ArticleThe Journal of physiology1997
Evidence of two mechanisms for the activation of the glucose transporter GLUT1 by anisomycin: p38(MAP kinase) activation and protein synthesis inhibition in mammalian cells.
Article in The Journal of physiology, 1997. 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, 80 citations in OpenAlex.
- Systematic Exploration of Functional Group Relevance for Anti-Leishmanial Activity of Anisomycin.Biomedicines · 2023Article
- Application of emetine in SARS-CoV-2 treatment: regulation of p38 MAPK signaling pathway for preventing emetine-induced cardiac complications.Cell cycle (Georgetown, Tex.) · 2022Article
- Different Aspects of Emetine's Capabilities as a Highly Potent SARS-CoV-2 Inhibitor against COVID-19.ACS pharmacology & translational science · 2022Review
- Anisomycin is active in preclinical models of pediatric acute myeloid leukemia via specifically inhibiting mitochondrial respiration.Journal of bioenergetics and biomembranes · 2021Article
- Global translation inhibition yields condition-dependent de-repression of ribosome biogenesis mRNAs.Nucleic acids research · 2019Article
- Antibiotic anisomycin induces cell cycle arrest and apoptosis through inhibiting mitochondrial biogenesis in osteosarcoma.Journal of bioenergetics and biomembranes · 2017Article
- Kinase-dependent Regulation of Monoamine Neurotransmitter Transporters.Pharmacological reviews · 2016Review
- Transforming growth factor-β1 impairs CFTR-mediated anion secretion across cultured porcine vas deferens epithelial monolayer via the p38 MAPK pathway.American journal of physiology. Cell physiology · 2013Article
- Article
- Post-transcriptional regulation of placenta growth factor mRNA by hydrogen peroxide.Microvascular research · 2012Article
- Bidirectional regulation of neutrophil migration by mitogen-activated protein kinases.Nature immunology · 2012Article
- Regulation of sodium iodide symporter gene expression by Rac1/p38β mitogen-activated protein kinase signaling pathway in MCF-7 breast cancer cells.The Journal of biological chemistry · 2012Article
- The metabolic life and times of a T-cell.Immunological reviews · 2010Review
- Rapid identification of inhibitors that interfere with poliovirus replication using a cell-based assay.Antiviral research · 2008Article
- Adrenaline increases glucose transport via a Rap1-p38MAPK pathway in rat vascular smooth muscle cells.British journal of pharmacology · 2007Article
- The cardioprotective effect of the low molecular weight isoform of fibroblast growth factor-2: the role of JNK signaling.Journal of molecular and cellular cardiology · 2007Article
- Intestinal sugar transport.World journal of gastroenterology · 2006Review
- Induction of human NF-IL6beta by epidermal growth factor is mediated through the p38 signaling pathway and cAMP response element-binding protein activation in A431 cells.Molecular biology of the cell · 2005Article
- Glutamate triggers rapid glucose transport stimulation in astrocytes as evidenced by real-time confocal microscopy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- The facilitated component of intestinal glucose absorption.The Journal of physiology · 2001Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
1. Inhibitors of protein synthesis stimulate sugar transport in mammalian cells through activation of plasma membrane GLUT1, the housekeeping isoform of the glucose transporter. However, it has been reported that some of these compounds, in addition to their effect on protein synthesis, also activate protein kinases. 2. In the present study we have explored the role of these two effects on GLUT1 activation. In 3T3-L1 adipocytes and Clone 9 cells, stimulation of sugar transport by puromycin, a translational inhibitor that does not activate kinases, was not detectable until 90 min after exposure. In contrast, stimulation by anisomycin, a potent Jun-NH2-terminal kinase (JNK) agonist, exhibited no lag phase. An intermediate response was observed to emetine and cycloheximide, weak activators of JNK. 3. The potency of anisomycin to stimulate transport acutely (30 min of exposure) was 5- to 10-fold greater than for its chronic stimulation of transport, measured after 4 h of exposure. The stimulation of transport by a low concentration of anisomycin (0.3 microM) was transient, peaked at 30-60 min and it was inhibited (IC50 < 1 microM) by SB203580, which indicates that its mediator is not JNK, but the homologous p38(MAP kinase) (p38(MAPK)). In contrast, the responses to 4 h exposure to 300 microM anisomycin or puromycin were refractory to SB203580. 4. Exposure to anisomycin resulted in rapid activation of p38(MAPK). Activation of both p38(MAPK) and GLUT1 by 0.3 microM anisomycin was cancelled by puromycin. 5. We conclude that the activation of GLUT1 in response to anisomycin includes two components: a delayed component involving translational inhibition and a fast, puromycin-inhibitable component that is secondary to activation of p38(MAPK).
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