Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse Liver Chromatin Circadian ChIP_seq for Bmal1 and Ruvbl2

ABSTRACT: Mouse livers were collected at 4 hours interval at constant darkness condition after 2 weeks synchronization to ambient light dark cycle, then conducted for the ChIP-seq (Bmal1, Ruvbl2). We found Ruvbl2 rhythmically co-occupancies with Bmal1 binding sites.

ORGANISM(S): Mus musculus

PROVIDER: GSE130505 | GEO | 2020/05/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Mouse Liver Chromatin Circadian ChIP_seq for Bmal1 and Ruvbl2

Project description:Mouse Liver Chromatin Circadian ChIP_seq for Bmal1 and Ruvbl2

| PRJNA540497 | ENA

ChIP-seq from Human U2OS Cell for BMAL1, CRY1, CRY2 and RUVBL2

Project description:To evaluate the chromatin binding of BMAL1, CRY1, CRY2 and RUVBL2 in U2OS cells.

2020-05-07 | GSE130602 | GEO

ChIP_seq for Bmal1 and Ruvbl2 in Mouse Liver and for BMAL1, RUVBL2, CRY1 and CRY2 in Human U2OS Cells

Project description:ChIP_seq for Bmal1 and Ruvbl2 in Mouse Liver and for BMAL1, RUVBL2, CRY1 and CRY2 in Human U2OS Cells

| PRJNA540491 | ENA

ChIP-seq from Human U2OS Cell for BMAL1, CRY1, CRY2 and RUVBL2

Project description:ChIP-seq from Human U2OS Cell for BMAL1, CRY1, CRY2 and RUVBL2

| PRJNA540717 | ENA

ChIP_seq for Bmal1 and Ruvbl2 in Mouse Liver and for BMAL1, RUVBL2, CRY1 and CRY2 in Human U2OS Cells

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

2020-05-07 | GSE130508 | GEO

Generation of tissue-specific circadian transcriptional programs by BMAL1 [ChIP-seq]

Project description:The mammalian circadian clock relies on the transcription factor CLOCK:BMAL1 to coordinate the rhythmic expression of thousands of genes and enable biological functions to anticipate the daily environmental variations. Consistent with the wide range of biological functions under clock control, rhythmic gene expression is tissue-specific, and this even if the clockwork mechanism is identical in every cell. Here we show that BMAL1 DNA binding is largely tissue-specific, through mechanisms involving differences in chromatin accessibility between tissues as well as co-binding of tissue-specific transcription factors. Our results also indicate that the ability of BMAL1 to drive tissue-specific rhythmic transcription not only relies on the activity of BMAL1 cis-regulatory elements (CREs), but also on the activity of neighboring CREs. Characterization of the physical interactions between BMAL1 CREs and other CREs by RNA Polymerase II ChIA-PET in the mouse liver reveals that most interactions are stable over the course of the day, and suggests that BMAL1-mediated rhythmic transcription relies on its ability to regulate the transcriptional activity of other CREs. Our data therefore suggest that much of BMAL1 target gene transcription depends on BMAL1 capacity at rhythmically regulating a network of enhancers.

2018-05-08 | GSE110602 | GEO

Context-specific regulation of BMAL1 target genes during the circadian cycle in mammals

Project description:While the circadian rhythm is a highly conserved phenomenon, it has highly specific functions, which differ from one cell type to another. Hence, although the master regulators BMAL1-CLOCK are conserved, the input and output conveying the tissue specificity vary. Through comparative analyses of ChIP-seq data in mouse liver and NIH3T3 fibroblasts, we reveal that only a fraction of BMAL1 binding sites are shared between different cell types and that many sites are bound, active and accessible in a cell-type-specific way. While we found a large fraction of the overall active liver transcriptome to be rhythmically expressed, rhythmic genes among BMAL1 targets are more enriched compared to the overall cyclic transcriptome in NIH3T3 than in liver. Thus, BMAL1 may launch and reinforce oscillations of a number of genes that propagate timing information rather than globally drive rhythmic gene expression.

2016-12-31 | GSE61775 | GEO

Molecular Chaperone RUVBL2 Activates Oncogenes by Modulation of Transcriptional Condensates [ChIP-Seq]

Project description:Transcription regulators and apparatuses compartmentalize into transcriptional condensates in part through molecular interactions among intrinsically disordered regions. To better understand how these fundamental condensates are regulated, we performed time-series analyses of transcriptome, genome and imaging to show that the previously characterized molecular chaperone RUVBL2 assembles Pol II condensates by its ATPase activity and prevalently interacting with diverse oncogenic transcription factors at promoters, thereby maintaining active transcription in mammalian cells. Besides, RUVBL2 is overexpressed in various cancers, has higher expression levels and preferential chromatin binding compared with RUVBL1. Remarkably, acute protein degradation and chemical perturbations of RUVBL2 with the nucleoside compound cordycepin result in the repression of oncogenes in embryonic stem cells and breast cancer cells, respectively. Our results suggest that molecular chaperone RUVBL2 safeguards the hemostasis of transcriptional condensates at promoters. Thus, pharmacological perturbations of RUVBL2 is a promising strategy to restore these condensates in breast cancers.

2022-08-30 | GSE160738 | GEO