| Name | caspase (protein family or complex) |
|---|---|
| Synonyms | caspase; caspases |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19646526 | Lee JY, Jung HJ, Song IS, Williams MS, Choi C, Rhee SG, Kim J, Kang SW: Protective role of cytosolic 2-cys peroxiredoxin in the TNF-alpha-induced apoptotic death of human cancer cells. Free Radic Biol Med. 2009 Oct 15;47(8):1162-71. Epub 2009 Jul 29. The HeLa cervical cancer cells expressing a dominant negative mutant (DN) of a cytosolic 2-cysPrx manifested remarkable increase in intracellular reactive species level, which was counteracted by catalase administration, and apoptotic cell death induced by combined treatment of TNF-alpha and cycloheximide compared to the control (CT) cells. The apoptosis enhanced by DN expression was shown to be dependent on a typical FADD/caspase pathway. |
2(0,0,0,2) | Details |
| 16546987 | Tang R, Faussat AM, Majdak P, Marzac C, Dubrulle S, Marjanovic Z, Legrand O, Marie JP: Semisynthetic homoharringtonine induces apoptosis via inhibition of protein synthesis and triggers rapid myeloid cell leukemia-1 down-regulation in myeloid leukemia cells. Mol Cancer Ther. 2006 Mar;5(3):723-31. The Bcl-2 cleavage could be inhibited by the Z-VAD.fmk caspase inhibitor. The Mcl-1 turnover was only induced by ssHHT and cycloheximide, but not by daunorubicin and cytosine arabinoside, and could be restored by proteasome inhibitors. |
2(0,0,0,2) | Details |
| 15542778 | Doi S, Soda H, Oka M, Tsurutani J, Kitazaki T, Nakamura Y, Fukuda M, Yamada Y, Kamihira S, Kohno S: The histone deacetylase inhibitor FR901228 induces caspase-dependent apoptosis via the mitochondrial pathway in small cell lung cancer cells. Mol Cancer Ther. 2004 Nov;3(11):1397-402. |
2(0,0,0,2) | Details |
| 17157182 | Pardo M, Melendez JA, Tirosh O: Manganese superoxide dismutase inactivation during Fas (CD95)-mediated apoptosis in Jurkat T cells. Free Radic Biol Med. 2006 Dec 15;41(12):1795-806. Epub 2006 Sep 16. In the presence of cycloheximide, an inhibitor of protein synthesis, the rates of cell death and MnSOD degradation were accelerated. Fas-induced MnSOD cleavage was partially inhibited in the presence of the pan-caspase inhibitor, z-VAD-fmk. |
2(0,0,0,2) | Details |
| 17647100 | Takadera T, Ohyashiki T: Calmodulin inhibitor-induced apoptosis was prevented by glycogen synthase kinase-3 inhibitors in PC12 cells. Cell Mol Neurobiol. 2007 Sep;27(6):783-90. Epub 2007 Jul 24. In order to determine the role of calmodulin in regulating neuronal survival and death, we examined, whether calmodulin inhibitors induce caspase-dependent apoptotic cell death, and whether glycogen synthase kinase-3 is involved in calmodulin inhibitor-induced cell death in PC12 cells. In addition, nerve growth factor and cycloheximide, a protein synthesis inhibitor, completely blocked cell death. |
2(0,0,0,2) | Details |
| 15808420 | Aronis A, Madar Z, Tirosh O: Mechanism underlying oxidative stress-mediated lipotoxicity: exposure of J774.2 macrophages to triacylglycerols facilitates mitochondrial reactive species production and cellular necrosis. Free Radic Biol Med. 2005 May 1;38(9):1221-30. We therefore evaluated the effect of TG on apoptotic cells showing high caspase activity. TG induced elevated ROS levels and suppressed caspase-3 in apoptotic cells pretreated for 24 h with cycloheximide. |
2(0,0,0,2) | Details |
| 17617453 | Ondrouskova E, Soucek K, Horvath V, Smarda J: Alternative pathways of programmed cell death are activated in cells with defective caspase-dependent apoptosis. Leuk Res. 2008 Apr;32(4):599-609. Epub 2007 Jul 6. We analysed programmed cell death pathways of v-myb-transformed BM2 monoblasts induced by arsenic trioxide, cycloheximide and camptothecin with U937 promonocytes as a reference cell line. |
2(0,0,0,2) | Details |
| 20080135 | Acrani GO, Gomes R, Proenca-Modena JL, da Silva AF, Carminati PO, Silva ML, Santos RI, Arruda E: Apoptosis induced by Oropouche virus infection in HeLa cells is dependent on virus protein expression. Virus Res. 2010 Apr;149(1):56-63. Epub 2010 Jan 18. Mitochondrial release of cytochrome C and activation of caspases 9 and 3 were also detected by western blot analysis. Results obtained in cells treated with chloroquine and cycloheximide indicated that viral uncoating and replication are required for apoptosis induction by OROV. |
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. Here, we demonstrated that the cell death promotion activity of MxA was caspase dependent when cell death was induced by UV irradiation or cycloheximide (CHX). |
2(0,0,0,2) | Details |
| 16109713 | Rahmani M, Davis EM, Bauer C, Dent P, Grant S: Apoptosis induced by the kinase inhibitor BAY 43-9006 in human leukemia cells involves down-regulation of Mcl-1 through inhibition of translation. J Biol Chem. 2005 Oct 21;280(42):35217-27. Epub 2005 Aug 18. These events were accompanied by ERK1/2 inactivation and caspase-independent down-regulation of Mcl-1. Inhibition of protein synthesis by cycloheximide or proteasome function with MG132 and pulse-chase studies with [35S] demonstrated that BAY 43-9006 did not diminish Mcl-1 protein stability, nor did it enhance Mcl-1 ubiquitination, but instead markedly attenuated Mcl-1 translation in association with the rapid and potent dephosphorylation of the eIF4E translation initiation factor. |
2(0,0,0,2) | Details |
| 17166486 | Takadera T, Ohyashiki T: Caspase-dependent apoptosis induced by calcineurin inhibitors was prevented by glycogen synthase kinase-3 inhibitors in cultured rat cortical cells. Brain Res. 2007 Feb 16;1133(1):20-6. Epub 2006 Dec 12. In addition, insulin growth factor-I (IGF-I) and cycloheximide completely blocked cell death. |
2(0,0,0,2) | Details |
| 16526045 | Hareramadas B, Rai U: Cellular mechanism of -induced thymic involution in wall lizard: caspase-dependent action. J Exp Zool A Comp Exp Biol. 2006 May 1;305(5):396-409. |
2(0,0,0,2) | Details |
| 15913957 | Kakinuma H, Inomata H, Kitamura N: Enhanced JNK activation by NESK without kinase activity upon caspase-mediated cleavage during apoptosis. Cell Signal. 2005 Nov;17(11):1439-48. Treatment of NESK-transfected HeLa cells with TNF-alpha in the presence of cycloheximide or with staurosporine induced proteolytic cleavage of NESK. |
2(0,0,0,2) | Details |
| 18497737 | He F, Doucet JA, Stephens JM: Caspase-mediated degradation of PPARgamma proteins in adipocytes. . Obesity (Silver Spring). 2008 Aug;16(8):1735-41. Epub 2008 May 22. RESULTS: We observed that TNFalpha can induce a caspase-mediated degradation of PPARgamma proteins in the presence of cycloheximide. |
116(1,2,2,6) | Details |
