Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-Seq data for AKT, BAD, ERBB2, IGF1R, RAF1 and ERK1 over-expressed samples with twelve green fluorescent protein control samples using human mammary epithelial cells

ABSTRACT: The goal was to capture the transcriptional activity due to over-expression of AKT, BAD, ERBB2, IGF1R, RAF1 and ERK1 genes.Over-expressions were validated using Western Blots. Illumina RNA-Seq technology was used to capture the downstream transcriptional activity. Reads were 101 base pairs long and single ended. An R open source package “Rsubread” was used to align and quantify the read using UCSC hg19 annotation. The integer-based gene counts were later normalized in TPM .

ORGANISM(S): Homo sapiens

PROVIDER: GSE73628 | GEO | 2017/01/01

SECONDARY ACCESSION(S): PRJNA297451

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-Seq data for AKT, BAD, ERBB2, IGF1R, RAF1 and KRAS(G12V) overexpressed samples with twelve green fluorescent protein control samples using human mammary epithelial cells

Project description:The goal was to capture the transcriptional activity due to over-expression of AKT, BAD, ERBB2, IGF1R, RAF1 and KRAS(G12V) genes .Overexpressions were validated using Western Blots. Illumina RNA-Seq technology was used to capture the downstream transcriptional activity. Reads were 101 base pairs long and single ended. An R open source package “Rsubread” was used to align and quantify the read using UCSC hg19 annotation. The integer-based gene counts were later normalized in TPM .

2017-06-01 | GSE83083 | GEO

RNA-Seq data for five HER2 over-expressed samples with twelve green fluorescent protein control samples using human mammary epithelial cells

Project description:Purpose: The goal was to capture the transcriptional activity due to over-expression of HER2 protein. We profiled this transcriptional activity using two different RNA-Seq alignment and quantification pipelines. We also used these samples to generate a gene expression signature of HER2 pathway activity. Over-expression was validated using Western blots. Illumina RNA-Seq technology was used to capture the downstream transcriptional activity. Reads were 101 base pairs long and single ended. An R open source package “Rsubread” was used to align and quantify the read using UCSC hg19 annotation. The integer-based gene counts were later normalized in FPKM and TPM .

2015-06-01 | GSE62820 | GEO

Endothelial Raf1 activation regulates arterial morphogenesis

Project description:Analyze effect of Raf1 S259A on gene expression in HUVEC Total RNA obtained from HUVEC infected with empty lentiviral vector pLVX-IRES-puro (control) or that expressing human RAF1 WT (WT) or RAF1 S259A (S259A).

2012-12-18 | E-GEOD-42964 | biostudies-arrayexpress

RNA-Seq data for KRAS wild-type(WT) and two mutant forms G12V and Q61H over-expressed samples with green fluorescent protein control samples using human mammary epithelial cells

Project description:The goal was to capture the transcriptional activity due to over-expression of KRAS gene. Over-expressions were validated using Western Blots. Illumina RNA-Seq technology was used to capture the downstream transcriptional activity. Reads were 101 base pairs long and single ended. An R open source package “Rsubread” was used to align and quantify the read using UCSC hg19 annotation. The integer-based gene counts were later normalized in TPM .

2017-05-01 | GSE76877 | GEO

Gene expression data from MCF7 cells overexpressing RAF1

Project description:In this study we performed gene transcription analysis of parental MCF7 cells and MCF7 engineered to overexpress oncoprotein RAF1. We demonstrate that overexpression of RAF1 leads to development of ivasive phenotype.

2017-08-31 | GSE100360 | GEO

Endothelial Raf1 activation regulates arterial morphogenesis

Project description:Analyze effect of Raf1 S259A on gene expression in HUVEC

2012-12-18 | GSE42964 | GEO

Cellular Interplay and Cytokine Hierarchy Cause Pathological Cardiac Hypertrophy in RAF1-Mutant Noonan Syndrome

