Disease relevance of Cicloheximide

• Effects of cycloheximide on virus RNA replication in an inducible line of polyoma-transformed rat cells [1].
• In this article, we describe two distinct effects of cycloheximide (CH), a potent inhibitior of protein synthesis, on the replication of polyoma virus (PV) DNA in an inducible line of PV-transformed rat cells (LPT cells) [1].
• Extracts of the EHS tumor, which produces an extracellular matrix containing basement membrane components, were tested for their ability to promote attachment to cycloheximide-treated PAM 212 cells [2].
• Infection with vaccinia virus (a poxvirus) quickly and efficiently shuts off host protein synthesis in the presence of actinomycin D (refs 3--5) or cycloheximide [3].
• The protein synthesis inhibitor cycloheximide, at a concentration of 0.08 microgram per milliliter, induced flat morphology within 24 to 48 hours and low saturation density in human osteosarcoma cells transformed by Kirsten murine sarcoma virus (Ki-MSV) or N-methyl-N' nitro-N-nitrosoguanidine [4].

Psychiatry related information on Cicloheximide

• Cycloheximide did not block the vitamin D suppression of Id message level [5].
• Effects of electroconvulsive shock and cycloheximide on the incorporation of amino acids into proteins of mouse brain subcellular fractions [6].
• Effects of DM-9384, a cyclic derivative of GABA, on amnesia and decreases in GABAA and muscarinic receptors induced by cycloheximide [7].
• In addition, the appearance of new junctional receptors was inhibited by cycloheximide and actinomycin D given at critical periods, implicating a protein synthetic step [8].
• Cycloheximide blocked the induction of permissiveness by butyrate suggesting that a protein(s) was responsible for allowing HSV synthesis in NB cells [9].

High impact information on Cicloheximide

• Consistent with the dependence of NMD on translation, the NMD of CBP80-bound mRNA is blocked by cycloheximide or suppressor tRNA [10].
• Mice strains deficient in their ability to detect cycloheximide have amino acid substitutions in the mT2R-5 gene; these changes render the receptor significantly less responsive to cycloheximide [11].
• We provide functional and mechanistic evidence that SRA acts as an RNA transcript; transfected SRA, unlike other steroid receptor coregulators, functions in the presence of cycloheximide, and SRA mutants containing multiple translational stop signals retain their ability to activate steroid receptor-dependent gene expression [12].
• Here, AP3/PI function was put under posttranslational control to analyze its immediate effect on the floral mRNA population, with indirect effects blocked by cycloheximide [13].
• We propose that reduced elongation rates in the presence of cycloheximide allow otherwise insufficient SRP to interact efficiently with ribosomes [14].

Chemical compound and disease context of Cicloheximide

• Mouse B16 melanoma cells, treated with high concentrations of cycloheximide or pactamycin for 1 hour and then washed repeatedly, recovered their ability to incorporate [3H]leucine into protein in about 4 hours, while cells treated with emetine recovered in 12 hours [15].
• We examined the effects of ATP depletion, a lysosomal protease inhibitor, and an inhibitor of actin polymerization on D2 activity in the presence or absence of cycloheximide or 3,3', 5'-triiodothyronine (reverse T3, rT3) in rat pituitary tumor cells (GH4C1) [16].
• Melanoma adhesion to this heparin-binding fragment was sensitive to the effects of cycloheximide, which contrasted adhesion to the haptotaxis-promoting fragment [17].
• Continuous treatment of the ocular circadian pacemaker of the mollusc Bulla gouldiana with anisomycin or cycloheximide substantially lengthened (up to 39 and 52 hr, respectively) the free-running period of the rhythm [18].
• Metabolic changes following estrogen stimulation and the inhibition of these changes in the presence of actinomycin D and cycloheximide were monitored continuously in perfused human breast cancer T47D clone 11 cells with 31P and 13C NMR techniques [19].

