Cycloheximide

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Erlend B Smeland - One of the best experts on this subject based on the ideXlab platform.

  • effect of Cycloheximide on epidermal growth factor receptor trafficking and signaling
    FEBS Letters, 2012
    Co-Authors: Morten P Oksvold, Nina Pedersen, Lise Forfang, Erlend B Smeland
    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.

Morten P Oksvold - One of the best experts on this subject based on the ideXlab platform.

  • effect of Cycloheximide on epidermal growth factor receptor trafficking and signaling
    FEBS Letters, 2012
    Co-Authors: Morten P Oksvold, Nina Pedersen, Lise Forfang, Erlend B Smeland
    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.

Nina Pedersen - One of the best experts on this subject based on the ideXlab platform.

  • effect of Cycloheximide on epidermal growth factor receptor trafficking and signaling
    FEBS Letters, 2012
    Co-Authors: Morten P Oksvold, Nina Pedersen, Lise Forfang, Erlend B Smeland
    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.

Lise Forfang - One of the best experts on this subject based on the ideXlab platform.

  • effect of Cycloheximide on epidermal growth factor receptor trafficking and signaling
    FEBS Letters, 2012
    Co-Authors: Morten P Oksvold, Nina Pedersen, Lise Forfang, Erlend B Smeland
    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.

M Costlow - One of the best experts on this subject based on the ideXlab platform.

  • tnf induction of el4 hyposensitivity to lysis by recombinant soluble and membrane associated tnfs tnf binding internalization and degradation
    Cellular Immunology, 1994
    Co-Authors: Marvin Fishman, M Costlow
    Abstract:

    Abstract EL4 mouse thymoma cells sensitive to TNF-mediated lysis only in the presence of Cycloheximide (S-EL4) or in the presence or absence of Cycloheximide (N-EL4) were used in these experiments. Murine tumor cell line (S-EL4) sensitivity to TNF cytotoxicity is augmented when Cycloheximide is added together with TNF or when Cycloheximide is added 1 hr before or after TNF. No enhanced sensitivity is observed when target cells are incubated with Cycloheximide 2-4 hr before or after the addition of TNF. In the absence of Cycloheximide, S-EL4 cells preexposed to murine TNF are less susceptible to lysis by TNF and TNF receptor-conjugated TNF but are lysed by integral membrane TNF. TNF-induced hyposensitivity is partially reversed by actinomycin D or by culturing the preexposed cells for 4 hr prior to TNF lytic assay. TNF preincubation of N- and SEL4 cells results in an immediate decrease in 125 1-TNF binding due to TNF receptor occupancy. Recovery of TNF-R occupancy and TNF internalization were subsequently noted.