| 18474237 | Lee JM, Kim YJ, Ra H, Kang SJ, Han S, Koh JY, Kim YH: The involvement of caspase-11 in TPEN-induced apoptosis. FEBS Lett. 2008 Jun 11;582(13):1871-6. Epub 2008 May 12. Cycloheximide or actinomycin D blocked caspase-11 induction, reduced caspase-11 and -3 activation, and attenuated TPEN-induced neuronal apoptosis. |
87(1,1,1,7) | Details |
| 19331698 | Wegrzyn P, Yarwood SJ, Fiegler N, Bzowska M, Koj A, Mizgalska D, Malicki S, Pajak M, Kasza A, Kachamakova-Trojanowska N, Bereta J, Jura J, Jura J: Mimitin - a novel cytokine-regulated mitochondrial protein. BMC Cell Biol. 2009 Mar 31;10:23. However, when apoptosis was induced by TNF and cycloheximide, and mimitin expression blocked, the activities of these caspases were significantly increased. |
82(1,1,1,2) | Details |
| 16003319 | Mori T, Doi R, Toyoda E, Koizumi M, Ito D, Kami K, Kida A, Masui T, Kawaguchi Y, Fujimoto K: Regulation of the resistance to TRAIL-induced apoptosis as a new strategy for pancreatic cancer. Surgery. 2005 Jul;138(1):71-7. Combined treatment with cycloheximide and TRAIL induced cleaved forms of caspases and simultaneously restored the sensitivity to TRAIL-induced apoptosis in the resistant cells. |
81(1,1,1,1) | Details |
| 20123115 | Pushpanjali P, Ramaiah KV: PKC activation contributes to caspase-mediated eIF2alpha phosphorylation and cell death. Biochim Biophys Acta. 2010 May;1800(5):518-525. Epub 2010 Feb 1. However, PMA enhances late stages of UV-irradiation or cycloheximide-induced caspase activation, eIF2alpha phosphorylation and apoptosis in Sf9 cells. |
38(0,1,1,8) | Details |
| 20032379 | Eriksson D, Lofroth PO, Johansson L, Riklund K, Stigbrand T: Apoptotic signalling in HeLa Hep2 cells following 5 Gy of -60 gamma radiation. Anticancer Res. 2009 Nov;29(11):4361-6. HeLa Hep2 cells were irradiated with or without preincubation with inhibitors of protein synthesis (cycloheximide, CHX) and caspases, followed by TUNEL staining and caspase assay plate evaluation. |
34(0,1,1,4) | Details |
| 16135563 | Werz O, Tretiakova I, Michel A, Ulke-Lemee A, Hornig M, Franke L, Schneider G, Samuelsson B, Radmark O, Steinhilber D: Caspase-mediated degradation of human 5-lipoxygenase in B lymphocytic cells. Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13164-9. Epub 2005 Aug 31. Caspase activation and 5-LO degradation were blocked by the protein-synthesis inhibitor cycloheximide, and cell-permeable peptide inhibitors of casp-6 and casp-8 prevented 5-LO cleavage. |
34(0,1,1,4) | Details |
| 15965903 | Stanic I, Facchini A, Borzi RM, Vitellozzi R, Stefanelli C, Goldring MB, Guarnieri C, Facchini A, Flamigni F: Polyamine depletion inhibits apoptosis following blocking of survival pathways in human chondrocytes stimulated by tumor necrosis factor-alpha. J Cell Physiol. 2006 Jan;206(1):138-46. The combined treatment of C-28/I2 chondrocytes with TNF and cycloheximide (CHX) resulted in a effector caspase activation and internucleosomal DNA fragmentation. |
34(0,1,1,4) | Details |
| 15545300 | Jaruga-Killeen E, Rayford W: TNF receptor 1 is involved in the induction of apoptosis by the cyclin dependent kinase inhibitor p27Kip1 in the prostate cancer cell line PC-3. FASEB J. 2005 Jan;19(1):139-41. Epub 2004 Nov 15. Cell cycle and typical markers of apoptosis were analyzed by flow cytometry in the presence of the following reagents: cycloheximide, pan-caspase inhibitor ZVAD-fmk, neutralizing anti-TNFR1, and anti-TNFR2. |
33(0,1,1,3) | Details |
| 15528219 | Kaur M, Agarwal C, Singh RP, Guan X, Dwivedi C, Agarwal R: Skin cancer chemopreventive agent, {alpha}-santalol, induces apoptotic death of human epidermoid carcinoma A431 cells via caspase activation together with dissipation of mitochondrial membrane potential and cytochrome c release. Carcinogenesis. 2005 Feb;26(2):369-80. Epub 2004 Nov 4. Pre-treatment of cells with caspase-8 or -9 inhibitor, pan caspase inhibitor or cycloheximide totally blocked alpha-santalol-caused caspase-3 activity and cleavage, but only partially reversed apoptotic cell death. |
33(0,1,1,3) | Details |
| 18522940 | Hellwig CT, Kohler BF, Lehtivarjo AK, Dussmann H, Courtney MJ, Prehn JH, Rehm M: Real time analysis of tumor necrosis factor-related apoptosis-inducing ligand/cycloheximide-induced caspase activities during apoptosis initiation. J Biol Chem. 2008 Aug 1;283(31):21676-85. Epub 2008 Jun 3. |
32(0,1,1,2) | Details |
| 17585910 | Ito S, Ihara T, Tamura H, Tanaka S, Ikeda T, Kajihara H, Dissanayake C, Abdel-Motaal FF, El-Sayed MA: alpha-Tomatine, the major saponin in tomato, induces programmed cell death mediated by reactive species in the fungal pathogen Fusarium oxysporum. FEBS Lett. 2007 Jul 10;581(17):3217-22. Epub 2007 Jun 15. In the present study, mechanisms involved in alpha-tomatine-induced cell death of fungi were examined using a filamentous pathogenic fungus Fusarium oxysporum. alpha-Tomatine-induced cell death of F. oxysporum (TICDF) occurred only under aerobic conditions and was blocked by the mitochondrial F (0) F (1)-ATPase inhibitor oligomycin, the caspase inhibitor D-VAD-fmk, and protein synthesis inhibitor cycloheximide. |
31(0,1,1,1) | Details |
| 16413676 | Yang W, Monroe J, Zhang Y, George D, Bremer E, Li H: Proteasome inhibition induces both pro- and anti-cell death pathways in prostate cancer cells. Cancer Lett. 2006 Nov 18;243(2):217-27. Epub 2006 Jan 18. MG132-induced cell death was partially inhibited by pan-caspase inhibitor zAVD-fmk and translational inhibitor cycloheximide. |
31(0,1,1,1) | Details |
| 17200126 | Adams KW, Cooper GM: Rapid turnover of mcl-1 couples translation to cell survival and apoptosis. J Biol Chem. 2007 Mar 2;282(9):6192-200. Epub 2007 Jan 2. Caspase inhibition and overexpression of Bcl-x (L) blocked cycloheximide-induced apoptosis. |
31(0,1,1,1) | Details |
| 17700538 | Deniaud A, Sharaf el dein O, Maillier E, Poncet D, Kroemer G, Lemaire C, Brenner C: Endoplasmic reticulum stress induces -dependent permeability transition, mitochondrial outer membrane permeabilization and apoptosis. Oncogene. 2008 Jan 10;27(3):285-99. Epub 2007 Aug 13. The specificity of this apoptosis pathway was validated in cells using a panel of pharmacological agents that chelate Ca2+ (BAPTA-AM) or inhibit receptor (IP (3) R; 2-aminoethoxydiphenyl borate), voltage-dependent anion channel (VDAC) (4,4'-diisothiocyanatostilbene-2,2'-disulfonate, the permeability transition pore (cyclosporin A and bongkrekic acid), caspases (z-VAD-fmk) and protein synthesis (cycloheximide). |
31(0,1,1,1) | Details |
| 16133868 | Autelli R, Crepaldi S, De Stefanis D, Parola M, Bonelli G, Baccino FM: Intracellular free iron and acidic pathways mediate TNF-induced death of rat hepatoma cells. Apoptosis. 2005 Aug;10(4):777-86. HTC cells, sensitized to TNF toxicity with cycloheximide, died in a caspase-independent apoptosis-like manner. |
7(0,0,1,2) | Details |
