ArticleMolecular and cellular biology2002
Cellular N-Ras promotes cell survival by downregulation of Jun N-terminal protein kinase and p38.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis.Cell death & disease · 2023Article
- CircPVT1 attenuates negative regulation of NRAS by let-7 and drives cancer cells towards oncogenicity.Scientific reports · 2021Article
- NRAS mutant E132K identified in young-onset sporadic colorectal cancer and the canonical mutants G12D and Q61K affect distinct oncogenic phenotypes.Scientific reports · 2020Article
- Classic Ras Proteins Promote Proliferation and Survival via Distinct Phosphoproteome Alterations in Neurofibromin-Null Malignant Peripheral Nerve Sheath Tumor Cells.Journal of neuropathology and experimental neurology · 2015Article
- RASSF7 expression and its regulatory roles on apoptosis in human intervertebral disc degeneration.International journal of clinical and experimental pathology · 2015Article
- Oncogenic Ras stimulates Eiger/TNF exocytosis to promote growth.Development (Cambridge, England) · 2014Article
- p38α MAPK pathway: a key factor in colorectal cancer therapy and chemoresistance.World journal of gastroenterology · 2014Review
- In TCR-stimulated T-cells, N-ras regulates specific genes and signal transduction pathways.PloS one · 2014Article
- Bevacizumab-based treatment in colorectal cancer with a NRAS Q61K mutation.Targeted oncology · 2013Article
- Dual effects of Ral-activated pathways on p27 localization and TGF-β signaling.Molecular biology of the cell · 2013Article
- Mutant N-RAS protects colorectal cancer cells from stress-induced apoptosis and contributes to cancer development and progression.Cancer discovery · 2013Article
- Antifouling surfaces for proteins labeled with dye-doped silica nanoparticles.Analytical chemistry · 2013Article
- Expression of c-Jun, p73, Casp9, and N-ras in thymic epithelial tumors: relationship with the current WHO classification systems.Diagnostic pathology · 2012Article
- RASSF7 negatively regulates pro-apoptotic JNK signaling by inhibiting the activity of phosphorylated-MKK7.Cell death and differentiation · 2011Article
- Functional specificity of ras isoforms: so similar but so different.Genes & cancer · 2011Article
- Ras, an actor on many stages: posttranslational modifications, localization, and site-specified events.Genes & cancer · 2011Article
- Integration of multiple signaling pathway activities resolves K-RAS/N-RAS mutation paradox in colon epithelial cell response to inflammatory cytokine stimulation.Integrative biology : quantitative biosciences from nano to macro · 2010Article
- RAS mutations affect tumor necrosis factor-induced apoptosis in colon carcinoma cells via ERK-modulatory negative and positive feedback circuits along with non-ERK pathway effects.Cancer research · 2009Article
- Reactive oxygen species: a double-edged sword in oncogenesis.World journal of gastroenterology · 2009Review
- Loss of integrin alpha1beta1 ameliorates Kras-induced lung cancer.Cancer research · 2008Article
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Authors and funding
4 authors.
Funding
Abstract
Cellular N-Ras provides a steady-state antiapoptotic signal, at least partially through the regulation of phosphorylated Akt and Bad levels. Fibroblasts lacking c-N-Ras expression are highly sensitive to the induction of apoptosis by a variety of agents. Reduction of pBad and pAkt levels using a phosphatidylinositol 3-kinase inhibitor was not sufficient to sensitize the control cell population to the high level of apoptosis observed in the N-Ras knockout cell lines, suggesting that c-N-Ras provides at least one other antiapoptotic signal. Stimulation of the control cells with apoptotic agents results in a transient increase in Jun N-terminal protein kinase (JNK)/p38 activity that decreased to baseline levels during the time course of the experiments. In all cases, however, sustained JNK/p38 activity was observed in cells lacking c-N-Ras expression. This correlated with sustained levels of phosphorylated MKK4 and MKK3/6, upstream activators of JNK and p38, respectively. Mimicking the sustained activation of JNK in the control cells did result in increasing their sensitivity to apoptotic agents, suggesting that prolonged JNK activity is a proapoptotic event. We also examined the potential downstream c-N-Ras targets that might be involved in regulating the duration of the JNK/p38 signal. Only the RalGDS 37G-N-Ras protein protected the N-Ras knockout cells from apoptosis and restored transient rather than sustained JNK activation. These data suggest that cellular N-Ras provides an antiapoptotic signal through at least two distinct mechanisms, one which regulates steady-state pBad and pAkt levels and one which regulates the duration of JNK/p38 activity following an apoptotic challenge.
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