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Chemical Compound Review

Acti-Dione     4-[2-(3,5-dimethyl-2-oxo- cyclohexyl)-2...

Synonyms: GNF-Pf-170, GNF-Pf-261, CHEMBL582062, CHEMBL600517, AG-J-67354, ...
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Disease relevance of cycloheximide


High impact information on cycloheximide

  • However, in C/EBPalpha growth-arrested cells, the level of the p21/SDI-1 did not change for > 80 min after CHX addition [4].
  • These findings indicated that CHX prevented the degradation of TNF mRNA by inhibiting the synthesis of a labile protein [5].
  • Since CHX and A23187 mediated induction of TCR mRNA is both rapid and reversible, it is unlikely that new DNA rearrangements are responsible for the induction [6].
  • Under these conditions, Cx selectively prevented the degradation of CK mRNA in a reversible manner [7].
  • The calcium ionophore A23187 induces the accumulation of TCR-alpha but not -beta transcripts; and in contrast to CHX, it increases the rate of TCR-alpha gene transcription and the expression of large nuclear TCR-alpha precursor transcripts [6].

Biological context of cycloheximide

  • CHX also induces full length TCR-beta transcripts greater than 90-fold while TCR-beta gene transcription increases only 2- to 4-fold [6].
  • The dissolution of microfilaments spread peripherally over time and preceded other TNF/CHI-induced effects such as cytoplasmic "boiling," decrease in cell volume, and lysis of the plasma membrane [8].
  • Finally, CHX, BIM, and SN50 facilitated the cleavage and activation of procaspase-8 in TRAIL-resistant cells, confirming that inhibition of TRAIL-induced apoptosis occurs at this level and that these agents sensitize MM cells by relieving this block [9].
  • In the culture system, hepatocellular DNA fragmentation in the presence of ActD/TNF was observed several hours before lactate dehydrogenase release and was inhibited by CHX [2].
  • Apoptosis induced by TNFalpha and CHX was facilitated by FLIP(S) antisense expression but attenuated by sense transfection [10].

Anatomical context of cycloheximide

  • Conditions were established for a time-window during which cycloheximide (Cx) produced a virtually total arrest of protein synthesis in myotubes that was reversible upon removal of the inhibitor [7].
  • In this report, we examine the mechanism of cytolysis in a 3T3-like mouse cell line, C3HA, which was sensitized to TNF by treatment with CHI [8].
  • The disruption of microfilaments, which was observed within 15 min of treatment, was not seen in untreated cells or in cells treated with either TNF or CHI alone [8].
  • We found that an early change in TNF/CHI-treated cells was a significant loss of stress fibers in perinuclear areas of the cytoplasm [8].
  • Cytochalasin E, which disrupts microfilaments, induced cytolysis of TNF-treated cells even in the absence of CHI; however, demecolcine, which depolymerizes microtubules, did not sensitize cells to TNF [8].

Associations of cycloheximide with other chemical compounds

  • Blocking protein synthesis promoted folding and export of ER-retained GFP-PDS, as demonstrated by surface-biotinylation analysis and by CHX- or puromycin-induced accumulation of YFP-PDS in the Golgi apparatus during a 20 degrees C temperature-block experiment [11].
  • The regulation of LPS-stimulated TNF alpha mRNA expression in vitro was also investigated by employing the protein synthesis inhibitor cycloheximide (CHX) [12].
  • Exposure of human fibroblasts to inhibitors of protein synthesis with different mechanisms of action (e.g., puromycin, pactamycin, or CHX) all generated hexose transport increases in a concentration-dependent fashion correlating with their increasing inhibitory effects on protein synthesis [13].
  • These apoptotic phenomena induced by 2CdA were inhibited by cycloheximide (CHX; a protein synthesis inhibitor), deoxycytidine (dC; a substrate of deoxycytidine kinase), acetyl Ile-Glu-Thr-Asp aldehyde (Ac-IETD-CHO; a caspase-8 inhibitor) and acetyl Asp-Glu-Val-Asp aldehyde (Ac-DEVD-CHO; a caspase-3 inhibitor) [14].
  • Further, dominant negative IkappaB attenuated the CHX and DENSPM-induced SSAT expression and mitochondria damage [15].

Gene context of cycloheximide

  • CHX increased the stability of both IL-1 alpha and IL-1 beta mRNA, demonstrating the existence of a post-transcriptional form of control [16].
  • In the absence of CHX, 259 and 125 genes were up or down-regulated respectively; only 38 and 24 of these genes were up and down-regulated by p53 also in the presence of CHX and are considered primary targets in this cell line [17].
  • The CHM-superinduced COX-2 mRNA was subject to a rapid degradation after removal of CHM (T1/2 < 1 hr) [18].
  • Irrespective of STAT1 status, TNF induced cytotoxic effects in the presence of cycloheximide (CHX) in both cell types [19].
  • In serum-free medium containing interleukin-3 (IL-3) or granulocyte-macrophage colony-stimulating factor (GM-CSF), the early induction of IFN-alpha mRNA became resistant to CHX, and, in contrast to FBS and CM supplemented medium, this was observed also without a preincubation of the PBMCs [20].

