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Transcripts (mRNA) during amino acid limitation after MEK was inhibited were analyzed. HepG2 cells were pretreated with MEK inhibitor, PD98059 for 1 hour, then incubated in complete medium and a medium depleted for Histidine for 8 hours. For Inhibitor treated cells, PD98059 was included in the mediu...
ORGANISM(S): Homo sapiens 
A375P melanoma cells were treated with 1uM of the MEK inhibitor PD184352 or 0.4uM of the V600EBRAF inhibitor PLX4720 for 2hr, 6hr and 24hrs. DMSO treatment for 2hr, 6hr and 24hrs serves as the negative control Triplicate experiments were performed for DMSO, PD184352 and PLX4720 treatment at 3 timepo...
ORGANISM(S): Homo sapiens 
Certain oncolytic viruses exploit activated Ras signalling in order to replicate in cancer cells. Constitutive activation of the Ras/MEK pathway is known to suppress the effectiveness of the interferon (IFN) antiviral response, which may contribute to Ras-dependent viral oncolysis. Here, we identifi...
ORGANISM(S): Homo sapiens 
Neurofibromatosis Type 1 (NF1) patients develop benign neurofibromas and malignant peripheral nerve sheath tumors (MPNST). These incurable peripheral nerve tumors result from loss of NF1 tumor suppressor gene function, causing hyperactive Ras signaling. Activated Ras controls numerous downstream eff...
ORGANISM(S): Mus musculus 
The impact of the cellular context and receptor type on the dynamics of phosphorylation cycles in signaling pathways are unclear. We employ an unbiased approach to identify network alterations that explain phosphorylation dynamics of the MEK/ERK module in response to hepatocyte growth factor or inte...
ORGANISM(S): Homo Sapiens (ncbitaxon:9606) 
2017-03-29 | MSV000080803 | MassIVE
Identification of MEK-ERK or p38MAPK dependent genes in human monocyte derived dendritic cells. Dendritic cells (DC) promote tolerance or immunity depending on their maturation state. Previous studies have revealed that DC maturation is enhanced or accelerated upon MEK-ERK signaling pathway inhibiti...
ORGANISM(S): Homo sapiens 
Anticancer drug development is an inefficient process, with potential therapeutics demonstrating a high attrition rate due to lack of efficacy in Phase II/III testing. In an effort to develop improved pre-clinical predictors of efficacy, we and others have turned to testing in genetically engineere...
ORGANISM(S): Mus musculus 
Mitogen-activated protein kinases (MEK 1/2) are central components of the RAS signaling pathway and attractive targets for cancer therapy. However, PIK3CA mutation, which commonly co-occurs with KRAS mutation, offered resistance to MEK inhibitor through activation of PI3K-AKT signaling. We identifie...
ORGANISM(S): Homo sapiens 
Data from ProteomeXchange, PXD ID: PXD000528. Experiment: GM_NKI_NRAS_Phospho_Mix2, file: OR9_20130426_GM_NKI_NRAS_Phospho_Mix2_repl1_ReRunFr10.mzml. Published as part of Pigment Cell Melanoma Res. 2015 Feb 28 . From the Abstract: {{i}} No effective targeted therapy is currently available for NRAS ...
ORGANISM(S): Homo_sapiens_viruses, Human 
Since direct pharmacological inhibition of RAS has thus far been unsuccessful, we explored system biology approaches to identify synergistic drug combination(s) that can mimic direct RAS inhibition. Leveraging an inducible mouse model of NRAS-mutant melanoma, we compare pharmacological MEK inhibitio...
ORGANISM(S): Mus musculus 
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