| 17097791 | Lock EA, Reed CJ, Kinsey GR, Schnellmann RG: Caspase-dependent and -independent induction of externalization during apoptosis in human renal carcinoma Cak (1)-1 and A-498 cells. Toxicology. 2007 Jan 5;229(1-2):79-90. Epub 2006 Oct 13. The endonuclease inhibitor aurintricarboxylic acid (ATA), phospholipase A (2) inhibitor bromoenol lactone (BEL), protein synthesis inhibitor cycloheximide (CH) and chloride channel blockers niflumic acid (NFA) and 5-nitro-2-(3-phenylpropylamino) (NPPB) all had no effect on staurosporine-induced annexin V binding in A-498 cells either in the presence or absence of ZVAD. |
5(0,0,0,5) | Details |
| 15905291 | Eley A, Hosseinzadeh S, Hakimi H, Geary I, Pacey AA: Apoptosis of ejaculated human sperm is induced by co-incubation with Chlamydia trachomatis lipopolysaccharide. Hum Reprod. 2005 Sep;20(9):2601-7. Epub 2005 May 19. Caspase activity was also investigated by fluorimetry and by use of a pan-caspase inhibitor and caspase-3 inhibitor. |
4(0,0,0,4) | Details |
| 17942133 | Chitnis NS, D'Costa SM, Paul ER, Bilimoria SL: Modulation of iridovirus-induced apoptosis by endocytosis, early expression, JNK, and apical caspase. Virology. 2008 Jan 20;370(2):333-42. Epub 2007 Oct 17. CIV infection of cells pretreated with cycloheximide induced apoptosis in 69% of the cells compared to 10% in normal infections. |
4(0,0,0,4) | Details |
| 17194804 | Lee SY, Cherla RP, Tesh VL: Simultaneous induction of apoptotic and survival signaling pathways in macrophage-like THP-1 cells by Shiga toxin 1. Infect Immun. 2007 Mar;75(3):1291-302. Epub 2006 Dec 28. Finally, the protein synthesis inhibitors Stx1 and anisomycin triggered limited apoptosis and prolonged JNK and p38 MAPK activation, while macrophage-like cells treated with cycloheximide remained viable and showed transient activation of MAPKs. Despite the partial resistance of macrophage-like THP-1 cells to Stx1-mediated killing, treatment of these cells with Stx1 activated a broad array of caspases, disrupted the mitochondrial membrane potential (DeltaPsi (m)), and released cytochrome c into the cytoplasm. |
3(0,0,0,3) | Details |
| 17613518 | McKay MM, Morrison DK: Caspase-dependent cleavage disrupts the ERK cascade scaffolding function of KSR1. J Biol Chem. 2007 Sep 7;282(36):26225-34. Epub 2007 Jul 5. In addition, we find that in comparison with KSR1 (-/-) mouse embryonic fibroblasts expressing wild type KSR1 (WT-KSR1), cells expressing a cleavage-resistant KSR1 protein (DEVA-KSR1) exhibit reduced apoptotic signaling in response to tumor necrosis factor-alpha/cycloheximide treatment. |
3(0,0,0,3) | Details |
| 15844877 | Jaganathan J, Petit JH, Lazio BE, Singh SK, Chin LS: Tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in established and primary glioma cell lines. Neurosurg Focus. 2002 Sep 15;13(3):ecp1. The A172 cells, by contrast, were susceptible only with cycloheximide, whereas U373MG cells were not susceptible to TRAIL. The JNK, caspase 3, and caspase 7 activity evaluated after treatment with TRAIL showed that TRAIL-sensitive cell lines exhibited downstream caspase activation, whereas TRAIL-resistant cells did not. |
3(0,0,0,3) | Details |
| 19112105 | Kadohara K, Nagumo M, Asami S, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Caspase-8 mediates mitochondrial release of pro-apoptotic proteins in a manner independent of its proteolytic activity in apoptosis induced by the protein synthesis inhibitor acetoxycycloheximide in human leukemia Jurkat cells. J Biol Chem. 2009 Feb 27;284(9):5478-87. Epub 2008 Dec 26. Jurkat cells deficient in caspase-8 were more resistant to Ac-CHX than wild-type Jurkat cells and manifested decreased apoptosis induction and caspase activation as well as inefficient release of cytochrome c, Smac/DIABLO, and AIF into the cytosol. |
3(0,0,0,3) | Details |
| 18329746 | Ravindra PV, Tiwari AK, Ratta B, Chaturvedi U, Palia SK, Subudhi PK, Kumar R, Sharma B, Rai A, Chauhan RS: Induction of apoptosis in Vero cells by Newcastle disease virus requires viral replication, de-novo protein synthesis and caspase activation. Virus Res. 2008 May;133(2):285-90. Epub 2008 Mar 10. Although cycloheximide blocked NDV-induced apoptosis, actinomycin-D did not, suggesting that de-novo viral protein synthesis was critical for the induction of apoptosis. |
3(0,0,0,3) | Details |
| 18465786 | Clermont F, Gonzalez NS, Communi D, Franken S, Dumont JE, Robaye B: HDGF is dephosphorylated during the early steps of endothelial cell apoptosis in a caspase-dependent way. J Cell Biochem. 2008 Jul 1;104(4):1161-71. We were looking by a proteomic approach for new phospho-proteins involved during the early steps of the TNF + cycloheximide (CHX)-induced apoptosis-preceding mitochondrial membrane permeabilization-of endothelial cells (BAEC). |
3(0,0,0,3) | Details |
| 17912641 | Ding WX, Ni HM, Yin XM: Absence of Bax switched MG132-induced apoptosis to non-apoptotic cell death that could be suppressed by transcriptional or translational inhibition. Apoptosis. 2007 Dec;12(12):2233-44. We previously showed that proteasome inhibitors including MG132 and Bortezomib could induce apoptosis in a Bax- and caspase-dependent way. |
2(0,0,0,2) | Details |
| 16409300 | Binet F, Cavalli H, Moisan E, Girard D: Arsenic trioxide (AT) is a novel human neutrophil pro-apoptotic agent: effects of catalase on AT-induced apoptosis, degradation of cytoskeletal proteins and de novo protein synthesis. Br J Haematol. 2006 Feb;132(3):349-58. Cycloheximide partially reversed AT-induced apoptosis. Herein, we found that AT-induced neutrophil apoptosis and gelsolin degradation via caspases. |
2(0,0,0,2) | 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. However, based on the use of proteinase inhibitors, cell death changes from being principally caspase-dependent to being principally cathepsin B (Cat B)-dependent. |
2(0,0,0,2) | Details |
| 17453339 | Guseva NV, Rokhlin OW, Taghiyev AF, Cohen MB: Unique resistance of breast carcinoma cell line T47D to TRAIL but not anti-Fas is linked to p43cFLIP (L). Breast Cancer Res Treat. 2008 Feb;107(3):349-57. Epub 2007 Apr 24. We observed that only anti-Fas mAb induces caspase activation and cell death in T47D. |
2(0,0,0,2) | Details |
| 16897441 | Popadic S, Popadic D, Ramic Z, Mostarica Stojkovic M, Trajkovic V, Milinkovic M, Medenica L: Chloramphenicol induces in vitro growth arrest and apoptosis of human keratinocytes. Cell Biol Toxicol. 2006 Sep;22(5):371-9. Epub 2006 Jul 23. CAP-induced keratinocyte apoptosis was associated with activation of caspases and increased production of reactive species. The pro-apoptotic action of CAP was antagonized by the antioxidant agent the protein synthesis inhibitor cycloheximide, and PD98059, a selective inhibitor of extracellular signal-regulated kinase (ERK) activation. |
2(0,0,0,2) | Details |
