| Name | interferon (protein family or complex) |
|---|---|
| Synonyms | Interferon |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 20167191 | Palm M, Garigliany MM, Cornet F, Desmecht D: Interferon-induced Sus scrofa Mx1 blocks endocytic traffic of incoming influenza A virus particles. Vet Res. 2010 5-6;41(3):29. Epub 2010 Jan 13. In infected cells expressing poMx1, the level of transcripts encoding the viral nucleoprotein is significantly lower than normal, even when secondary transcription is prevented by exposure to cycloheximide. |
2(0,0,0,2) | Details |
| 16704297 | Numajiri A, Mibayashi M, Nagata K: Stimulus-dependent and domain-dependent cell death acceleration by an IFN-inducible protein, human MxA. J Interferon Cytokine Res. 2006 Apr;26(4):214-9. Human MxA is an interferon- alpha / beta (IFN-alpha/beta)-inducible protein that inhibits multiplication of influenza viruses and other RNA viruses. |
1(0,0,0,1) | Details |
| 17368049 | DeWitte-Orr SJ, Leong JA, Bols NC: Induction of antiviral genes, Mx and vig-1, by dsRNA and Chum salmon reovirus in rainbow trout monocyte/macrophage and fibroblast cell lines. Fish Shellfish Immunol. 2007 Sep;23(3):670-82. Epub 2007 Feb 1. Medium conditioned by cells previously exposed to poly IC or CSV and assumed to contain interferon (IFN) induced the antiviral genes in RTS11. In both cell lines, poly IC and CSV induced Mx transcripts in the presence of cycloheximide, suggesting a direct induction mechanism, independent of IFN, was also possible. |
1(0,0,0,1) | Details |
| 16313564 | Roxstrom-Lindquist K, Assefaw-Redda Y, Rosinska K, Faye I: 20-Hydroxyecdysone indirectly regulates Hemolin gene expression in Hyalophora cecropia. Insect Mol Biol. 2005 Dec;14(6):645-52. The third conserved motif is similar to the interferon (IFN) regulatory factor binding element (IRF-E) and IFN-stimulated response element (ISRE). Using the protein synthesis inhibitor cycloheximide we demonstrate that Hemolin up-regulation by 20E requires ongoing protein synthesis. |
1(0,0,0,1) | Details |
| 19661440 | Li JH, D'Alessio A, Pober JS: Lipopolysaccharide can trigger a cathepsin B-dependent programmed death response in human endothelial cells. Am J Pathol. 2009 Sep;175(3):1124-35. Epub 2009 Aug 6. In the presence of the protein synthesis inhibitor cycloheximide, LPS primarily induces caspase-dependent apoptotic cell death of HUVECs, which is blocked by siRNA-mediated knockdown of myeloid differentiation factor 88 adaptor protein but not of Toll-like receptor-associated interferon-inducing factor. We conclude that LPS can activate a Cat-B-dependent programmed death response in human endothelial cells that is independent of both myeloid differentiation factor 88 and Toll-like receptor-associated interferon-inducing factor, is blocked by both FADD and phosphatidylinositol 3 kinase, and is potentiated by interferon-gamma. |
1(0,0,0,1) | Details |
| 15858025 | DeFilippis V, Fruh K: Rhesus cytomegalovirus particles prevent activation of interferon regulatory factor 3. J Virol. 2005 May;79(10):6419-31. Since infection during inhibition of protein expression by cycloheximide or inactivation of viral gene expression by UV treatment did not trigger IRF3 activation or ISG expression by RhCMV, we conclude that RhCMV virions contain a novel inhibitor of IFN-independent viral induction of ISG expression by IRF3. One of the most important innate host defense mechanisms against viral infection is the induction of interferon (IFN)-stimulated genes (ISGs). |
1(0,0,0,1) | Details |
| 16136269 | Danforth DN, Zhu Y: Conversion of Fas-resistant to Fas-sensitive MCF-7 breast cancer cells by the synergistic interaction of interferon-gamma and Breast Cancer Res Treat. 2005 Nov;94(1):81-91. MCF-7 human breast cancer cells have low levels of Fas receptor (FasR) and are resistant to anti-FasR antibody mediated apoptosis, however two naturally occurring substances, interferon and (AT), act synergistically to enhance antiproliferative processes in these cells, suggesting this combination may also be an effective means for enhancing FasR expression. FasR-induced cells were resistant to stimulation of apoptosis by anti-FasR antibody, however treatment with cycloheximide rendered these cells sensitive to antibody-induced apoptosis, suggesting endogenous blockade to signaling. |
