ArticleOncogene2003
Selective activation of the c-Jun N-terminal kinase (JNK) pathway fails to elicit Bax activation or apoptosis unless the phosphoinositide 3'-kinase (PI3K) pathway is inhibited.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
The trial behind it
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Who cites it
18 citing papers in PubMed, 49 citations in OpenAlex.
- Potential Mechanisms of Plant-Derived Natural Products in the Treatment of Cervical Cancer.Biomolecules · 2021Review
- NGF and the Amyloid Precursor Protein in Alzheimer's Disease: From Molecular Players to Neuronal Circuits.Advances in experimental medicine and biology · 2021Review
- Naringin inhibits colorectal cancer cell growth by repressing the PI3K/AKT/mTOR signaling pathway.Experimental and therapeutic medicine · 2020Article
- Endoplasmic Reticulum Stress Impaired Uncoupling Protein 1 Expression via the Suppression of Peroxisome Proliferator-Activated Receptor γ Binding Activity in Mice Beige Adipocytes.International journal of molecular sciences · 2019Article
- NGF controls APP cleavage by downregulating APP phosphorylation at Thr668: relevance for Alzheimer's disease.Aging cell · 2016Article
- JNK signaling pathway is involved in piperlongumine-mediated apoptosis in human colorectal cancer HCT116 cells.Oncology letters · 2015Article
- Regulation of cell survival by sphingosine-1-phosphate receptor S1P1 via reciprocal ERK-dependent suppression of Bim and PI-3-kinase/protein kinase C-mediated upregulation of Mcl-1.Cell death & disease · 2013Article
- Hepatic apoptosis postburn is mediated by c-Jun N-terminal kinase 2.Shock (Augusta, Ga.) · 2013Article
- Alpinetin suppresses proliferation of human hepatoma cells by the activation of MKK7 and elevates sensitization to cis-diammined dichloridoplatium.Oncology reports · 2012Article
- Crosstalk and signaling switches in mitogen-activated protein kinase cascades.Frontiers in physiology · 2012Article
- The SUMO E3-ligase PIAS1 couples reactive oxygen species-dependent JNK activation to oxidative cell death.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Article
- Silencing of the JNK pathway maintains progesterone receptor activity in decidualizing human endometrial stromal cells exposed to oxidative stress signals.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- p38 MAP kinase mediates arsenite-induced apoptosis through FOXO3a activation and induction of Bim transcription.Apoptosis : an international journal on programmed cell death · 2008Article
- Two distinct signaling pathways regulate peroxynitrite-induced apoptosis in PC12 cells.Cell death and differentiation · 2006Article
- Prologation of c-Jun N-terminal kinase is associated with cell death induced by tumor necrosis factor alpha in human chondrocytes.Journal of Korean medical science · 2004Article
- Article
- JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins.The EMBO journal · 2004Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
c-Jun N-terminal kinase (JNK) is activated when cells are exposed to noxious stimuli. The role of JNK in apoptosis is subject to considerable debate; for example, JNK activation may promote or inhibit apoptosis depending on the cell type and stimulus involved. These conflicting results have arisen in part because few studies have successfully separated JNK activation from the primary stress-induced damage or from other stress-induced signalling pathways. Here we describe a conditional mutant, deltaMEKK1:ER*, which allows selective activation of the JNK cascade in the absence of any cellular stress. Activation of deltaMEKK1:ER* in CC139 fibroblasts resulted in the rapid and sustained activation of JNK without activating ERK or p38 or promoting IkappaBalpha phosphorylation. Activation of deltaMEKK1:ER* caused a reversible halt in cell growth but failed to induce apoptosis. In contrast, treatment of cells with LY294002, to inhibit phosphoinositide 3-kinase (PI3K), caused downregulation of Bcl-2 and Mcl-1 and allowed deltaMEKK1:ER* to elicit a robust apoptotic response characterized by activation of Bax and caspases. This PI3K-inhibitable, JNK-induced death response was not impeded, but actually accelerated, by cycloheximide. This suggests that JNK-induced activation of Bax and cell death does not require the upregulation of pro-death genes such as Bim or FasL, but rather proceeds through pre-existing components. However, if the PI3K cell survival pathway is not inhibited, even sustained activation of JNK exerts no overt proapoptotic effect in CC139 cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.