| 16891117 | Zhou D, Chu W, Rothfuss J, Zeng C, Xu J, Jones L, Welch MJ, Mach RH: Synthesis, radiolabeling, and in vivo evaluation of an 18F-labeled isatin analog for imaging caspase-3 activation in apoptosis. Bioorg Med Chem Lett. 2006 Oct 1;16(19):5041-6. Epub 2006 Aug 7. A non-peptide-based isatin sulfonamide analog, WC-II-89, was synthesized and its inhibition toward recombinant human caspase-3 and other caspases was determined. Biodistribution studies using [(18) F] WC-II-89 revealed higher uptake in liver and spleen of cycloheximide-treated rats, an animal model of apoptosis, relative to control animals. |
2(0,0,0,2) | Details |
| 17804721 | Endo H, Murata K, Mukai M, Ishikawa O, Inoue M: Activation of insulin-like growth factor signaling induces apoptotic cell death under prolonged hypoxia by enhancing endoplasmic reticulum stress response. Cancer Res. 2007 Sep 1;67(17):8095-103. We show that stimulating IGF signaling provoked caspase-dependent apoptosis under low tension in two cancer cell lines, COLO 320 and AsPC-1. IGF-induced cell death under hypoxic conditions was prevented by treatment with cycloheximide, suggesting that de novo protein synthesis is required. |
1(0,0,0,1) | Details |
| 18977202 | Nakashima T, Tanaka R, Yamashita Y, Kanda Y, Hara M: Aranorosin and a novel derivative inhibit the anti-apoptotic functions regulated by Bcl-2. Biochem Biophys Res Commun. 2008 Dec 26;377(4):1085-90. Epub 2008 Oct 31. It negatively regulates mitochondrial outer membrane permeabilization, which is responsible for the release of apoptogenic factors and the subsequent activation of caspases. |
1(0,0,0,1) | Details |
| 16648577 | Andersson Y, Le H, Juell S, Fodstad O: AMP-activated protein kinase protects against anti-epidermal growth factor receptor-Pseudomonas exotoxin A immunotoxin-induced MA11 breast cancer cell death. Mol Cancer Ther. 2006 Apr;5(4):1050-9. An immunotoxin-induced activation of c-Jun NH2-terminal kinase (JNK) preceded and overlapped caspase-mediated cleavage of the alpha-subunit of AMPK in a time- and dose-dependent manner. In contrast, cycloheximide, even at a concentration causing a 90% inhibition of protein synthesis, did neither affect the ATP level nor activate JNK and AMPK. |
1(0,0,0,1) | Details |
| 15657395 | Croft DR, Coleman ML, Li S, Robertson D, Sullivan T, Stewart CL, Olson MF: Actin-myosin-based contraction is responsible for apoptotic nuclear disintegration. J Cell Biol. 2005 Jan 17;168(2):245-55. Membrane blebbing during the apoptotic execution phase results from caspase-mediated cleavage and activation of ROCK I. |
1(0,0,0,1) | Details |
| 18445680 | Solinet S, Vitale ML: Isoform B of myosin II heavy chain mediates actomyosin contractility during TNFalpha-induced apoptosis. J Cell Sci. 2008 May 15;121(Pt 10):1681-92. Epub 2008 Apr 29. Cells that are treated long-term with TNFalpha or short-term with TGFalpha together with cycloheximide (CHX) undergo apoptosis. We show that TNFalpha induces caspase-dependent MHCIIA degradation, whereas MHCIIB levels and association with the cytoskeleton remained virtually unchanged in TtT/GF cells and NIH 3T3 fibroblasts. |
1(0,0,0,1) | Details |
| 16152591 | Akahane M, Akahane T, Matheny SL, Shah A, Okajima E, Thorgeirsson UP: Vascular endothelial growth factor-D is a survival factor for human breast carcinoma cells. Int J Cancer. 2006 Feb 15;118(4):841-9. The VEGF-D-expressing MCF-7 and MDA-MB-231 lines displayed resistance to apoptosis induced by hypoxia, staurosporin and cycloheximide. Increased Bcl-2 expression, decreased homogenous caspase activities and inhibition of poly (ADP- polymerase cleavage were associated with inhibition of apoptosis in VEGF-D-expressing clones. |
1(0,0,0,1) | Details |
| 16087277 | Zupanska A, Dziembowska M, Ellert-Miklaszewska A, Gaweda-Walerych K, Kaminska B: Cyclosporine a induces growth arrest or programmed cell death of human glioma cells. Neurochem Int. 2005 Nov;47(6):430-41. Moreover, CsA-induced cell death was accompanied by activation of executory caspases followed by PARP cleavage. |
1(0,0,0,1) | Details |
| 18466319 | Santa-Catalina MO, Garcia-Marin LJ, Bragado MJ: Lovastatin effect in rat neuroblasts of the CNS: inhibition of cap-dependent translation. J Neurochem. 2008 Aug;106(3):1078-91. Epub 2008 May 3. Cycloheximide treatment, which blocked protein synthesis, does not induce neuroblasts apoptosis. Concomitantly, lovastatin causes a decrease in eIF4G cellular amount, which is partially mediated by caspase (s) activity excluding caspase 3. |
1(0,0,0,1) | Details |
| 16966373 | Gyrd-Hansen M, Farkas T, Fehrenbacher N, Bastholm L, Hoyer-Hansen M, Elling F, Wallach D, Flavell R, Kroemer G, Nylandsted J, Jaattela M: Apoptosome-independent activation of the lysosomal cell death pathway by caspase-9. Mol Cell Biol. 2006 Nov;26(21):7880-91. Epub 2006 Sep 11. Taken together, the findings indicate that caspase-9 plays a dual role in cell death signaling, as an activator of effector caspases and lysosomal membrane permeabilization. |
1(0,0,0,1) | Details |
| 20108032 | Chopra M, Gahrs M, Haben M, Michels C, Schrenk D: Inhibition of apoptosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin depends on protein biosynthesis. Cell Biol Toxicol. 2010 Jan 27. In this study, we examined the effects of TCDD on apoptosis induced by UV-C light, ochratoxin A (OTA), and cycloheximide (CHX) in primary rat hepatocytes. Both UV-C light and OTA caused caspase activation and nuclear apoptotic effects. |
1(0,0,0,1) | Details |
| 16133866 | Drexler HC, Euler M: Synergistic apoptosis induction by proteasome and histone deacetylase inhibitors is dependent on protein synthesis. Apoptosis. 2005 Aug;10(4):743-58. The pan-caspase inhibitor Z-VAD-FMK and the caspase-8 inhibitor Z-IETD-FMK could inhibit K562 cell apoptosis. The most striking anti-apoptotic effect though was obtained by the translational inhibitor cycloheximide, which abolished caspase 8 processing, blocked Bid cleavage and maintained the mitochondrial transmembrane potential. |
2(0,0,0,2) | Details |
| 19454725 | Karahashi H, Michelsen KS, Arditi M: Lipopolysaccharide-induced apoptosis in transformed bovine brain endothelial cells and human dermal microvessel endothelial cells: the role of JNK. J Immunol. 2009 Jun 1;182(11):7280-6. Stimulation of transformed bovine brain endothelial cells (TBBEC) with LPS leads to apoptosis while human microvessel endothelial cells (HMEC) need the presence of cycloheximide (CHX) with LPS to induce apoptosis. Herbimycin A, a kinase inhibitor, and SP600125, a JNK inhibitor, suppressed the activation of caspases and lactate dehydrogenase release. |
2(0,0,0,2) | Details |