Biological context of Cicloheximide

• In serum-stimulated normal fibroblasts, the kinetics of inactivation of p42MAPK coincides with the appearance of newly synthesized 3CH134 protein, and the protein synthesis inhibitor cycloheximide leads to persistent activation of MAP kinase [20].
• In starved cells, stress-induced phosphorylation is rapid, involves a large percentage of the H1, occurs at multiple sites on the H1 molecule and is inhibited by cycloheximide [21].
• The midblastula transition (MBT) in Xenopus can be initiated prematurely by blocking the fundamental cell-cycle oscillator with cycloheximide, in which case motility and transcription are quickly initiated [22].
• Cooperative alignment of nu bodies during chromosome replication in the presence of cycloheximide [23].
• L1 mRNA accumulates in the cytoplasm in the presence of cycloheximide, which blocks DNA replication and the onset of the late phase [24].

Anatomical context of Cicloheximide

• Effects of cycloheximide on the "autocatalytic" nature of the maturation promoting factor (MPF) in oocytes of Xenopus laevis [25].
• Overexpression of MnSOD confers increased resistance to TNF plus cycloheximide on the 293 human embryonic kidney cell line [26].
• As cycloheximide, a protein synthesis inhibitor, also inhibits presentation of protein antigens to class II-restricted T cells, the data indicate that peptides generated by processing of exogenous proteins binds to newly synthesized class II molecules for presentation to T cells [27].
• Differential hybridization was used to screen a complementary DNA library constructed from PC12 cells treated with NGF and cycloheximide [28].
• Immediately after training, each animal received one of the following amnestic treatments: stimulation of the frontal cortex or amygdala, pentylenetetrazol, diethyldithiocarbamate, or cycloheximide [29].

Associations of Cicloheximide with other chemical compounds

• Additional experiments indicate that the effect of the ras protein requires entry into the cells, is temporary, is inhibited by cycloheximide or actinomycin D, and is seen only in established cell lines [30].
• We show here that the tumor promoter okadaic acid, which inhibits protein phosphatases 1 and 2A, and the protein synthesis inhibitors anisomycin and cycloheximide also stimulate pp33 and pp15 phosphorylation [31].
• Tumor necrosis factor (TNF) induces the synthesis of protein(s) that can protect cells against subsequent killing by TNF in the presence of cycloheximide [26].
• Protein synthesis inhibition by cycloheximide (CHX) treatment indicated that the half-life of p21/SDI-1 in dividing HT1 cells was approximately 30 min [32].
• Incubation of delta psi mlow cells in the presence of excess amount of the GC receptor antagonist RU38486 (which displaces DEX from the GC receptor), cytokines that inhibit DEX-induced cell death, or cycloheximide fails to prevent cytolysis [33].

Gene context of Cicloheximide

• These effects of TNF-alpha and IL-1 on target cells may contribute to their reported protective activity against radiation as well as their ability to induce resistance to cell killing induced by the combination of TNF-alpha and cycloheximide [34].
• These effects appear to result from stabilization of the ftz protein, since ftz stripes decay much more slowly in mutant embryos than in wild type after injection of the protein synthesis inhibitor cycloheximide [35].
• Here, we show that cells released from cdc28ts arrest in the presence of cycloheximide show wild-type levels of induction for HO, CLN1, and CDC9 (DNA ligase) [36].
• Insertion of a 20-bp fragment from the CDC9 promoter (containing a MluI element) upstream of LacZ confers both periodic expression and transcriptional induction in cycloheximide following release from cdc28ts arrest [36].
• Consistent with this, release from pheromone arrest (where CLN1 and CLN2 are not expressed) in cycloheximide shows no induction at all [36].

Analytical, diagnostic and therapeutic context of Cicloheximide

• In agreement with this interpretation, we detected myc RNA as stable transcripts in differentiated F9 cells after treatment of the cells with cycloheximide [37].
• Denervation and hypophysectomy block the increase in medullary and cortical enzyme activity, respectively, whereas cycloheximide presents the increase in both tissues [38].
• The addition of actinomycin D or cycloheximide to the HIV-infected monocytes before coculture reduced, > 2.5-fold, the levels of TNF-alpha [39].
• Incubation of neonatal kidney cell cultures with the protein synthesis inhibitor cycloheximide resulted in a significant decrease in both the cellular and media AP [40].
• Whereas cycloheximide and actinomycin D both inhibited BK-induced IL-1beta synthesis, results from Northern blot and nuclear run-on assays suggested that BK acted primarily at the transcription level which led to the accumulation of IL-1beta message in stimulated cells [41].

References