of 10g cRNA, using bacterial control mRNA.

2008-04-29 | E-GEOD-11053 | biostudies-arrayexpress

Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (RNA-Seq BGI)

Project description:Multi-omics profiling of cholangiocytes reveals chromatin state dynamics during hepatic cystogenesis in polycystic liver disease (RNA-Seq BGI)

| PRJNA834045 | ENA

Targeting UBC9-mediated Protein Hyper-SUMOylation in Cystic Cholangiocytes Halts Polycystic Liver Disease in Experimental Models

Project description:Background & Aims: polycystic liver diseases (PLDs) are genetic disorders characterized by progressive development of multiple fluid-filled biliary cysts. Most PLD-causative genes participate in protein biogenesis and/or transport. Post-translational modifications (PTMs) are implicated in protein stability, localization and activity, contributing to human pathobiology; however, their role in PLD is unknown. Here, we aimed to unveil the role of protein SUMOylation in PLD and its potential therapeutic targeting. Methods: levels and function of SUMOylation, along with response to S-adenosylmethionine (SAMe, inhibitor of the SUMOylation enzyme UBC9) and/or short-hairpin RNAs (shRNAs) against UBE2I (UBC9), were evaluated in vitro, in vivo and/or in patients with PLD. SUMOylated proteins were determined by immunoprecipitation and proteomic analyses by mass spectrometry. Results: most SUMOylation-related genes were found overexpressed (mRNA) in polycystic human and rat liver tissue, as well as in cystic cholangiocytes in culture compared to controls. Increased SUMOylated protein levels were also observed in cystic human cholangiocytes in culture, which decreased after SAMe administration. Chronic treatment of polycystic (PCK: Pkdh1-mut) rats with SAMe halted hepatic cystogenesis and fibrosis, and reduced liver/body weight ratio and liver volume. In vitro, both SAMe and shRNA-mediated UBE2I knockdown increased apoptosis and reduced cell proliferation of cystic cholangiocytes. High-throughput proteomic analysis of SUMO1-immunoprecipitated proteins in cystic cholangiocytes identified candidates involved in protein biogenesis, ciliogenesis and proteasome degradation. Accordingly, SAMe hampered the proteasome hyperactivity in cystic cholangiocytes, leading to the activation the unfolded protein response (UPR) and stress-related apoptosis.

2020-09-29 | PXD021139 | Pride

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