Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIPseq experiments for chromatin modification in S.cerevisiae upon truncations of CTR9

ABSTRACT: ChIPseq experiments for chromatin modification in S.cerevisiae upon truncations of CTR9

PROVIDER: PRJNA725913 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14352027.fastq.gz	Fastqsanger.gz
	SRR14352028.fastq.gz	Fastqsanger.gz
	SRR14352029.fastq.gz	Fastqsanger.gz
	SRR14352030.fastq.gz	Fastqsanger.gz
	SRR14352031.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

ChIPseq experiments for chromatin modification in S.cerevisiae upon truncations of CTR9

Project description:ChIPseq experiments for chromatin modification in S.cerevisiae upon truncations of CTR9

2021-04-29 | GSE173534 | GEO

Ctr9 Promoter Region Binding

Project description:To study the function of Paf1C in mouse ESCs, we generated an ES cell line stably expressing a location and affinity purification (LAP)-tagged Ctr9 fusiuon protein using the bacterial astificial chromosome (BAC)-based TransgeneOmics approach. To investigate whether pluripotency and lineage control genes differentially regulated upon Paf1C depletion are direct targets of the Paf1C, we analyzed the binding of the Ctr9-LAP fusion protein by ChIP-chip and identified 2175 promoter regions that were bound by Ctr9. The supplementary bed file contains promoter regions bound by Ctr9. Keywords: ChIP-chip

2009-01-31 | GSE14654 | GEO

H3K9me3 ChIPseq experiments from PD IMR90s

Project description:H3K9me3 ChIPseq in Proliferating and Senescent IMR90s

2014-12-15 | GSE53329 | GEO

RNAi profiling of mouse ES cells knocked down for Ctr9

Project description:To monitor global transcript changes after Paf1C depletion we transfected ESCs with esiRNA targeting Ctr9 and control esiRNA (Luc). Experiment Overall Design: 4 replicates of esiRNA tranfection controls (luciferase esiRNA) and 4 replicates of Ctr9 esiRNA tranfection samples

2008-10-21 | E-GEOD-12078 | biostudies-arrayexpress

Multiple Histone modifications ChIP-seq in MCF7 cells corresponding to Ctr9 KD (paper title: Ctr9, the scaffold subunit of PAFc, govens PRC2-mediated H3K27me3 domains in breast cancer cells)

Project description:We want to examine the alternation of histone modification spectrum on chormatin in corresponding to Ctr9 loss either in an inducible KD or stable KD fashion in MCF7 breast cancer cells.

2022-06-25 | GSE133318 | GEO

Systematic identification of Ctr9 regulome in ERα-positive breast cancer

Project description:Ctr9, the key scaffold subunit of the human RNA polymerase II (RNAPII) associated factor complex (PAFc), has been demonstrated as a positive regulator of ERα-positive breast cancer progression and ERα-target gene expression. Previously, we found that knockdown of Ctr9 reduces ERα protein stability and decreases the occupancy of ERα and RNAPII at select ERα-target genes. However, the genome-wide regulation of the occupancy of ERα and RNAPII mediated by Ctr9 is still unclear. Here, we determined the genome-wide ERα and RNAPII occupancy in response to estrogen induction and/or Ctr9 knockdown by performing chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq). We found that loss of Ctr9 dramatically decreases the global occupancy of ERα and RNAPII, highlighting the significance of Ctr9 in regulating estrogen signaling in ERα-positive breast cancer cells. Combining this resource with previously published genomic data sets, we identified a unique subset of ERα and Ctr9 target genes, and further delineates the possible independent function of Ctr9 from other subunits in PAFc.

2016-10-10 | GSE80728 | GEO

Determine the chromatin association change of H3K27me3 and PRC2 in response to CTR9 inducible loss as well as genome-wide mapping of Flag-CTR9 binding sites in MCF7 cells

Project description:CTR9 is the scaffold subunit in PAFc (Polymerase associated factor complex), a multifunctional complex employed in multiple steps of RNA Pol II-mediated transcription. CTR9/PAFc is well known as an evolutionarily conserved elongation factor regulating gene activation via coupling with histone modifications enzymes. However, little is known about its function to restrain repressive histone markers. Using inducible and stable CTR9 knockdown breast cancer cell lines, we discovered that the amount of H3K27me3 is strictly controlled by CTR9. Quantitative profiling on histone modifications revealed a striking increase of H3K27me3 level upon loss of CTR9. Moreover, loss of CTR9 leads to genome-wide expansion of H3K27me3, as well as increased recruitment of PRC2 on chromatin, which can be reversed by CTR9 restoration. Moreover, CTR9 depletion triggers a PRC2 subtype switch from less active PRC2.2 to PRC2.1 with higher methyltransferase activity. As a consequence, CTR9 depletion generates vulnerability that renders breast cancer cells hypersensitive to PRC2 inhibitors. Our findings that CTR9 demarcates PRC2-mediated H3K27me3 levels and genomic distribution provide a unique mechanism of transition from transcriptionally active to repressive chromatin states and shed light on the biological functions of CTR9 in development and cancer.

2021-10-19 | GSE173176 | GEO

Histone modification and transcription factor ChIPseq of Xenopus laevis epithelial progenitors

Project description:To determine the positions of promoters and enhancers in developing Xenopus laevis epithelial progenitors, we performed ChIPseq on the histone modifications H3K4me3 and H3K27ac. We also performed ChIPseq on the transcription factors foxj1 (in the presence or absence of rfx2), myb (in the presence or absence of multicilin), and rad21. Some embryos were harvested as wild-types; in other experiments, we injected embryos with mRNAs encoding FLAG-foxj1 (with and without rfx2 morpholino) or GFP-myb (with and without an inducible form of multicilin (mcidas-HGR)). We then isolated epithelial progenitors surgically and, when injected with multicilin, induced at mid-stage 11. We then harvested chromatin at 9 hours after induction (roughly stage 18) and performed ChIPseq using antibodies against endogenous targets (H3K4me3, H3K27ac, rad21) or protein tags (FLAG, GFP). We then sequenced these libraries, aligned the reads to the X. laevis genome (version 9.1) with bwa mem and called peaks with HOMER, using input as background.

2016-02-23 | E-GEOD-78176 | biostudies-arrayexpress

H3K9me3 ChIPseq experiments from PD IMR90s

Project description:H3K9me3 ChIPseq in Proliferating and Senescent IMR90s We used ChIP-seq to examine the global binding of H3K9me3 in human IMR90 replicative senescence (RS) and oncogene-induced (OIS)

2014-12-15 | E-GEOD-53329 | biostudies-arrayexpress

Ctr9 knockdown in mouse ES cells

Project description:To monitor global transcript changes after Paf1C depletion we transfected ESCs with esiRNA targeting Ctr9 and control esiRNA (Luc).

2008-07-18 | GSE12078 | 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