1(0,0,0,1) | Details |
| 15685448 | Tahara E Jr, Tahara H, Kanno M, Naka K, Takeda Y, Matsuzaki T, Yamazaki R, Ishihara H, Yasui W, Barrett JC, Ide T, Tahara E: G1P3, an interferon inducible gene 6-16, is expressed in gastric cancers and inhibits mitochondrial-mediated apoptosis in gastric cancer cell line TMK-1 cell. Cancer Immunol Immunother. 2005 Aug;54(8):729-40. Epub 2005 Feb 1. One of exceptional gastric cancer cell line, TMK-1, which do not express detectable 6-16, is sensitive to apoptosis induced by cycloheximide (CHX), 5-fluorouracil (5-FU) and serum-deprivation. |
1(0,0,0,1) | Details |
| 16479515 | Green J, Khabar KS, Koo BC, Williams BR, Polyak SJ: Stability of CXCL-8 and related AU-rich mRNAs in the context of hepatitis C virus replication in vitro. J Infect Dis. 2006 Mar 15;193(6):802-11. Epub 2006 Feb 13. BACKGROUND: Previous studies have shown that levels of CXCL-8 are elevated in patients with chronic hepatitis C virus (HCV) infection and are highest in nonresponders to interferon (IFN) therapy and that CXCL-8 inhibits IFN antiviral action. CXCL-8 mRNA was superinduced by TNF- alpha in the presence of the protein-synthesis inhibitor cycloheximide. |
1(0,0,0,1) | Details |
| 17583676 | Kamachi M, Aramaki T, Tanimura S, Ichinose K, Fujikawa K, Iwamoto N, Yoshizaki A, Ida H, Kawakami A, Kohno M, Eguchi K: Activation of protein phosphatase causes alternative splicing of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL): potential effect on immune surveillance. Biochem Biophys Res Commun. 2007 Aug 17;360(1):280-5. Epub 2007 Jun 15. Etoposide and cycloheximide induced alternative splicing, whereas staurosporine (a broad kinase inhibitor) blocked both constitutive and alternative splicing. |
0(0,0,0,0) | Details |
| 15919906 | Ousman SS, Wang J, Campbell IL: Differential regulation of interferon regulatory factor (IRF)-7 and IRF-9 gene expression in the central nervous system during viral infection. J Virol. 2005 Jun;79(12):7514-27. The stimulation of IRF-7 gene expression by IFN-alpha in glial cell culture was prevented by cycloheximide. |
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| 18494554 | Masuda K, Teshima-Kondo S, Mukaijo M, Yamagishi N, Nishikawa Y, Nishida K, Kawai T, Rokutan K: A novel tumor-promoting function residing in the 5' non-coding region of vascular endothelial growth factor mRNA. PLoS Med. 2008 May 20;5(5):e94. The 5'UTR-mediated activity was not affected by a protein synthesis inhibitor, cycloheximide. |
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| 16049355 | Hidajat R, Nagano-Fujii M, Deng L, Hotta H: Cleavage of the hepatitis C virus NS5A protein by caspase-3 in the interferon sensitivity-determining region in a sequence-dependent manner. Kobe J Med Sci. 2004;50(5-6):153-66. |
2(0,0,0,2) | Details |
| 15728246 | Gugliesi F, Mondini M, Ravera R, Robotti A, de Andrea M, Gribaudo G, Gariglio M, Landolfo S: Up-regulation of the interferon-inducible IFI16 gene by oxidative stress triggers p53 transcriptional activity in endothelial cells. J Leukoc Biol. 2005 May;77(5):820-9. Epub 2005 Feb 22. To investigate the mechanism of IFI16 accumulation, cells were incubated for 6 h in the presence of H2O2 or IFN-beta, and then cycloheximide was added to inhibit further protein synthesis. |
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| 15684817 | Liu M, Hummer BT, Li X, Hassel BA: Camptothecin induces the ubiquitin-like protein, ISG15, and enhances ISG15 conjugation in response to interferon. J Interferon Cytokine Res. 2004 Nov;24(11):647-54. |
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| 17200614 | Pandey M, Bajaj GD, Rath PC: Induction of the interferon-inducible RNA-degrading enzyme, RNase L, by stress-inducing agents in the human cervical carcinoma cells. RNA Biol. 2004 May;1(1):21-7. Epub 2004 May 5. We checked the stress-inducible transcription factor, nuclear factor kappa B (NF-kappaB), which was persistently activated by cycloheximide but not by other agents after 24 hours indicating no role of NFkappaB in the RNase L-induction. |
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