Project description:Noonan syndrome (NS) is caused by mutations in RAS/ERK pathway genes, and is characterized by craniofacial, growth, cognitive and cardiac defects. NS patients with kinase-activating RAF1 alleles typically develop pathological left ventricular hypertrophy (LVH), which is reproduced in Raf1 L613V/+ knock-in mice. Here, using inducible Raf1 L613V expression, we show that LVH results from the interplay of cardiac cell types. Cardiomyocyte Raf1 L613V enhances Ca 2+ sensitivity and cardiac contractility without causing hypertrophy. Raf1 L613V expression in cardiomyocytes or activated fibroblasts exacerbates pressure overload-evoked fibrosis. Endothelial/endocardial (EC) Raf1 L613V causes cardiac hypertrophy without affecting contractility. Co-culture and neutralizing antibody experiments reveal a cytokine hierarchy (TNFα->IL6) from Raf1 L613V -expressing ECs that drives cardiomyocyte hypertrophy in vitro. Furthermore, post-natal TNFα inhibition normalizes the increased wall thickness and cardiomyocyte hypertrophy in vivo. We conclude that NS cardiomyopathy involves cardiomyocytes, ECs, and fibroblasts, TNFα/IL6 signaling components represent potential therapeutic targets, and abnormal EC signaling might contribute to other forms of LVH.

2017-05-22 | GSE95739 | GEO

Interactome dynamics of RAF1-BRAF kinase monomers and dimers

Project description:RAF kinases play major roles in cancer. BRAFV600E mutants drive ~6% of human cancers. Potent kinase inhibitors exist but show variable effects in different cancer types, sometimes even inducing paradoxical RAF kinase activation. Both paradoxical activation and drug resistance are frequently due to enhanced dimerization between RAF1 and BRAF, which maintains or restores the activity of the downstream MEK-ERK pathway. Here, using quantitative proteomics we mapped the interactomes of RAF1 monomers, RAF1-BRAF and RAF1-BRAFV600E dimers identifying and quantifying >1,000 proteins. In addition, we examined the effects of vemurafenib and sorafenib, two different types of clinically used RAF inhibitors. Using regression analysis to compare different conditions we found a large overlapping core interactome but also distinct condition specific differences. Given that RAF proteins have kinase independent functions such dynamic interactome changes could contribute to their functional diversification. Analysing this dataset may provide a deeper understanding of RAF signalling and mechanisms of resistance to RAF inhibitors.

2023-02-27 | PXD036792 | Pride

Circular ANRIL isoforms switch from repressors to activators of p15/CDKN2B expression during RAF1 oncogene-induced senescence

Project description:Long non-coding RNAs (ncRNAs) are major regulators of gene expression and cell fate. The INK4 locus encodes the tumour suppressor proteins p15INK4b, p16INK4a and p14ARF required for cell cycle arrest and whose expression increases during senescence. ANRIL is a ncRNA antisense to the p15 gene. In proliferative cells, ANRIL prevents senescence by repressing INK4 genes through the recruitment of Polycomb-group proteins. In models of replicative and RASval12 oncogene-induced senescence (OIS), the expression of ANRIL and Polycomb proteins decreases, thus allowing INK4 derepression. Here, we found in a model of RAF1 OIS that ANRIL expression rather increases, due in particular to an increased stability. This led us to search for circular ANRIL isoforms, as circular RNAs are rather stable species. We found that the expression of two circular ANRIL increases in several OIS models (RAF1, MEK1 and BRAF). In proliferative cells, they repress p15 expression, while in RAF1 OIS, they promote full induction of p15, p16 and p14ARF expression. Further analysis of one of these circular ANRIL shows that it interacts with Polycomb proteins and decreases EZH2 Polycomb protein localization and H3K27me3 at the p15 and p16 promoters, respectively. We propose that changes in the ratio between Polycomb proteins and circular ANRIL isoforms allow these isoforms to switch from repressors of p15 gene to activators of all INK4 genes in RAF1 OIS. Our data reveal that regulation of ANRIL expression depends on the senescence inducer and underline the importance of circular ANRIL in the regulation of INK4 gene expression and senescence.

2020-12-31 | GSE143957 | GEO

Time-course expression data from HEK293âRAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF

Project description:We integrate experimental data and mathematical modelling to unveil how ERK signal duration is relayed to mRNA dynamics. HEK293 cells were transfected with an inducible form of RAF (âRAF1:ER) and induced with tamoxifen (4OHT) or stimulated with different growth factors (EGF, FGF, iGF). Effects of RAF signalling were perturbed subsequently or in parallel with MEK inhibtor U0126, translation inhibtor cycloheximide (CYHX) and actinomycin D (ActD).

2017-04-28 | E-GEOD-72919 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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