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Effect of cycloheximide on epidermal growth factor receptor trafficking and signaling
Authors:Morten P. Oksvold  Nina Marie Pedersen  Lise Forfang  Erlend B. Smeland
Affiliation:a Dept. of Immunology, Institute for Cancer Research, Oslo University Hospital HF, Montebello, Oslo, Norway
b Dept. of Biochemistry, Institute for Cancer Research, Oslo University Hospital HF, Norway
c Centre for Cancer Biomedicine, Faculty of Medicine, University of Oslo, Norway
Abstract:
Cycloheximide is the most common protein synthesis inhibitor, and is believed to specifically inhibit the cytoplasmic protein synthesis. Here we demonstrate that cycloheximide induces internalization and redistribution of EGF receptor to early endosomes in HeLa cells independent of receptor tyrosine phosphorylation, but dependent on p38 MAPK activity. Degradation of EGF receptor or its downstream effectors was not observed. EGF-induced activation of ERK1/2 was inhibited upon pre-treatment with cycloheximide, but did not activate JNK. The observed effects of treatment with cycloheximide alone are significant and therefore results involving the use of cycloheximide for inhibition of protein synthesis must be interpreted with caution.

Structured summary of protein interactions

EEA1 and EGFRcolocalize by fluorescence microscopy (View interaction).
Keywords:Cycloheximide   EGF receptor   p38 MAPK   Signaling   Stress
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