Analytical, diagnostic and therapeutic context of cycloheximide


  1. Regulation of tumor necrosis factor-related apoptosis-inducing ligand sensitivity in primary and transformed human keratinocytes. Leverkus, M., Neumann, M., Mengling, T., Rauch, C.T., Bröcker, E.B., Krammer, P.H., Walczak, H. Cancer Res. (2000) [Pubmed]
  2. Murine hepatocyte apoptosis induced in vitro and in vivo by TNF-alpha requires transcriptional arrest. Leist, M., Gantner, F., Bohlinger, I., Germann, P.G., Tiegs, G., Wendel, A. J. Immunol. (1994) [Pubmed]
  3. Interleukin-1 beta induction of tumor necrosis factor-alpha gene expression in human astroglioma cells. Bethea, J.R., Chung, I.Y., Sparacio, S.M., Gillespie, G.Y., Benveniste, E.N. J. Neuroimmunol. (1992) [Pubmed]
  4. CCAAT/enhancer-binding protein alpha (C/EBP alpha) inhibits cell proliferation through the p21 (WAF-1/CIP-1/SDI-1) protein. Timchenko, N.A., Wilde, M., Nakanishi, M., Smith, J.R., Darlington, G.J. Genes Dev. (1996) [Pubmed]
  5. Transcriptional and posttranscriptional regulation of tumor necrosis factor gene expression in human monocytes. Sariban, E., Imamura, K., Luebbers, R., Kufe, D. J. Clin. Invest. (1988) [Pubmed]
  6. Induction of T-cell receptor-alpha and -beta mRNA in SL12 cells can occur by transcriptional and post-transcriptional mechanisms. Wilkinson, M.F., MacLeod, C.L. EMBO J. (1988) [Pubmed]
  7. Selective degradation of mRNA: the role of short-lived proteins in differential destabilization of insulin-induced creatine phosphokinase and myosin heavy chain mRNAs during rat skeletal muscle L6 cell differentiation. Pontecorvi, A., Tata, J.R., Phyillaier, M., Robbins, J. EMBO J. (1988) [Pubmed]
  8. Cytolysis by tumor necrosis factor is preceded by a rapid and specific dissolution of microfilaments. Scanlon, M., Laster, S.M., Wood, J.G., Gooding, L.R. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  9. Intracellular regulation of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human multiple myeloma cells. Mitsiades, N., Mitsiades, C.S., Poulaki, V., Anderson, K.C., Treon, S.P. Blood (2002) [Pubmed]
  10. Resistance of human ovarian cancer cells to tumor necrosis factor alpha is a consequence of nuclear factor kappaB-mediated induction of Fas-associated death domain-like interleukin-1beta-converting enzyme-like inhibitory protein. Xiao, C.W., Yan, X., Li, Y., Reddy, S.A., Tsang, B.K. Endocrinology (2003) [Pubmed]
  11. Protein synthesis inhibitors and the chemical chaperone TMAO reverse endoplasmic reticulum perturbation induced by overexpression of the iodide transporter pendrin. Shepshelovich, J., Goldstein-Magal, L., Globerson, A., Yen, P.M., Rotman-Pikielny, P., Hirschberg, K. J. Cell. Sci. (2005) [Pubmed]
  12. Expression, regulation, and production of tumor necrosis factor-alpha in mouse testicular interstitial macrophages in vitro. Xiong, Y., Hales, D.B. Endocrinology (1993) [Pubmed]
  13. Inhibitors of protein synthesis cause increased hexose transport in cultured human fibroblasts by a mechanism other than transporter translocation. Germinario, R.J., Manuel, S., Chang, Z., Leckett, B. J. Cell. Physiol. (1992) [Pubmed]
  14. 2-Chloro-2'-deoxyadenosine induces apoptosis through the Fas/Fas ligand pathway in human leukemia cell line MOLT-4. Nomura, Y., Inanami, O., Takahashi, K., Matsuda, A., Kuwabara, M. Leukemia (2000) [Pubmed]
  15. Inactivation of IkappaB contributes to transcriptional activation of spermidine/spermine N(1)-acetyltransferase. Choi, W., Proctor, L., Xia, Q., Feng, Y., Gerner, E.W., Chiao, P.J., Hamilton, S.R., Zhang, W. Mol. Carcinog. (2006) [Pubmed]
  16. Regulation of expression of human IL-1 alpha and IL-1 beta genes. Turner, M., Chantry, D., Buchan, G., Barrett, K., Feldmann, M. J. Immunol. (1989) [Pubmed]
  17. DNA microarrays identification of primary and secondary target genes regulated by p53. Kannan, K., Amariglio, N., Rechavi, G., Jakob-Hirsch, J., Kela, I., Kaminski, N., Getz, G., Domany, E., Givol, D. Oncogene (2001) [Pubmed]
  18. Differential regulation of cyclooxygenase-2 (COX-2) mRNA stability by interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) in human in vitro differentiated macrophages. Huang, Z.F., Massey, J.B., Via, D.P. Biochem. Pharmacol. (2000) [Pubmed]
  19. Lack of requirement of STAT1 for activation of nuclear factor-kappaB, c-Jun NH2-terminal protein kinase, and apoptosis by tumor necrosis factor-alpha. Mukhopadhyay, A., Shishodia, S., Fu, X.Y., Aggarwal, B.B. J. Cell. Biochem. (2002) [Pubmed]
  20. The induction of interferon-alpha and interferon-beta mRNA in human natural interferon-producing blood leukocytes requires de novo protein synthesis. Cederblad, B., Gobl, A.E., Alm, G.V. J. Interferon Res. (1991) [Pubmed]
  21. Peroxynitrite contributes to spontaneous loss of cardiac efficiency in isolated working rat hearts. Ferdinandy, P., Panas, D., Schulz, R. Am. J. Physiol. (1999) [Pubmed]
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