Disease relevance of cycloheximide

• Moreover, studies with cyclohexamide demonstrated that the survival effect of hypoxia was fully dependent on continuing protein synthesis [1].
• Cyclohexamide up-regulated the expression of ICAM-1 on chondrosarcoma cells but had little or no effect on carcinoma cells [2].
• When the same fused cells were treated with the protein synthesis inhibitor cyclohexamide, the pX17-dependent activation of the HIV-1 LTR was abolished [3].
• Partial elimination of latent Epstein-Barr virus genomes from virus-producing cells by cyclohexamide [4].
• These data suggest that Fas is a potential protein related to apoptosis in osteosarcomas when the sensitizing activity of cyclohexamide on anti-Fas-mediated cytotoxicity was exerted [5].

High impact information on cycloheximide

• The incubation of OKT8(-) T cells with LTB4 for 18 h resulted in the appearance of the OKT8(+) on 10-20% of the cells, and this could be blocked by cyclohexamide but not by mitomycin C [6].
• This LTB4-induced suppressor cell was radiosensitive, and its generation could be blocked by cyclohexamide but not by mitomycin C [6].
• The inability of cyclohexamide treatment to effect the TGR localization of GLUT-4 indicates that GLUT-4 enters the ANF secretory granules at the TGR via the recycling pathway and not via the biosynthetic pathway [7].
• The inhibitory effect of 1,25(OH)2D3 on erythroid differentiation of K562 cells was abrogated by cyclohexamide (20 micrograms/mL), an inhibitor of protein synthesis [8].
• We also performed studies on lymphocytes cultured in the presence of cyclohexamide, which suggested that the expression of class I HLA antigens and B2 microglobulin are highly sensitive to the inhibition of protein synthesis, whereas the expression of class II HLA antigens, Leu-4, and HLe-1 are not [9].

Chemical compound and disease context of cycloheximide

• Studies on fatty liver with isolated hepatocytes. I. The action of colchicine, phalloidin, cytochalasin B, and cyclohexamide on protein and triglyceride synthesis and secretion [10].

Biological context of cycloheximide

• In addition, cyclohexamide treatment was found to markedly increase the stability of pim-1 transcripts in bovine PBMC suggesting that a protein synthesis-dependent posttranscriptional pim-1 mRNA degradation pathway may be involved in the regulation of pim-1 mRNA levels in lymphoid cells [11].
• Quantitation of the levels of the BEF-1 isoforms, and studies in the presence of cyclohexamide, provided evidence for the phosphorylation of an existing intracellular pool of BEF-1, with no change in the total intracellular level [12].
• This detection of CD80 is attributable to the acquisition of CD80 from APCs, as opposed to the up-regulation of endogenous CD80, as demonstrated by CD4(+) T cells treated with cyclohexamide [13].
• RNA expression experiments with transgenic tobacco seedlings or with transfected pea protoplasts using PS-IAA4/5 promoter GUS or CAT fusions reveal that CHX transcriptionally activates PS-IAA4/5 gene expression [14].
• The inducibility of DNA synthesis after treatment with cyclohexamide (CHM) during mitosis and the G1 phase of WI38 cells has been studied in the heterokaryons following fusion with HeLa cells in S phase [15].

Anatomical context of cycloheximide

• Inhibitors of microtubules (colchicine and vinca alkaloids) and of protein synthesis (cyclohexamide) had no effect [16].
• This priming by LPS is dependent on protein synthesis, given that cyclohexamide blocks the ability of LPS to prime macrophages for activation of caspase-1 by the P2X7R [17].
• In this study human fibroblast monolayers that were incubated with cyclohexamide (50 micrograms/ml) for 14 h at 37 C had no detectable 35 K protein on their cell surface, but type I Sm-C/IGF-I receptors were still present [18].
• Effects of cyclohexamide on a cytoplasmic factor initiating meiotic naturation in Xenopus oocytes [19].
• In explant cultures, Bmp activation of Odd-skipped related 1 (Odd-1), the earliest known gene expressed in the intermediate mesoderm, is blocked by cyclohexamide, indicating that the activation of Odd-1 by Bmp signaling is translation-dependent [20].

Associations of cycloheximide with other chemical compounds

• TGF-beta 1 secretion was inhibited in a dose-dependent manner by pretreatment with cyclohexamide, but was not affected by pretreatment with actinomycin D [21].
• This increase in BKB1R mRNA level is protein synthesis-independent as indicated by treatment of cells with cycloheximide (CHX) or puromycin (PUR) [22].
• Cyclohexamide when used alone (i.e., in non-FBS- or TGF-beta1-treated cultures), moreover, effectively stimulated PAI-1 induction whereas puromycin was ineffective [23].
• In addition to the IL-1beta effects, translation inhibitors, CHX and PUR increase the steady state BKB1R mRNA level by inhibiting BKB1R mRNA degradation [22].
• MDM exposure to recombinant macrophage-tropic (R5) gp120 led to dose- and donor-dependent release of TNF-alpha, which was cyclohexamide-sensitive and associated with up-regulated message [24].

Gene context of cycloheximide

• Experiments with cyclohexamide-dependent block of protein synthesis showed that the half-life of CUGBP1 is increased in cells expressing CUG repeats [25].
• The induction of BRCA1 mRNA was blocked by cyclohexamide [26].
• It is interesting that activation of these signaling molecules by G-CSF was prolonged by pretreating cells with actinomycin D or cyclohexamide, suggesting that de novo protein synthesis is required for appropriate termination of G-CSF-R signaling [27].
• These BR isoforms were activated by 20E in fat bodies cultured in vitro and behaved as early genes, with a self-repressive autoregulatory loop that can be blocked by the protein inhibitor, cyclohexamide [28].
• Inhibitor studies revealed no significant difference among control, cyclohexamide, and actinomycin D supernatants for tPA, suggesting release of protein rather than active synthesis [29].

Analytical, diagnostic and therapeutic context of cycloheximide

• Analysis of poly(A+)RNA by northern blots revealed hybridization of an IGF-I cDNA to a 7.5- to 7.0-kb transcript and superinduction of the 7.5-7.0-kb mRNA by the translational inhibitor, cyclohexamide [30].
• Western blot analysis showed that IFN-tau and CHX treatment resulted in a greater expression of the proapoptotic protein Bax-alpha compared with that in control cultures [31].
• 6. RT-PCR revealed elevated iNOS mRNA levels after 12 h of exposure to CH [32].
• Cyclohexamide did not affect rosette formation, suggesting that agglutinins may be preformed and stored in leukocytes prior to secretion [33].
• Immunoprecipitation of NR1 following the block of protein synthesis by cyclohexamide revealed that the rapidly and slowly degrading pools mainly consisted of the NR1 splice variants NR1-4a and NR1-2a [34].

References