| 19041363 | Asare N, Lag M, Lagadic-Gossmann D, Rissel M, Schwarze P, Holme JA: 3-Nitrofluoranthene (3-NF) but not 3-aminofluoranthene (3-AF) elicits apoptosis as well as programmed necrosis in Hepa1c1c7 cells. Toxicology. 2009 Jan 31;255(3):140-50. Epub 2008 Nov 7. Taken together, 3-NF elicits both apoptosis and a caspase-independent programmed cell death (PCD) with autophagic characteristics. Cycloheximide completely attenuated 3-NF-induced cell death. |
1(0,0,0,1) | Details |
| 16151639 | Brecht K, Simonen M, Heim J: Upregulation of alpha globin promotes apoptotic cell death in the hematopoietic cell line FL5.12. Apoptosis. 2005 Oct;10(5):1043-62. Antisense alpha globin downregulated the expression of endogenous alpha globin und reduced caspase activity. |
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| 19395591 | Kumagai K, Ito K, Ando Y, Hakamata S, Teranishi M, Nakayama H, Manabe S: Neutralization of IL-10 exacerbates cycloheximide-induced hepatocellular apoptosis and necrosis. Toxicol Pathol. 2009;37(4):536-46. Epub 2009 Apr 24. The caspase activities and mRNA levels of Cc120, LOX-1, and E-selectin in the livers were significantly higher in the IL-10Ab/CHX group than the CHX group. |
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| 16004999 | Hareramadas B, Rai U: Mechanism of androgen-induced thymic atrophy in the wall lizard, Hemidactylus flaviviridis: an in vitro study. Gen Comp Endocrinol. 2005 Oct;144(1):10-9. DHT-induced thymocyte apoptosis was found to be caspase-dependent since it activated the initiator (caspase-9) and effector caspases (caspases-3 and -7) as well as cleaved the enzyme substrate poly (ADP- polymerase (PARP). |
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| 17123514 | Theiss C, Mazur A, Meller K, Mannherz HG: Changes in gap junction organization and decreased coupling during induced apoptosis in lens epithelial and NIH-3T3 cells. Exp Cell Res. 2007 Jan 1;313(1):38-52. Epub 2006 Oct 13. We demonstrate that global induction of apoptosis in primary bovine lens epithelial (LEC) or fibroblastic mouse NIH-3T3 cells by staurosporine, puromycin, cycloheximide, or etoposide is accompanied by a decrease in coupling by gap junctions. Cell coupling as tested by neurobiotin spreading was maintained when the LEC or NIH-3T3 cells were pre-incubated with the pan-caspase inhibitor zVAD or the caspase-3 inhibiting tetrapeptide DEVD. |
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| 18571430 | Gangadhar NM, Firestein SJ, Stockwell BR: A novel role for jun N-terminal kinase signaling in olfactory sensory neuronal death. Mol Cell Neurosci. 2008 Aug;38(4):518-25. Epub 2008 May 11. Here, we show that inhibition of transcription or translation, by actinomycin D or cycloheximide, respectively, suppresses pathways leading to death, prolonging the survival of OSNs in culture. We discovered that caspase activity and jun N-terminal kinase (JNK) signaling both play a role in OSN death, and inhibition of JNK activity suppresses effector caspase (caspase-3) activation. |
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| 17352013 | Ustundag Y, Bronk SF, Gores GJ: Proteasome inhibition-induces endoplasmic reticulum dysfunction and cell death of human cholangiocarcinoma cells. World J Gastroenterol. 2007 Feb 14;13(6):851-7. The protein synthesis inhibitor, cycloheximide, blocked apoptosis induced by proteasome inhibitor indicating that ER dysfunction was dependent upon the formation of new proteins. CONCLUSION: Proteasome inhibition induces ER dysfunction and caspase-independent cell death selectively in human cholangiocarcinoma cells. |
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| 18300075 | Shih SR, Weng KF, Stollar V, Li ML: Viral protein synthesis is required for Enterovirus 71 to induce apoptosis in human glioblastoma cells. J Neurovirol. 2008 Jan;14(1):53-61. Human glioblastoma cells (SF268) develop apoptosis, as characterized by DNA fragmentation and caspase activation, upon infection with Enterovirus 71 (EV71). Apoptosis was inhibited when EV71-infected cells were treated with chloroquine, HCl, or cycloheximide. |
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| 19561079 | Tardito S, Isella C, Medico E, Marchio L, Bevilacqua E, Hatzoglou M, Bussolati O, Franchi-Gazzola R: The thioxotriazole (II) complex A0 induces endoplasmic reticulum stress and paraptotic death in human cancer cells. J Biol Chem. 2009 Sep 4;284(36):24306-19. Epub 2009 Jun 26. Paraptosis involves extensive endoplasmic reticulum vacuolization in the absence of caspase activation. Cycloheximide inhibited the accumulation of ubiquitinylated proteins and hampered A0-induced cell death process. |
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| 15748153 | Steinbach JP, Wolburg H, Klumpp A, Weller M: Hypoxia sensitizes human malignant glioma cells towards CD95L-induced cell death. J Neurochem. 2005 Mar;92(6):1340-9. Furthermore, inhibition of protein synthesis by cycloheximide also reduced consumption and conferred protection from hypoxia, but did not modulate CD95L-induced cell death under hypoxic conditions. The mitochondrial injury induced by hypoxia was enhanced by co-treatment, and caspase cleavage became prominent. |
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| 16446372 | Caruso JA, Mathieu PA, Joiakim A, Zhang H, Reiners JJ Jr: Aryl hydrocarbon receptor modulation of tumor necrosis factor-alpha-induced apoptosis and lysosomal disruption in a hepatoma model that is caspase-8-independent. J Biol Chem. 2006 Apr 21;281(16):10954-67. Epub 2006 Jan 30. It also delayed the induction of apoptosis and partially prevented Bid cleavage and the activation of pro-caspases-3/7 in cultures treated with TNFalpha + CHX. |
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| 20017956 | Cho SH, Chung KS, Choi JH, Kim DH, Lee KT: Compound K, a metabolite of ginseng saponin, induces apoptosis via caspase-8-dependent pathway in HL-60 human leukemia cells. BMC Cancer. 2009 Dec 18;9:449. Interestingly, the activation of caspase-3 and -8 and DNA fragmentation were significantly prevented in the presence of cycloheximide, suggesting that Compound K-induced apoptosis is dependent on de novo protein synthesis. In addition, compound-K induced a series of intracellular events associated with both the mitochondrial- and death receptor-dependent apoptotic pathways, namely, (1) the activation of caspases-3, -8, and -9; (2) the loss of mitochondrial membrane potential; (3) the release of cytochrome c and Smac/DIABLO to the cytosol; (4) the translocation of Bid and Bax to mitochondria; and (5) the downregulations of Bcl-2 and Bcl-xL. |
