Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Myh9 knockdown and PEG950 treatment on in vitro differentiated hepatocyte gene expression

ABSTRACT: Effect of Myh9 knockdown and PEG950 treatment on in vitro differentiated hepatocyte gene expression

PROVIDER: PRJNA1167646 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Effect of Myh9 knockdown and PEG950 treatment on in vitro differentiated hepatocyte gene expression

Project description:Myh9 knockdown reduces the strength of the apical actomyosin cortex from hepatocytes, which causes isotropic growth of the bile canaliculus (BC) and ultimately results in the formation of hepatocyte cysts with a large central apical lumen. Treatment of hepatocytes with the osmotically active bioinert polymer PEG950 causes and increase in intraluminal pressure, which causes expansion of the bile canaliculus (BC) and ultimately results in the formation of hepatocyte cysts with a large central apical lumen. In these cysts, hepatocytes have common apico-basal polarity, such as observed for simple epithelia like cholangiocytes. To investigate whether this change in apical lumen morphology and polarization is associated with alterations in gene expression we compared hepatocytes with and without Myh9 knockdown and with and without PEG950 treatment.

2024-10-16 | GSE278503 | GEO

Effect of Rab35 knockdown on in vitro differentiated hepatocyte gene expression (time-course)

Project description:Effect of Rab35 knockdown on in vitro differentiated hepatocyte gene expression (time-course)

| PRJNA862855 | ENA

Effect of Rab35 knockdown on in vitro differentiated hepatocyte gene expression (time-course)

Project description:Rab35 knockdown results in a loss of apical bulkheads from hepatocytes, which causes isotropic growth of the bile canaliculus (BC) and ultimately results in the formation of hepatocyte cysts. In these cysts, hepatocytes have common apico-basal polarity, such as observed for simple epithelia like cholangiocytes. To investigate whether this change in polarization is associated with alterations in gene expression we compared hepatocytes with and without Rab35 knockdown in a previous RNA-sequencing experiment and found changes in gene expression after 5 days of culture. In this experiment, we want to investigate when Rab35 knockdown starts to affect gene expression. For this, we performed a time-course RNA-sequencing experiment in hepatocytes with and without Rab35 knockdown.

2024-10-16 | GSE209876 | GEO

CD248 knockdown in in vitro differentiated adipocytes exposed to hypoxia

Project description:CD248 knockdown in in vitro differentiated adipocytes exposed to hypoxia

| PRJNA544327 | ENA

Myh9 plays essential role in hematopoietic stem/progenitor cells survival and maintenance

Project description:Myosin heavy chain 9 (MYH9) gene encodes a protein named non-muscle heavy chain IIA (NMHC IIA), interacting with actin and participating in various biological processes. Mutations in MYH9 cause an array of autosomal dominant disorders, known as MYH9-related diseases (MYH9-RD). However, the role of MYH9 in normal hematopoiesis remains largely unexplored. By using Mx1-cre Myh9 conditional knockout mice, we established an inducible system to precisely inactivate Myh9 function in hematopoietic cells in vivo. The results showed that deletion of Myh9 led to severe defects in hematopoiesis, characterized by pancytopenia, drastic decreases of hematopoietic stem/progenitor cells (HSPC), and bone marrow failure, causing early lethality in mice. The defect in hematopoiesis caused by Myh9 ablation is cell autonomous. In addition, Myh9 deletion impairs HSPC repopulation capacity and increases apoptosis. RNA sequencing results revealed significant alterations in the expression of genes related to HSC self-renewal and maintenance, while multiple signal pathways were also involved, including genes for HSC and myeloid cell development, intrinsic apoptosis, targets of mTOR signaling, and maturity of hematopoietic cells. Collectively, our findings suggest an essential role for Myh9 in the survival and maintenance of HSPC in normal hematopoiesis.

2022-06-01 | GSE198134 | GEO

Expression data from in vitro differentiated MDSC

Project description:Expression data from in vitro differentiated MDSC

| PRJNA623778 | ENA

CD248 knockdown in in vitro differentiated adipocytes exposed to hypoxia

Project description:Human adipose tissue derived stem cells were differentiated to adipocytes in vitro. At the end of differentiation, cells were treated with siRNA targeting CD248 followed by exposure to 1% oxygen levels. Microarray analysis were performed to identify differentially regulated genes.

2019-05-23 | GSE131667 | GEO

RNA-seq of in vitro differentiated human abdominal and gluteal adipocyte cell lines following doxycycline induced RSPO3-knockdown

Project description:GWAS studies and our own work have identified RSPO3 as a gene modulating human body fat distribution. The GWAS signal at RSPO3 is coincident with an eQTL in mature adipocytes. To assess the effects of RSPO3 on abdominal and gluteal adipocyte biology, we undertook inducible RSPO3-knockdown in in vitro differentiated immortalized human abdominal and gluteal adipocyte cell lines (DFAT cells).

2020-06-01 | GSE149294 | GEO

Rab35 knock-down during in vitro hepatocyte differentiation

Project description:Rab35 knock-down during in vitro hepatocyte differentiation

| PRJNA1130838 | ENA

Expression data from hepatocyte-like cells (HLCs) differentiated from human induced pluripotent stem cells (iPSCs)

Project description:We devised two hepatocyte differentiation methods, namely Method 1 (M1) and Method 2 (M2), through modifying existing well-known hepatocyte differentiation strategies, and compared the resultant cells phenotypically, functionally and transcriptomically at different stages of hepatocyte differentiation. !Series_summary =We used microarrays to compare the global gene expression of the HLCs differentiated using the two methods, M1 and M2.

2021-11-03 | GSE187011 | 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