ArticleProceedings of the National Academy of Sciences of the United States of America1994
Oncogenic Ras activates c-Jun via a separate pathway from the activation of extracellular signal-regulated kinases.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 187 citations in OpenAlex.
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- A mechanism study of DUSP1 in inhibiting malignant progression of endometrial carcinoma by regulating ERK/AP-1 axis and dephosphorylation of EPHA2.Journal of Cancer · 2023Article
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- Ras Signaling in Breast Cancer.Advances in experimental medicine and biology · 2021Article
- Cisplatin contributes to programmed death-ligand 1 expression in bladder cancer through ERK1/2-AP-1 signaling pathway.Bioscience reports · 2019Article
- Suppression of MicroRNA 200 Family Expression by Oncogenic KRAS Activation Promotes Cell Survival and Epithelial-Mesenchymal Transition in KRAS-Driven Cancer.Molecular and cellular biology · 2016Article
- The Effector Protein BPE005 from Brucella abortus Induces Collagen Deposition and Matrix Metalloproteinase 9 Downmodulation via Transforming Growth Factor β1 in Hepatic Stellate Cells.Infection and immunity · 2016Article
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- Deficiency of cardiomyocyte-specific microRNA-378 contributes to the development of cardiac fibrosis involving a transforming growth factor β (TGFβ1)-dependent paracrine mechanism.The Journal of biological chemistry · 2014Article
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- siRNA-mediated downregulation of TC21 sensitizes esophageal cancer cells to cisplatin.World journal of gastroenterology · 2012Article
- RAS oncogenes: weaving a tumorigenic web.Nature reviews. Cancer · 2011Review
- Therapeutic strategies for targeting ras proteins.Genes & cancer · 2011Article
- Ets1 blocks terminal differentiation of keratinocytes and induces expression of matrix metalloproteases and innate immune mediators.Journal of cell science · 2010Article
- Mechanisms of regulation of oligodendrocyte development by p38 mitogen-activated protein kinase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Laboratory and clinical studies of cancer chemoprevention by antioxidants in berries.Carcinogenesis · 2008Review
- Gene expression-based screening for inhibitors of PDGFR signaling.Genome biology · 2008Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
c-Jun transcriptional activity is augmented by expression of oncogenic Ras and Raf proteins. This study demonstrates a direct correlation between Ras transforming activity and c-Jun activation, supporting an important role for c-Jun in transformation by Ras. Since we observed that Ras activated c-Jun transcriptional activity by increasing phosphorylation of the c-Jun activation domain at residues Ser-63/Ser-73 and that oncogenic Ras proteins activated extracellular signal-regulated protein kinases (ERK1 and ERK2) (also known as mitogen-activated protein kinases), we evaluated the possibility that ERKs were directly responsible for c-Jun activation. Coexpression of wild-type ERKs with oncogenic Ras proteins potentiated, while kinase-defective ERKs inhibited, Ras-induced transcriptional activation from the Ras-responsive element (Ets-1/AP-1) present in the NVL-3 enhancer and the serum-response element in the c-fos promoter. In contrast, coexpression of either wild-type or kinase-defective ERKs inhibited Ras and Raf activation of c-Jun transcriptional activity. Thus, although activation of both ERK and c-Jun are downstream consequences of activation of the Ras signal transduction pathway, our results suggest that Ras-induced c-Jun phosphorylation and transcriptional activation are not a direct consequence of ERK1 and ERK2 activation.
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