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| 16728660 | von Wnuck Lipinski K, Keul P, Ferri N, Lucke S, Heusch G, Fischer JW, Levkau B: Integrin-mediated transcriptional activation of inhibitor of apoptosis proteins protects smooth muscle cells against apoptosis induced by degraded collagen. Circ Res. 2006 Jun 23;98(12):1490-7. Epub 2006 May 25. The mechanism by which NF-kappaB was protecting SMC against collagen fragment-induced apoptosis was a transcriptional activation of several endogenous caspase inhibitors of the inhibitor of apoptosis protein (IAP) family as: (1) the expression of xIAP, c-IAP2, and survivin was potently induced by collagen fragments; (2) IAP expression was abrogated by superrepressor IkappaBalpha; and (3) knockdown of each of the 3 IAPs by small interfering RNA (siRNA) resulted in enhanced apoptosis after collagen fragment treatment. |
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| 15637055 | Weng C, Li Y, Xu D, Shi Y, Tang H: Specific cleavage of Mcl-1 by caspase-3 in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in Jurkat leukemia T cells. J Biol Chem. 2005 Mar 18;280(11):10491-500. Epub 2005 Jan 6. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces programmed cell death through the caspase activation cascade and translocation of cleaved Bid (tBid) by the apical caspase-8 to mitochondria to induce oligomerization of multidomain Bax and Bak. In sharp contrast to cycloheximide-induced Mcl-1 dilapidation, TRAIL did not activate proteasomal degradation of Mcl-1 in Jurkat cells. |
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| 19339992 | Mendes CS, Levet C, Chatelain G, Dourlen P, Fouillet A, Dichtel-Danjoy ML, Gambis A, Ryoo HD, Steller H, Mollereau B: ER stress protects from retinal degeneration. . EMBO J. 2009 May 6;28(9):1296-307. Epub 2009 Apr 2. In addition, Drosophila S2 cultured cells, when pre-exposed to mild ER stress, are protected from H (2) O (2), cycloheximide- or ultraviolet-induced cell death. We show that a specific ER-mediated signal promotes antioxidant defences and inhibits caspase-dependent cell death. |
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| 17391795 | DeWitte-Orr SJ, Bols NC: Cytopathic effects of chum salmon reovirus to salmonid epithelial, fibroblast and macrophage cell lines. Virus Res. 2007 Jun;126(1-2):159-71. Epub 2007 Mar 27. Syncytia and HA formation were blocked by cycloheximide and ribavirin but not actinomycin D, suggesting that expression of CSV genes were required for both phenomena. Cultures with syncytia underwent a decline in cell viability, which appeared to be via apoptosis, as determined by intranucleosomal fragmentation and caspase dependence assays using the pan-caspase inhibitor, zVAD-fmk. |
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| 15812552 | de Groot DJ, Timmer T, Spierings DC, Le TK, de Jong S, de Vries EG: Indomethacin-induced activation of the death receptor-mediated apoptosis pathway circumvents acquired doxorubicin resistance in SCLC cells. Br J Cancer. 2005 Apr 25;92(8):1459-66. In GLC4-Adr, doxorubicin plus indomethacin resulted in elevated caspase activity and a 2.7-fold enhanced sensitivity to doxorubicin. Both lines were resistant to anti-Fas antibody, but plus the protein synthesis inhibitor cycloheximide anti-Fas antibody induced 40% apoptosis in GLC4-Adr. |
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| 17107344 | Arlt A, Minkenberg J, Kruse ML, Grohmann F, Folsch UR, Schafer H: Immediate early gene-X1 interferes with 26 S proteasome activity by attenuating expression of the 19 S proteasomal components S5a/Rpn10 and S1/Rpn2. Biochem J. 2007 Mar 1;402(2):367-75. In contrast with direct apoptotic stimuli, such as the anti-cancer drug etoposide, leading to caspase-dependent degradation of S1 and S5a, the effect of IEX-1 is independent of proteolytic cleavage of these proteins. Furthermore, the decreasing effect of IEX-1 on S5a and S1 expression is still seen in the presence of cycloheximide, but not in the presence of actinomycin D, and quantitative real-time PCR revealed lower mRNA levels of S5a and S1 in IEX-1-overexpressing cells, suggesting an interference of IEX-1 with the gene transcription of S5a and S1. |
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| 15670574 | Kadohara K, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Acetoxycycloheximide (E-73) rapidly induces apoptosis mediated by the release of cytochrome c via activation of c-Jun N-terminal kinase. Biochem Pharmacol. 2005 Feb 15;69(4):551-60. Epub 2004 Dec 28. Cycloheximide (CHX) is an inhibitor of protein synthesis and commonly used to modulate death receptor-mediated apoptosis or to induce apoptosis in a number of normal and transformed cells. E-73 induced the release of cytochrome c from mitochondria even in the presence of the caspase inhibitor benzyloxycarbonyl-Val--Asp (OMe)-fluoromethyl ketone. |
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| 15561559 | Dewitte-Orr SJ, Zorzitto JR, Sutton LP, Bols NC: Preferential induction of apoptosis in the rainbow trout macrophage cell line, RTS11, by actinomycin D, cycloheximide and double stranded RNA. Fish Shellfish Immunol. 2005 Apr;18(4):279-95. The rainbow trout macrophage cell line RTS11 was found to be considerably more sensitive than rainbow trout fibroblast (RTG-2) and Chinook salmon epithelial (CHSE-214) cell lines to killing by macromolecular synthesis inhibitors, actinomycin D (AMD) and cycloheximide (CHX), a synthetic double stranded RNA (dsRNA), polyinosinic:polycytidylic acid (poly IC), and combinations of poly IC with AMD or CHX. By contrast, z-VAD-fmk almost completely abrogated killing by co-treatments of poly IC and low concentrations of AMD or CHX, suggesting caspase dependence. |
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| 19671668 | Huang SK, White ES, Wettlaufer SH, Grifka H, Hogaboam CM, Thannickal VJ, Horowitz JC, Peters-Golden M: (2) induces fibroblast apoptosis by modulating multiple survival pathways. FASEB J. 2009 Dec;23(12):4317-26. Epub 2009 Aug 11. PGE (2) also potentiated apoptosis elicited by Fas ligand plus cycloheximide. These proapoptotic actions were dependent on signaling through the EP2/EP4 receptors and by downstream activation of both caspases 8 and 9. |
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| 15685617 | Suy S, Mitchell JB, Samuni A, Mueller S, Kasid U: tempo, a small molecule, induces apoptosis in prostate carcinoma cells and suppresses tumor growth in athymic mice. Cancer. 2005 Mar 15;103(6):1302-13. Tempo-induced loss of cell viability was blocked partially or completely after pretreatment of cells with actinomycin-D or cycloheximide, suggesting a de novo macromolecule synthesis-dependent mechanism of cell death. CONCLUSIONS: These data demonstrated that tempo induced apoptosis and activated a caspase-mediated signaling pathway in prostate carcinoma cells. |
