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Homo sapiens

ABSTRACT: ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (ChIP-Seq)

OTHER RELATED OMICS DATASETS IN: E-GEOD-59020

PROVIDER: PRJNA254144 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1504810.fastq.gz	Fastqsanger.gz
	SRR1504811.fastq.gz	Fastqsanger.gz
	SRR1504812.fastq.gz	Fastqsanger.gz
	SRR1504813.fastq.gz	Fastqsanger.gz
	SRR1504814.fastq.gz	Fastqsanger.gz

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Similar Datasets

Homo sapiens

Project description:ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (RNA-Seq)

| PRJNA254145 | ENA

E-GEOD-59020

Project description:ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (RNA-Seq)

2025-01-24 | E-GEOD-59020 | ExpressionAtlas

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells

Project description:ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells

| PRJNA254143 | ENA

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (ChIP-Seq)

Project description:ETS1 and RAS/ERK regulate a common gene expression program in establishing enviroment suitable for prostate cancer cell migration. ChIP-sequencing of various transcription factors

2014-10-07 | E-GEOD-59021 | biostudies-arrayexpress

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (ChIP-Seq)

Project description:ETS1 and RAS/ERK regulate a common gene expression program in establishing enviroment suitable for prostate cancer cell migration.

2014-10-07 | GSE59021 | GEO

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (RNA-Seq)

Project description:ETS1 and RAS/ERK regulate a common gene expression program in establishing enviroment suitable for prostate cancer cell migration.

2014-10-07 | GSE59020 | GEO

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (RNA-Seq)

Project description:ETS1 and RAS/ERK regulate a common gene expression program in establishing enviroment suitable for prostate cancer cell migration. mRNA profiles of luciferase knockdown (WT), ETS1 knockdown, and U0126 treated DU145 cells were generated using deep sequencing, in triplicate, using Illumina HiSeq. Knockdowns were stable shRNA expression from a lentiviral construct selected with puromycin.

2014-10-07 | E-GEOD-59020 | biostudies-arrayexpress

Kinome profiling of HRAS Q61K mutant SMS-CTR rhabdomyosarcoma cell line treated with tipifarnib

Project description:Hyperactive RAS signaling drives tumorigenesis in PAX 3/7::FOXO1 fusion-negative rhabdomyosarcoma (FN-RMS). Despite the frequency of these mutations, RAS pathway-directed therapies have been ineffective for RAS-driven RMS. Farnesyltransferase (FTase) inhibitors (FTIs), such as tipifarnib, inhibit HRAS membrane localization and blunt HRAS effector signaling, leading to an antitumor effect in HRAS-mutant FN-RMS preclinical models. Response to FTI is limited by adaptive feedback reactivation of ERK signaling and upregulation of wild-type (WT) RAS. We found that the combination of HRAS suppression with FTI and MEK inhibition (MEKi) impaired ERK reactivation and reduced ERK transcriptional output in HRAS-mutant RMS models. Co-targeting FTase and MEK restrained tumor progression and induced terminal myogenic differentiation. These findings highlight an effective combinatorial strategy and support its preclinical translation for patients with HRAS-mutant RMS. Here, kinome profiling was performed on the SMS-CTR(HRAS Q61K) RMS cell line after 24 or 48 hour exposure to 100 nM tipifarnib.

2026-02-12 | PXD062989 | Pride

Mus musculus

Project description:Deregulation of the Ras-Erk Signaling Axis Modulates the Enhancer Landscape [ChIP-seq]

| PRJNA270358 | ENA

Combined inhibition of HRAS and MEK induces tumor regression and restores myogenic differentiation in HRAS-mutant rhabdomyosarcoma

Project description:Hyperactive RAS signaling drives tumorigenesis in PAX 3/7::FOXO1 fusion-negative rhabdomyosarcoma (FN-RMS). Despite the frequency of these mutations, indirect RAS pathway-directed therapies have been ineffective for RAS-driven RMS. Farnesyltransferase (FTase) inhibitors (FTIs), such as tipifarnib, inhibit HRAS membrane localization and blunt HRAS effector signaling, leading to an antitumor effect in HRAS-mutant FN-RMS preclinical models. Response to FTase inhibition is limited by adaptive feedback reactivation of ERK signaling and upregulation of wild-type (WT) RAS. We found that the combination of HRAS suppression with FTI and MEK inhibition (MEKi) impaired ERK reactivation and reduced ERK transcriptional output in HRAS-mutant RMS models. Co-targeting FTase and MEK restrained tumor progression and induced terminal myogenic differentiation. These findings highlight an effective combinatorial strategy and support its preclinical translation for patients with HRAS-mutant RMS.

2025-12-08 | GSE312030 | GEO

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