The mechanism of sodium fluoride and cycloheximide inhibition of hemoglobin biosynthesis in the cell-free reticulocyte system

Lin, Syr-Yaung; Mosteller, Raymond D.; Hardesty, Boyd

doi:10.1016/0022-2836(66)90079-9

Cited by 198 publications

(37 citation statements)

References 18 publications

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“…In parallel, cycloheximide (CHX) was used as a control, which inhibits protein biosynthesis by the ribosomal machinery. 28 The experiment showed that Roc-AR strongly inhibited 35 S-methionine incorporation with an IC 50 of approximately 30 nM (Figure 4b). These data suggest that Roc-AR may downregulate c-FLIP expression through inhibition of translation.…”

Section: Resultsmentioning

confidence: 95%

Rocaglamide breaks TRAIL resistance in HTLV-1-associated adult T-cell leukemia/lymphoma by translational suppression of c-FLIP expression

et al. 2010

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The human T-cell leukemia virus type-1 (HTLV-1)-associated adult T-cell leukemia/lymphoma (ATL) is incurable by currently known therapies. ATL samples and cell lines derived from ATL patients show restricted sensitivity to tumor necrosis factorrelated apoptosis-inducing ligand (TRAIL) and CD95 ligand (CD95L). We have recently shown that HTLV-1-infected cells express elevated levels of cellular caspase-8 FLICE-inhibitory protein (c-FLIP) conferring resistance to receptor-mediated apoptosis. This finding underscores the demand to develop new strategies for treatment of ATL. In this study, we show that the naturally occurring herbal compound Rocaglamide (Roc) sensitizes CD95L-and TRAIL-induced apoptosis in HTLV-1-infected cells by downregulation of c-FLIP expression. Investigation of the molecular mechanism of Roc-mediated downregulation of c-FLIP revealed that it inhibits phosphorylation of the translation initiation factor 4E (eIF4E), a key factor that controls the rate-limiting step of translation, through inhibition of the MEK-ERK-MNK1 signaling pathway. This event prevents de novo synthesis of short-lived proteins such as c-FLIP in HTLV-1-infected cells. Our data suggest that Roc may serve as an adjuvant for TRAIL-based anticancer therapy.

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Section: Resultsmentioning

confidence: 95%

Rocaglamide breaks TRAIL resistance in HTLV-1-associated adult T-cell leukemia/lymphoma by translational suppression of c-FLIP expression

et al. 2010

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“…NaF blocks a step between the binding of initiator tRNA and mRNA to the 40 S subunit and the binding of the first aminoacyl-tRNA to the ribosome [ 13,14], presumably by preventing the addition of the 60 S subunit [15]. Sodium fluoride also inhibits the initiation of protein synthesis in an endogenous cell free system as well as in a poly U dependent cell free system [ 16,17]. Sodium azide, however, has no inhibitory effect on the poly U dependent polyphenylalanine synthesis in a cell free system In summary, it is concluded that NaN 3 leads to an instant inhibition of protein synthesis in protoplasts of S. carlsbergensis, the inhibition being complete at concentrations of 10 -3 M of NaN 3 or higher.…”

Section: Resultsmentioning

confidence: 99%

Azide as inhibitor of protein synthesis in yeast protoplasts

Amesz¹,

Zeijst²

1972

FEBS Letters

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“…Cycloheximide is known to be a potent inhibitor of translation in both plants (10) and animals (11). Its ability to inhibit elongation in plants is well documented (7).…”

Section: Resultsmentioning

confidence: 99%

Timing of the Auxin Response in Etiolated Pea Stem Sections

Barkley

Evans

1970

Plant Physiol.

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The short term growth response of etiolated pea stem segments (Pisum sativum L., var. Alaska) was investigated with the use of a high resolution growth-recording device. The immediate effect of treatment with indole-3-acetic acid is an inhibition of growth. This inhibition lasts about 10 minutes, and then the rate of elongation rises abruptly to a new steady rate about 4 times the rate of elongation before auxin treatment. This rapid steady rate of elongation, however, continues for only about 25 minutes before declining suddenly to a lower steady rate of growth about 2 times the rate of elongation before the addition of auxin.Pretreatment of the segments with cycloheximide or actinomycin strongly inhibits both phases of auxin-promoted elongation without altering the length of the latent period in response to the hormone.

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The mechanism of sodium fluoride and cycloheximide inhibition of hemoglobin biosynthesis in the cell-free reticulocyte system

Cited by 198 publications

References 18 publications

Rocaglamide breaks TRAIL resistance in HTLV-1-associated adult T-cell leukemia/lymphoma by translational suppression of c-FLIP expression

Rocaglamide breaks TRAIL resistance in HTLV-1-associated adult T-cell leukemia/lymphoma by translational suppression of c-FLIP expression

Azide as inhibitor of protein synthesis in yeast protoplasts

Timing of the Auxin Response in Etiolated Pea Stem Sections

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