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| 15678148 | Figarella K, Rawer M, Uzcategui NL, Kubata BK, Lauber K, Madeo F, Wesselborg S, Duszenko M: induces programmed cell death in Trypanosoma brucei bloodstream form. Cell Death Differ. 2005 Apr;12(4):335-46. The use of caspase inhibitors cannot prevent the cell death, indicating that the process is caspase-independent. |
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| 16427675 | Chen D, Texada DE, Duggan C, Deng Y, Redens TB, Langford MP: Caspase-3 and -7 mediate apoptosis of human Chang's conjunctival cells induced by enterovirus 70. Virology. 2006 Apr 10;347(2):307-22. Epub 2006 Jan 20. EV70-induced apoptosis was inhibited by cycloheximide and methoxysuccinyl---Pro-Val-chloromethylketone (MPCMK), but not actinomycin D and guanidine.HCl (although guanidine.HCl inhibited the apoptosis induced by EV70 infection at 0.5 PFU/cell for 18 h). |
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| 15935204 | Dreiem A, Ring A, Fonnum F: Organic solvent-induced cell death in rat cerebellar granule cells: structure dependence of c10 hydrocarbons and relationship to reactive species formation. Neurotoxicology. 2005 Jun;26(3):321-30. However, there was no internucleosomal DNA fragmentation and no protection by the pan-caspase inhibitor Boc-D-FMK or the protein synthesis inhibitor cycloheximide. |
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| 16777169 | Choudhary SK, Walker RM, Powell DM, Planelles V, Walsh C, Camerini D: CXCR4 tropic human immunodeficiency virus type 1 induces an apoptotic cascade in immature infected thymocytes that resembles thymocyte negative selection. Virology. 2006 Sep 1;352(2):268-84. Epub 2006 Jun 14. Furthermore, treatment of thymocytes with cycloheximide abrogated HIV-1-induced apoptosis, implying a requirement for de novo protein synthesis. |
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| 18231987 | Stanic I, Cetrullo S, Facchini A, Stefanelli C, Borzi RM, Tantini B, Guarnieri C, Caldarera CM, Flamigni F: Effect of the polyamine analogue N1,N11-diethylnorspermine on cell survival and susceptibility to apoptosis of human chondrocytes. J Cell Physiol. 2008 Jul;216(1):153-61. In conclusion, following DENSPM treatment, C-28/I2 chondrocytes are initially sensitized to caspase 9-dependent apoptosis in the presence of TNF and CHX and may eventually undergo a late and mainly caspase-independent cell death in the absence of other stimuli. |
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| 18819247 | Bosio E, Seveso M, Dedja A, Luca G, Calvitti M, Calafiore R, Rigotti P, Busetto R, Ancona E, Cozzi E: protoporpyhrin reduces caspase-3,-7 enzyme activity in neonatal porcine islets, but does not inhibit cell death induced by TNF-alpha. Cell Transplant. 2008;17(6):587-98. Indeed, the inhibition of caspase enzyme activity resulted in decreased PARP-1 cleavage, which may lead to heightened levels of necrosis in treated NPICC cultures, possibly explaining the observed commitment of NPICC to the death pathway. In in vitro assessments of NPICC apoptosis, NPICC showed a high sensitivity to apoptotic stimulation using a combination of TNF-alpha and cycloheximide. |
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| 17635918 | Jang BC, Sung SH, Park JG, Park JW, Bae JH, Shin DH, Park GY, Han SB, Suh SI: hydrochloride specifically inhibits COX-2 by preventing COX-2 N-glycosylation and by increasing COX-2 protein turnover in a proteasome-dependent manner. J Biol Chem. 2007 Sep 21;282(38):27622-32. Epub 2007 Jul 16. Remarkably, GS-HCl-mediated decrease in COX-2 molecular mass was associated with inhibition of COX-2 N-glycosylation during translation, as assessed by the effect of tunicamycin, the protein N-glycosylation inhibitor, or of cycloheximide, the translation inhibitor, on COX-2 modification. |
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| 17245642 | Chen SP, Wu JL, Su YC, Hong JR: Anti-Bcl-2 family members, zfBcl-x (L) and zfMcl-1a, prevent cytochrome c release from cells undergoing betanodavirus-induced secondary necrotic cell death. Apoptosis. 2007 Jun;12(6):1043-60. To identify the mediator (s) of this necrotic process, a protein synthesis inhibitor (cycloheximide; CHX; 0.33 microg/ml) was used to block cytochrome c release as well as PS exposure and mitochondrial membrane permeability transition pore (MMP) loss. |
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| 18417179 | Asare N, Landvik NE, Lagadic-Gossmann D, Rissel M, Tekpli X, Ask K, Lag M, Holme JA: 1-Nitropyrene (1-NP) induces apoptosis and apparently a non-apoptotic programmed cell death (paraptosis) in Hepa1c1c7 cells. Toxicol Appl Pharmacol. 2008 Jul 15;230(2):175-86. Epub 2008 Feb 29. In contrast, cycloheximide markedly reduced both the number of apoptotic and PI-positive cells as well as the cytoplasmic vacuolization, suggesting that 1-NP induced paraptotic cell death. |
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| 15657078 | Depuydt B, van Loo G, Vandenabeele P, Declercq W: Induction of apoptosis by TNF receptor 2 in a T-cell hybridoma is FADD dependent and blocked by caspase-8 inhibitors. J Cell Sci. 2005 Feb 1;118(Pt 3):497-504. Epub 2005 Jan 18. We show here that TNFR2-mediated apoptosis in PVC60 cells can be blocked by the broad-spectrum caspase inhibitor zVAD-fmk, the caspase-8 inhibitor zIETD-fmk and by CrmA, a viral inhibitor of caspase-1 and caspase-8. |
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| 16432762 | Xia Y, Novak R, Lewis J, Duckett CS, Phillips AC: Xaf1 can cooperate with TNFalpha in the induction of apoptosis, independently of interaction with XIAP. Mol Cell Biochem. 2006 Jun;286(1-2):67-76. Epub 2006 Jan 24. Xaf1 expression promotes cytochrome c release that cannot be blocked by inhibition of caspase activity. |
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| 15626483 | Fischer SF, Rehm M, Bauer A, Hofling F, Kirschnek S, Rutz M, Bauer S, Wagner H, Hacker G: Toll-like receptor 9 signaling can sensitize fibroblasts for apoptosis. Immunol Lett. 2005 Feb 15;97(1):115-22. Analysis of the apoptotic signaling showed that the mitochondrial pathway of apoptosis was triggered by TLR9, as mitochondrial Bax was activated upstream of caspase-cleavage. CpG-DNA-induced apoptosis was reduced by cycloheximide suggesting that de novo protein synthesis was required. |
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| 16158421 | Jin HO, Park IC, An S, Lee HC, Woo SH, Hong YJ, Lee SJ, Park MJ, Yoo DH, Rhee CH, Hong SI: Up-regulation of Bak and Bim via JNK downstream pathway in the response to in human glioblastoma cells. J Cell Physiol. 2006 Feb;206(2):477-86. In addition, de novo protein synthesis was required for the initiation of apoptosis in that the protein synthesis inhibitor, cycloheximide (CHX), inhibited NO-induced apoptotic cell death as well as up-regulation of Bak and Bim. |
