Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bmal1 -/- RNA-seq in mouse embryonic stem cells

ABSTRACT: RNA seq experiment comparing mRNA expression in Bmal1 -/- and parental wild-type mESCs

ORGANISM(S): Mus musculus

PROVIDER: GSE134884 | GEO | 2020/03/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Bmal1 -/- RNA-seq in mouse embryonic stem cells

Project description:Bmal1 -/- RNA-seq in mouse embryonic stem cells

| PRJNA556693 | ENA

Influence of SB431542 on J1 mouse embryonic stem cells growth

Project description:To know exactly how SB431542 contribute to mouse embryonic stem cells (mESCs) undifferentiated state maintenance, microarray experiment for DMSO mock treated and SB431542 treated J1 mESCs was performed

2014-10-29 | GSE55729 | GEO

ATAC-seq of mouse embryonic stem cells

Project description:To identify the accessible chromatin in wild-type mouse embryonic stem cells (mESCs), we performed ATAC-seq in mESCs.

2021-01-05 | E-MTAB-9245 | biostudies-arrayexpress

Circadian key component CLOCK/BMAL1 interferes with segmentation clock in mouse embryonic organoids

Project description:In mammals, circadian clocks are strictly suppressed during early embryonic stages as well as pluripotent stem cells, by the lack of CLOCK/BMAL1 mediated circadian feedback loops. During ontogenesis, the innate circadian clocks emerge gradually at a late developmental stage, then, with which the circadian temporal order is invested in each cell level throughout a body. Meanwhile, in the early developmental stage, a segmented body plan is essential for an intact developmental process and somitogenesis is controlled by another cell-autonomous oscillator, the segmentation clock, in the posterior presomitic mesoderm (PSM). In the present study, focusing upon the interaction between circadian key components and the segmentation clock, we investigated the effect of the CLOCK/BMAL1 on the segmentation clock Hes7 oscillation, revealing that the expression of functional CLOCK/BMAL1 severely interferes with the ultradian rhythm of segmentation clock in induced PSM and gastruloids. RNA sequencing analysis showed that the premature expression of CLOCK/BMAL1 affects the Hes7 transcription and its regulatory pathways. These results suggest that the suppression of CLOCK/BMAL1-mediated transcriptional regulation during the somitogenesis may be inevitable for intact mammalian development.

2021-12-09 | GSE181295 | GEO

CTCF ChIP-MS from crosslinked chromatin in mouse embryonic stem cells (mESCs) and motor neurons (MNs)

Project description:To identify CTCF partners and co-localizing proteins from crosslinked chromatin in mESCs and MNs in endogenous conditions. The goal is to identify proteins within each sample with respect to wild-type control for each.

2022-02-15 | PXD030543 | Pride

CTCF ChIP-MS from native chromatin in mouse embryonic stem cells (mESCs) and motor neurons (MNs)

Project description:To identify CTCF partners and co-localizing proteins from native chromatin in mESCs and MNs in endogenous conditions. The goal is to identify proteins within each sample with respect to wild-type control for each.

2022-02-11 | PXD030452 | Pride

RNA-seq experiment of mouse embryonic stem cells (mESCs), comparing TCF/LEF quadruple knock-out cells with wild type cells

Project description:RNA-seq experiment of mouse embryonic stem cells (mESCs), comparing TCF/LEF quadruple knock-out cells with wild type cells

| PRJEB45649 | ENA

Mouse embryonic stem cells LCMS-MS

Project description:We hypothesized that uncovering interactions between Pfkp and other proteins could help resolve the mechanism whereby Pfkp regulates germ layer differentiation. Towards this, Pfkp was immunoprecipitated from mESCs and mass spectrometry analysis used to identify a number of potential Pfkp-interacting proteins

2023-02-23 | PXD038944 | Pride

The molecular clock protein Bmal1 regulates cell differentiation in mouse embryonic stem cells.

Project description:Mammals optimize their physiology to the light-dark cycle by synchronization of the master circadian clock in the brain with peripheral clocks in the rest of the tissues of the body. Circadian oscillations rely on a negative feedback loop exerted by the molecular clock that is composed by transcriptional activators Bmal1 and Clock, and their negative regulators Period and Cryptochrome. Components of the molecular clock are expressed during early development, but onset of robust circadian oscillations is only detected later during embryogenesis. Here, we have used naïve pluripotent mouse embryonic stem cells (mESCs) to study the role of Bmal1 during early development. We found that, compared to wild-type cells, Bmal1-/- mESCs express higher levels of Nanog protein and altered expression of pluripotency-associated signalling pathways. Importantly, Bmal1-/- mESCs display deficient multi-lineage cell differentiation capacity during the formation of teratomas and gastrula-like organoids. Overall, we reveal that Bmal1 regulates pluripotent cell differentiation and propose that the molecular clock is an hitherto unrecognized regulator of mammalian development.

| S-EPMC7156284 | biostudies-literature

Diurnal profiling of mouse liver of hepatocyte specific BMAL1 KO mice (Bmal1 HepKO)

Project description:Obesity and liver diseases are associated with the disruption of the circadian clock that orchestrates mammalian physiology to optimize nutrient metabolism and storage. We show here that the activity of the circadian clock regulator BMAL1 is perturbed during liver fibrosis in humans. To understand the impact of BMAL1 perturbation in obesity and liver diseases, we assessed the impact of a high fat diet or leptin deficiency on Bmal1 knockout mice. While Bmal1 knockout mice were prone to obesity, they were protected against insulin resistance, hepatic steatosis, inflammation, and fibrosis. In addition to direct transcriptional regulation of metabolic programs by BMAL1, we show that adaptation of the growth hormone and sex hormone pathways plays a critical role in this protection. Similar endocrine perturbations correlate with the development of liver fibrosis in humans, suggesting that endocrine perturbation associated with circadian disruption is critical for the pathogenesis of metabolic and liver diseases.

2022-01-26 | GSE190221 | 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