Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [ssRNA-seq]

ABSTRACT: BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [ssRNA-seq]

PROVIDER: PRJNA1096630 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [ssRNA-seq]

Project description:Genome profiling of BMAL1,TRIM28 and H3K9me3 analyzed by ChIP-seq in JM8+/+ and Bmal1-/- mESCs. Genome profiling of FlagBMAL1 in mESCs. High throughput capture chromosome conformation analysis (Hi-C) in JM8+/+ and Bmal1-/- mESCs. mRNA-seq analysis of JM8+/+ and Clock-/- mESCs

2025-08-14 | GSE263284 | GEO

BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [ChIP-seq]

Project description:BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [ChIP-seq]

| PRJNA1096625 | ENA

BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [Hi-C]

Project description:BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [Hi-C]

| PRJNA1096626 | ENA

BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [Hi-C]

2025-08-14 | GSE263283 | GEO

BMAL1 represses transposable elements independently of CLOCK in pluripotent cells [ChIP-seq]

2025-08-14 | GSE263279 | GEO

BMAL1 represses transposable elements independently of CLOCK in pluripotent cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-14 | GSE263285 | GEO

Twenty-four hour rhythms in the absence of the clock gene Bmal1

Project description:Circadian (~24 hour) clocks exist in almost all types of living organism and play a fundamental role in regulating daily physiological and behavioural processes. The transcription factor BMAL1 (ARNTL) is thought to be one of the principal drivers of the molecular clock in mammals since its deletion abolishes 24-hour activity patterning, an important physiological output of the clockwork. However, whether or not Bmal1-/- mice can nevertheless display molecular 24-hour rhythms is unknown. Here, we determined whether Bmal1 function is necessary for daily molecular oscillations in two tissues – skin fibroblasts and liver. Unexpectedly, both tissues exhibited robust 24-hour oscillations over 2-3 days in the absence of any exogenous synchronizers such as daily light or temperature cycles. This demonstrates a competent 24-hour molecular pacemaker in Bmal1 knockouts. Indeed, molecular oscillations were pervasive throughout the transcriptome, proteome and phosphoproteome of Bmal1-/- mice. In particular, several proteins exhibited rhythmic phosphorylation in both Bmal1-proficient and -deficient cells, highlighting an unanticipated role for post-translational regulators in 24-hour rhythms in the absence of any known clock mechanisms.

2020-02-17 | PXD009243 | Pride

rice ssRNA-seq

Project description:rice ssRNA-seq

| PRJEB2597 | ENA

Transcriptional Repressor Gm129 Modulates the Circadian Gene Expression by Inhibiting CLOCK:BMAL1 Activity

Project description:The mammalian circadian clock is a molecular oscillator composed of a feedback loop that involves transcriptional activators CLOCK and BMAL1, and repressors Cryptochrome (CRY) and Period (PER). Here we show that a direct CLOCK-BMAL1 target gene, Gm129, is a novel regulator of the feedback loop. ChIP analysis revealed that the CLOCK:BMAL1:CRY1 complex strongly occupies the promoter region of Gm129. Both mRNA and protein levels of GM129 exhibit high amplitude circadian oscillations in mouse liver, and Gm129 gene encodes a nuclear-localized protein that directly interacts with BMAL1 and represses CLOCK:BMAL1 activity. In vitro and in vivo protein-DNA interaction results demonstrate that, like CRY1, GM129 functions as a repressor by binding to the CLOCK:BMAL1 complex on DNA. Although Gm129-/- or Cry1-/- Gm129-/- mice retain a robust circadian rhythm, the peaks of Nr1d1 and Dbp mRNAs in liver exhibit significant phase delay compared to control. Our results suggest that, in addition to CRYs and PERs, GM129 protein contributes to the transcriptional feedback loop by modulating CLOCK:BMAL1 activity as a transcriptional repressor. Examination of 3 transcriptional regulators in mouse liver

2014-01-07 | E-GEOD-53828 | 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

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