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| 15754039 | Lai MD, Lin WC, Sun YM, Chang FL: Phosphorylated and hypoacetylated mutant p53 enhances cisplatin-induced apoptosis through caspase-9 pathway in the absence of transcriptional activation or translation. Int J Mol Med. 2005 Apr;15(4):725-34. Both transcriptional inhibitor actinomycin D and translational inhibitor cycloheximide did not inhibit apoptosis. |
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| 15832948 | Concannon CG, FitzGerald U, Holmberg CI, Szegezdi E, Sistonen L, Samali A: CD95-mediated alteration in Hsp70 levels is dependent on protein stabilization. Cell Stress Chaperones. 2005 Spring;10(1):59-65. Engagement of death receptors induces caspase activation and apoptosis. Inhibition of translation and de novo protein synthesis by cycloheximide resulted in Hsp70 protein levels diminishing over time in control cells, whereas its level remained constant during CD95 signaling. |
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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. It has been reported that NS5A is cleaved into a few fragments by a caspase (s) or caspase-like enzyme (s) under certain conditions. |
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| 16814338 | Chen YC, Chow JM, Lin CW, Wu CY, Shen SC: Baicalein inhibition of oxidative-stress-induced apoptosis via modulation of ERKs activation and induction of HO-1 gene expression in rat glioma cells C6. Toxicol Appl Pharmacol. 2006 Oct 15;216(2):263-73. Epub 2006 May 19. In the absence of H (2) O (2), BE induces ERKs protein phosphorylation, and HO-1 protein expression induced by BE was blocked by the addition of cycloheximide, actinomycin D, and the ERK inhibitor PD98059. |
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| 16910777 | Dasgupta J, Subbaram S, Connor KM, Rodriguez AM, Tirosh O, Beckman JS, Jourd'Heuil D, Melendez JA: Manganese superoxide dismutase protects from TNF-alpha-induced apoptosis by increasing the steady-state production of H2O2. Antioxid Redox Signal. 2006 Jul-Aug;8(7-8):1295-305. The increase in H (2) O (2) was associated with decreased sensitivity to TNF-alpha-mediated apoptosis, as measured by monitoring the loss of mitochondrial membrane potential (MMP), caspase activation, poly-ADP polymerase (PARP) cleavage, and accumulation of hypodiploid DNA content. |
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| 16215688 | Singh S, Khar A: Differential gene expression during apoptosis induced by a serum factor: role of mitochondrial F0-F1 ATP synthase complex. Apoptosis. 2005 Dec;10(6):1469-82. Caspase 1 and caspase 3 activity and the loss of mitochondrial membrane potential were also inhibited by oligomycin during apoptosis in these cells, suggesting that the oligomycin induced inhibition of apoptosis could be due to inhibition of caspase activity and inhibition of mitochondrial depolarization. |
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| 15977640 | Nowoslawski L, Klocke BJ, Roth KA: Molecular regulation of acute -induced neuron apoptosis. J Neuropathol Exp Neurol. 2005 Jun;64(6):490-7. This effect was recapitulated in vitro and required new gene transcription, protein translation, Bax expression, and caspase activation. |
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| 19097065 | Stanic' I, Facchini A, Borzi RM, Stefanelli C, Flamigni F: The polyamine analogue N1,N11-diethylnorspermine can induce chondrocyte apoptosis independently of its ability to alter metabolism and levels of natural polyamines. J Cell Physiol. 2009 Apr;219(1):109-16. However, the simultaneous addition of DENSPM and CHX rapidly increased caspase activity in C-28/I2 cells in the absence of SSAT and SMO induction or significant reduction of polyamine levels. |
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| 18056701 | Fei Q, McCormack AL, Di Monte DA, Ethell DW: Paraquat neurotoxicity is mediated by a Bak-dependent mechanism. . J Biol Chem. 2008 Feb 8;283(6):3357-64. Epub 2007 Dec 4. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. |
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| 19137541 | Rizzi F, Caccamo AE, Belloni L, Bettuzzi S: Clusterin is a short half-life, poly-ubiquitinated protein, which controls the fate of prostate cancer cells. J Cell Physiol. 2009 May;219(2):314-23. Inhibition of protein synthesis by cycloheximide showed that CLU half-life is less than 2 h. Proteasome inhibition by MG132 caused stabilization and accumulation of all CLU protein products, including the nuclear form of CLU (nCLU), and committing cells to caspase-dependent death. |
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| 19647171 | Chen DL, Zhou D, Chu W, Herrbrich PE, Jones LA, Rothfuss JM, Engle JT, Geraci M, Welch MJ, Mach RH: Comparison of radiolabeled isatin analogs for imaging apoptosis with positron emission tomography. Nucl Med Biol. 2009 Aug;36(6):651-8. INTRODUCTION: Caspase-3 is one of the executioner caspases activated as a result of apoptosis. We compared the ability of two novel radiolabeled isatins, [18F] WC-IV-3 and [11C] WC-98, to detect caspase-3 activation in a rat model of cycloheximide-induced liver injury. |
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| 15647476 | Verma P, Chierzi S, Codd AM, Campbell DS, Meyer RL, Holt CE, Fawcett JW: Axonal protein synthesis and degradation are necessary for efficient growth cone regeneration. J Neurosci. 2005 Jan 12;25(2):331-42. Collectively, these findings suggest that local protein synthesis and degradation, controlled by various TOR-, p38 MAPK-, and caspase-dependent pathways, underlie growth cone initiation after axotomy. Application of protein synthesis inhibitors (cycloheximide and anisomycin) to cut axons, including axons whose cell bodies were removed, or proteasome inhibitors (lactacystin and N-acetyl-Nor---Al) all result in a reduction in the proportion of transected axons able to reform growth cones. |
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| 15541727 | McNeish IA, Lopes R, Bell SJ, McKay TR, Fernandez M, Lockley M, Wheatley SP, Lemoine NR: Survivin interacts with Smac/DIABLO in ovarian carcinoma cells but is redundant in Smac-mediated apoptosis. Exp Cell Res. 2005 Jan 1;302(1):69-82. We sought to stimulate the mitochondrial pathway of apoptosis by constructing a recombinant adenovirus encoding mature, processed Smac/DIABLO (Ad CMV tSmac), the second mitochondrial activator of caspases. This down-regulation does not result from transcriptional changes, as determined by quantitative real-time PCR, but cycloheximide treatment indicates that survivin half-life is reduced from 6 to 2 h, which is secondary to ubiquitination and proteasomal degradation. |
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