Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of HBV-infected Primary Human Hepatocytes treatment by Tazarotene

ABSTRACT: Monitor HBV mRNA reduction in response to Tazarotene and to identify global transcriptome-wide gene expression associated with Tazarotene treatment in HBV infected PHH using RNA-Seq

ORGANISM(S): Homo sapiens

PROVIDER: GSE114003 | GEO | 2018/09/09

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA Expression Profile of HBV-infected Primary Human Hepatocytes treatment by Interferon subtypes.

Project description:Microarray-dependent transcriptional analysis of interferon stimulated genes treated with different kind of interferon subtypes in HBV-infected PHH.

2020-04-20 | GSE138566 | GEO

RNA-seq of HBV-infected Primary Human Hepatocytes treatment by Tazarotene

Project description:RNA-seq of HBV-infected Primary Human Hepatocytes treatment by Tazarotene

| PRJNA454860 | ENA

Selective depletion of HBV-infected hepatocytes by class A capsid assembly modulators require high levels of intrahepatic HBV core protein

Project description:Several classes of capsid assembly modulators (CAMs) are currently being developed for chronic hepatitis B (CHB) cure. Both class A (CAM-A) and class E (CAM-E) CAMs disrupt nucleocapsid assembly and reduce extracellular hepatitis B virus (HBV) DNA. However, only CAM-As have been shown to reduce the number of HBV-infected cells in the animal models. However, there has been limited efficacy to date of CAM-A molecules achieving this secondary mechanism of HBV-infected cell clearance in CHB clinical trials. To investigate this disconnect, we performed comparative experiments with tool compounds from each class to further explore these unique features and antiviral activity of CAM-A across HBV-infected primary human hepatocytes (PHH), as well as in two different HBV mouse models (immunodeficient mice repopulated with human hepatocytes and AAV-HBV). Mechanistic studies in HBV-infected PHH revealed that CAM-A, but not CAM-E, induced dose-dependent aggregation of HBV core protein (HBc) in the nucleus. Experiments with siRNA, resulted in identification of the ubiquitin-binding protein p62 as a factor negatively regulating the size of these aggregates. Furthermore, we found that only the CAM-A is able to induce HBc-positive cell death in vivo with the loss of HBV-infected cells positively correlated to the levels of intrahepatic HBc. Profiling of intrahepatic HBc levels across CHB patient liver biopsies demonstrated a significantly lower level of HBc per hepatocyte than either of the HBV mouse models. Taken together, these data demonstrate that CAMs of class A have a unique secondary mechanism that has potential to specifically affect viability of HBV-infected hepatocytes. At the same time, the clearance of infected hepatocytes may depend on the level of HBc expression thereby limiting the therapeutic potential for this class of molecules.

2024-05-21 | GSE260966 | GEO

ChIP-Seq data of H3K79succ modification of mononuclear bodies in PHH cells infected with HBV

Project description:Cell: HBV-infected PHH cells. Methods: PHH cells were infected with 2000 genome equivalents/cell of HBV particles in the presence of 4% PEG8000. Seven days after HBV infection, ChIP-Seq analysis of cccDNA in HBV-infected PHHs was carried out. HBV-infected PHH cells were digested with micrococcal nuclease and resulting mononucleosomes purified by sucrose gradient centrifugation. Nucleosomes were enriched with anti-H3K79succ antibodies by ChIP assay and the associated DNA contained both human and HBV DNA fragments was analyzed by deep sequencing. The HBV-specific reads in ChIP-Seq pilot experiments was quantified and normalized by the reads mapped to the human genome.

2021-11-14 | GSE188634 | GEO

Effect of two compounds on HBV gene expression in HBV-infected primary human hepatocytes.

Project description:HBV gene expression in HBV-infected primary human hepatocytes.

2022-07-15 | GSE208115 | GEO

Changes of microRNA expression levels in HBV-infected human primary hepatocytes

Project description:Human primary hepatocytes isolated from chimeric mice were infected with HBV for 7 days. The comprehensive changes of miRNA levels were determined by miRNA array. MicroRNA expression levels were compared in between control and HBV-replicating primary hepatocytes by 2K microRNA microarrays

2014-03-15 | E-GEOD-55929 | biostudies-arrayexpress

HBV-infected Primary Human Hepatocytes and HBV-infected HepG2-NTCP cells treatment by Interferon subtypes

Project description:HBV-infected Primary Human Hepatocytes and HBV-infected HepG2-NTCP cells treatment by Interferon subtypes

| PRJNA576399 | ENA

Changes of microRNA expression levels in HBV-infected human primary hepatocytes

Project description:Human primary hepatocytes isolated from chimeric mice were infected with HBV for 7 days. The comprehensive changes of miRNA levels were determined by miRNA array.

2014-03-15 | GSE55929 | GEO

Long-Term Hepatitis B Virus Infection Induces Cytopathic Effects in Primary Human Hepatocytes, and Can be Partially Reversed by Antiviral Therapy

Project description:Based on our recently developed 5 chemicals-cultured primary human hepatocytes (5C-PHH) model that supports long-term HBV infection, we performed multiplexed quantitative analysis of temporal changes of host proteome and transcriptome on PHH cells infected by HBV for up to 4 weeks. We showed that metabolic-, complement-, cytoskeleton-, mitochondrial- and oxidation-related pathways were modulated at transcriptional or post-transcriptional levels during long-term HBV infection, which led to cytopathic effects and could be partially rescued by early rather than late nucleot(s)ide analogs (NAs) administration.

2021-09-02 | GSE183156 | GEO

Deciphering hepatitis B virus phospho-signature in primary human hepatocytes

Project description:Phosphorylation is a major post-translation modification (PTM) of proteins, and small molecules, which is finely tuned by the activity of several hundred kinases and phosphatases. It controls most if not all cellular pathways including anti-viral responses. Accordingly, viruses often induce important changes in the phosphorylation of host factors that can either help or counteract viral replication. Surprisingly, among more than 500 kinases constituting the human kinome only few have been described as important for the Hepatitis B virus (HBV) infectious cycle, and most of them intervene during early or late infectious steps by phosphorylating the viral Core protein (HBc) protein. In addition, scarce information is available on the consequences of HBV infection on the activity of cellular kinases. The objective of this study was to investigate the global impact of HBV infection on the cellular phosphorylation landscape at early after infection. For this, primary human hepatocytes (PHH) were challenged or not with HBV, and a mass spectrometry (MS)-based quantitative phospho-proteomic analysis was conducted two- and seven-days post-infection.

2024-05-02 | PXD051216 | 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