ArticleOncogene2000
Differential roles of JNK and Smad2 signaling pathways in the inhibition of c-Myc-induced cell death by TGF-beta.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 29 citations in OpenAlex.
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- miR-137-3p Modulates the Progression of Prostate Cancer by Regulating the JNK3/EZH2 Axis.OncoTargets and therapy · 2020Article
- Analysis of differentially expressed proteins in Yersinia enterocolitica-infected HeLa cells.Biochimica et biophysica acta · 2016Article
- Identification of the ZAK-MKK4-JNK-TGFβ signaling pathway as a molecular target for novel synthetic iminoquinone anticancer compound BA-TPQ.Current cancer drug targets · 2013Article
- Rac1 modulates acute and subacute genotoxin-induced hepatic stress responses, fibrosis and liver aging.Cell death & disease · 2013Article
- Transforming growth factor beta enhances epithelial cell survival via Akt-dependent regulation of FKHRL1.Molecular biology of the cell · 2001Article
- The MLK family mediates c-Jun N-terminal kinase activation in neuronal apoptosis.Molecular and cellular biology · 2001Article
- c-Jun interacts with the corepressor TG-interacting factor (TGIF) to suppress Smad2 transcriptional activity.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Smad7 inhibits the survival nuclear factor kappaB and potentiates apoptosis in epithelial cells.Oncogene · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transforming growth factor beta (TGF-beta) plays an important role in constraining cellular proliferation, but it is also a potent inducer of programmed cell death or apoptosis. Here, we demonstrate that TGF-beta can have an opposite effect, acting as a survival factor to prevent c-Myc-induced cell death in Rat-1 fibroblasts. However, in marked contrast to TGF-beta, Smad2, which is a critical intracellular mediator of the TGF-beta signaling pathway, functions as an antagonist to induce increased cell death. The protective activity of TGF-beta was associated with the activation of c-Jun N-terminal Kinase (JNK) and was not linked to the ability of TGF-beta to promote cell cycle progression. Expression of dominant-interfering forms of various components of the JNK signaling pathway, including Rac1, Cdc42, mitogen-activated protein kinase kinase 4 (MKK4), and c-Jun, abolished TGF-beta-mediated cell survival. Furthermore, overexpression of the constitutively activated mutant RacL61F37A, which selectively stimulates JNK cascade but not G1 cell cycle progression or actin polymerization, was sufficient to prevent apoptosis induced by c-Myc. These findings describe a differential effect of two separated signaling pathways of TGF-beta and indicate for the first time that Smad2 can act as antagonist to suppress TGF-beta-dependent cell survival. Oncogene (2000) 19, 1277 - 1287.
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