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k-ras oncogene was transduced into the HPV16-E6E7 immortalized normal human pancreatic duct epithelial cell line (H6c7) to generate a stable K-ras oncogene-expressing cell line (H6c7-Kr). The gene expression profile of the H6c7-Kr cells was compared to that of H6c7 cells. We have excluded (subtracte...
ORGANISM(S): Homo sapiens 
RAS genes are frequently mutated in cancer and have for decades eluded effective therapeutic attack. The National Cancer Institute’s RAS Initiative has a focus on understanding pathways and discovering therapies for RAS-driven cancers. Part of these efforts is the generation of novel reagents to ena...
ORGANISM(S): Homo Sapiens 
Mutations in both RAS and the PTEN/PIK3CA/AKT signaling module are found in the same human tumors. PIK3CA and AKT are downstream effectors of RAS, and the selective advantage conferred by mutation of two genes in the same pathway is unclear. Based on a comparative molecular analysis, we show that ac...
ORGANISM(S): Homo sapiens 
We have compared the response to TGFbeta1 in normal and v-rasHa transduced primary mouse keratinocytes using NCI cDNA microarrays. This analysis reveals that Ha-ras alters global TGFbeta1 mediated gene expression in a gene specific manner. The expression pattern of TGFbeta1 immediate early response ...
ORGANISM(S): Mus musculus 
Upon perturbations by RAS and by shBMAL, differential effects on the circadian phenotype were observed in wild type and Ink4a/Arf knockout MEFs which could be reproduced by modelling simulations and correlated with opposing cell cycle fate decisions.
ORGANISM(S): Mus musculus 
The c-H-ras proto-oncogene undergoes alternative splicing of the exon termed IDX giving rise to a novel protein of the Ras family, p19 (H-RasIDX). The experiment tests the effect on the transcriptome of overexpressing the wild type and W164A mutated forms of p19. Keywords: genetic modification Thre...
ORGANISM(S): Homo sapiens 
We compared the transformation efficiencies of mutant NRAS and KRAS in immortal, non-transformed Ink4a/Arf-deficient melanocytes. NRAS mutation leads to increased cellular proliferation and is potently tumorigenic. In contrast, KRAS mutation does not enhance melanocyte proliferation and is only weak...
ORGANISM(S): Mus musculus 
To gain more information about EMT induced by oncogenic Ras in MDCK cells, we performed RNA-seq of MDCK and MDCK-Ras cells and compared their genome-wide gene expression profiles.
ORGANISM(S): Canis lupus familiaris 
Oncolytic viruses exploit common molecular changes in cancer cells, which are not present in normal cells, to target and kill cancer cells. Ras transformation and defects in type I interferon (IFN)-mediated antiviral responses are known to be the major mechanisms underlying viral oncolysis. Previous...
ORGANISM(S): Mus musculus 
Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis
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