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ChIP-seq from Human U2OS Cell for BMAL1 and CRY1 with DMSO or Cordycepin Treatment

ABSTRACT: ChIP-seq from Human U2OS Cell for BMAL1 and CRY1 with DMSO or Cordycepin Treatment

PROVIDER: PRJNA540498 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8992340.fastq.gz	Fastqsanger.gz
	SRR8992341.fastq.gz	Fastqsanger.gz
	SRR8992342.fastq.gz	Fastqsanger.gz
	SRR8992343.fastq.gz	Fastqsanger.gz
	SRR8992344.fastq.gz	Fastqsanger.gz

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ChIP-seq from Human U2OS Cell for BMAL1 and CRY1 with DMSO or Cordycepin Treatment

Project description:To evaluate the effects of cordycepin on CRY1 and BMAL1 binding on the chromatin sites, non-synchronized U2OS cells were treated with cordycepin (100 uM) for 1 h, then performed ChIP-seq. We found cordycepin relieves CRY1 proteins from the chromatin for more than 60-70%, while unaffects BMAL1 from the chromatin.

2020-05-07 | GSE130506 | GEO

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.

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ChIP-seq of three core components of the circadian clock (BMAL1, CLOCK and CRY1) in unsynchronized human U2OS cells

Project description:The human osteosarcoma cell line U2OS contains a functional circadian clock but expresses only a few rhythmic genes. We identified by ChIP-seq analysis 3040 binding sites of the circadian transcription factors BMAL1, CLOCK, and CRY1 in the genome of U2OS cells, comparable to the number found in highly rhythmic tissues like liver. ChIP was performed as described previously (Rey et al, 2011; doi:10.1371/journal.pbio.1000595) using confluent desynchronized U2OS cells and BMAL1, CLOCK, and CRY1-antibodies. Immunoprecipitated chromatin (10 ng DNA of 8 independent BMAL1 ChIPs with enrichment levels > 80-fold, 9 ng DNA of a CRY1 ChIP with 10-fold enrichment, and 8 ng DNA of a CLOCK ChIP with 40-fold enrichment) was used for library preparation. Three lanes of the BMAL1 library, and one lane each of the CRY1 and CLOCK library were sequenced on the Illumina Genome Analyzer IIx using Single-Read Cluster Generation Kit and 36 Cycle Sequencing Kit v2 (Lausanne Genomics Technologies Facility).

2016-02-11 | E-GEOD-44236 | biostudies-arrayexpress

ChIP-seq of three core components of the circadian clock (BMAL1, CLOCK and CRY1) in unsynchronized human U2OS cells

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ChIP-seq from Human U2OS Cell for CRY2 and RUVBL2 with DMSO or Cordycepin Treatment

Project description:To evaluate the effects of cordycepin on CRY2 and RUVBL2 binding on the chromatin sites, non-synchronized U2OS cells were treated with cordycepin (100 uM) for 1 h, then performed ChIP-seq. We found that cordycepin relieves CRY2 and RUVBL2 proteins from the chromatin for more than 60-70%.

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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

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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

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ChIP-seq from Human U2OS Cell for CRY2 and RUVBL2 with DMSO or Cordycepin Treatment

Project description:ChIP-seq from Human U2OS Cell for CRY2 and RUVBL2 with DMSO or Cordycepin Treatment

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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

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Non-circadian expression masking clock-driven weak transcription rhythms in U2OS cells

Project description:U2OS cells harbor a circadian clock but express only a few rhythmic genes in constant conditions. We identified 3040 binding sites of the circadian regulators BMAL1, CLOCK and CRY1 in the U2OS genome. Most binding sites even in promoters do not correlate with detectable rhythmic transcript levels. Luciferase fusions reveal that the circadian clock supports robust but low amplitude transcription rhythms of representative promoters. However, rhythmic transcription of these potentially clock-controlled genes is masked by non-circadian transcription that overwrites the weaker contribution of the clock in constant conditions. Our data suggest that U2OS cells harbor an intrinsically rather weak circadian oscillator. The oscillator has the potential to regulate a large number of genes. The contribution of circadian versus non-circadian transcription is dependent on the metabolic state of the cell and may determine the apparent complexity of the circadian transcriptome. Analysis of temporal expression profiles of 5708 expressed genes in synchronized U2OS cells.

2014-05-23 | GSE57891 | GEO

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