ArticleThe Journal of biological chemistry2008
Regulation of arsenic trioxide-induced cellular responses by Mnk1 and Mnk2.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Arsenic Trioxide and the MNK1 Inhibitor AUM001 Exert Synergistic Anti-Glioblastoma Effects by Modulating Key Translational, Cell Cycle, and Transmembrane Transport Pathways.Brain sciences · 2026Article
- Mechanistic update of Trisenox in blood cancer.Current research in pharmacology and drug discovery · 2023Review
- Global signalling network analysis of luminal T47D breast cancer cells in response to progesterone.Frontiers in endocrinology · 2022Article
- The Differential Phosphorylation-Dependent Signaling and Glucose Immunometabolic Responses Induced during Infection byMicroorganisms · 2020Article
- Discovery of novel Mnk inhibitors using mutation-based induced-fit virtual high-throughput screening.Chemical biology & drug design · 2019Article
- Induction of MNK Kinase-dependent eIF4E Phosphorylation by Inhibitors Targeting BET Proteins Limits Efficacy of BET Inhibitors.Molecular cancer therapeutics · 2019Article
- Differential Response of Glioma Stem Cells to Arsenic Trioxide Therapy Is Regulated by MNK1 and mRNA Translation.Molecular cancer research : MCR · 2018Article
- Quercetin and Cisplatin combined treatment altered cell cycle and mitogen activated protein kinase expressions in malignant mesotelioma cells.BMC complementary and alternative medicine · 2016Article
- Translational control of PML contributes to TNFα-induced apoptosis of MCF7 breast cancer cells and decreased angiogenesis in HUVECs.Cell death and differentiation · 2016Article
- Direct binding of arsenic trioxide to AMPK and generation of inhibitory effects on acute myeloid leukemia precursors.Molecular cancer therapeutics · 2015Article
- Resveratrol enhances the suppressive effects of arsenic trioxide on primitive leukemic progenitors.Cancer biology & therapy · 2014Article
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- Regulation of the kinase RSK1 by arsenic trioxide and generation of antileukemic responses.Cancer biology & therapy · 2013Article
- Article
- p38α mitogen-activated protein kinase depletion and repression of signal transduction to translation machinery by miR-124 and -128 in neurons.Molecular and cellular biology · 2013Article
- Article
- Interferon regulatory factor-1 binds c-Cbl, enhances mitogen activated protein kinase signaling and promotes retinoic acid-induced differentiation of HL-60 human myelo-monoblastic leukemia cells.Leukemia & lymphoma · 2011Article
- Essential role for Mnk kinases in type II interferon (IFNgamma) signaling and its suppressive effects on normal hematopoiesis.The Journal of biological chemistry · 2011Article
- Negative regulatory effects of Mnk kinases in the generation of chemotherapy-induced antileukemic responses.Molecular pharmacology · 2010Article
- Autophagy is a critical mechanism for the induction of the antileukemic effects of arsenic trioxide.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Arsenic trioxide (As(2)O(3)) is a potent inducer of apoptosis of malignant cells in vitro and in vivo, but the precise mechanisms by which it mediates such effects are not well defined. We provide evidence that As(2)O(3) induces phosphorylation/activation of the MAPK signal-integrating kinases (Mnks) 1 and 2 in leukemia cell lines. Such activation is defective in cells with targeted disruption of the p38alpha MAPK gene, indicating that it requires upstream engagement of the p38 MAPK pathway. Studies using Mnk1(-/-) or Mnk2(-/-), or double Mnk1(-/-)Mnk2(-/-) knock-out cells, establish that activation of Mnk1 and Mnk2 by arsenic trioxide regulates downstream phosphorylation of the eukaryotic initiation factor 4E at Ser-209. Importantly, arsenic-induced apoptosis is enhanced in cells with targeted disruption of the Mnk1 and/or Mnk2 genes, suggesting that these kinases are activated in a negative-feedback regulatory manner, to control generation of arsenic trioxide responses. Consistent with this, pharmacological inhibition of Mnk activity enhances the suppressive effects of arsenic trioxide on primary leukemic progenitors from patients with acute leukemias. Taken together, these findings indicate an important role for Mnk kinases, acting as negative regulators for signals that control generation of arsenic trioxide-dependent apoptosis and antileukemic responses.
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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.