Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: ERF deletion rescues RAS deficiency in mouse embryonic stem cells [ChIP-seq]

PROVIDER: PRJNA388571 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5631350.fastq.gz	Fastqsanger.gz
	SRR5631351.fastq.gz	Fastqsanger.gz
	SRR5631352.fastq.gz	Fastqsanger.gz
	SRR5631353.fastq.gz	Fastqsanger.gz
	SRR5631354.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Mus musculus

Project description:ERF deletion rescues RAS deficiency in mouse embryonic stem cells [expression profiling]

| PRJNA388151 | ENA

ERF deletion rescues RAS deficiency in mouse embryonic stem cells

Project description:ERF deletion rescues RAS deficiency in mouse embryonic stem cells

| PRJNA388568 | ENA

ERF deletion rescues RAS deficiency in mouse embryonic stem cells [ChIP-seq]

Project description:RAS proteins are key regulators of growth factor signaling. Here we show that deletion of all RAS genes in mouse embryonic stem cells (mES) leads to an overall reduction in protein translation, limits their long-term proliferative capacity and incapacitates them to differentiate. Deletion of ERF, a transcriptional repressor of the ETS family, rescues proliferation and differentiation of RAS-deficient mES cells and allows the development of teratomas lacking RAS genes. Upon RAS deletion, ERF translocates to the nucleus where it binds to multiple enhancers of key RAS targets suppressing their expression. We also reveal recurrent losses of ERF in cancer and show that ERF deficiency increases the resistance of cancer cells to pharmacological inhibition of the RAS pathway. In summary, we here reveal a central role for ERF in coordinating RAS signaling in pluripotent cells, and identify a synthetic viable interaction that bypasses the requirement for RAS proteins in mammalian cells.

2018-05-08 | GSE99476 | GEO

ERF deletion rescues RAS deficiency in mouse embryonic stem cells [expression profiling]

2018-05-08 | GSE99336 | GEO

Mus musculus

Project description:Chip-chip from mouse embryonic stem (mES) cells

| PRJNA106653 | ENA

Mus musculus

Project description:ChIP-chip from mouse embryonic stem (mES) cells

| PRJNA125311 | ENA

Mus musculus

Project description:Chd4 deficiency effect on mouse embryonic stem cells

| PRJNA352927 | ENA

Erf chromatin binding-sites in E13.5 mouse embryo fibroblasts

Project description:We show that reduced dosage of ERF, which encodes an inhibitory ETS transcription factor directly bound by ERK1/2 , causes complex craniosynostosis (premature fusion of the cranial sutures) in humans and mice. Features of this newly recognized clinical disorder include multiple suture synostosis, craniofacial dysmorphism, Chiari malformation and language delay. Mice with functional Erf reduced to ~30% of normal exhibit postnatal multisuture synostosis; by contrast, embryonic calvarial development appears mildly delayed. Using chromatin immunoprecipitation in mouse embryonic fibroblasts and high-throughput sequencing, we find that ERF binds preferentially to distal regulatory elements containing RUNX or AP1 motifs. This work identifies ERF as a novel regulator of osteogenic stimulation by RAS-ERK signaling, potentially by competing with activating ETS factors in multifactor transcriptional complexes. Examination of Erf binding site in E13.5 mouse embryo fibroblasts, growing in the presence or absence of serum for 4 hours

2013-01-15 | E-GEOD-42936 | biostudies-arrayexpress