| Name | caspase 8 |
|---|---|
| Synonyms | Apoptotic cysteine protease; Apoptotic protease Mch 5; CAP 4; CAP4; CASP 8; CASP8; CASP8 protein; Caspase 8… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. |
83(1,1,1,3) | Details |
| 18485876 | Wang L, Du F, Wang X: TNF-alpha induces two distinct caspase-8 activation pathways. Cell. 2008 May 16;133(4):693-703. Cycloheximide promotes caspase-8 activation by eliminating endogenous caspase-8 inhibitor, c-FLIP, while Smac mimetic does so by triggering autodegradation of cIAP1 and cIAP2 (cIAP1/2), leading to the release of receptor interacting protein kinase (RIPK1) from the activated TNF receptor complex to form a caspase-8-activating complex consisting of RIPK1, FADD, and caspase-8. |
64(0,2,2,4) | 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. By using a large panel of genetically modified murine embryonic fibroblasts, we show here that, in response to tumor necrosis factor (TNF), caspase-8 cleaves and activates caspase-9 in an apoptosome-independent manner. |
1(0,0,0,1) | Details |
| 19453217 | Vinken M, Decrock E, De Vuyst E, Leybaert L, Vanhaecke T, Rogiers V: Biochemical characterisation of an in vitro model of hepatocellular apoptotic cell death. Altern Lab Anim. 2009 Apr;37(2):209-18. This study was set up to critically evaluate a commonly-used in vitro model of hepatocellular apoptotic cell death, in which freshly isolated hepatocytes, cultured in a monolayer configuration, are exposed to a combination of Fas ligand and cycloheximide for six hours. The initiation of apoptosis was evidenced by the activation of caspase 8 and caspase 9, and increased Annexin-V reactivity. |
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. Caspase-8, -9 and -3 as well as the proapoptotic factor Bax and cytochrome c were activated. |
1(0,0,0,1) | Details |
| 19228791 | Garcia S, Mera A, Gomez-Reino JJ, Conde C: Poly (ADP- polymerase suppression protects rheumatoid synovial fibroblasts from Fas-induced apoptosis. Rheumatology. 2009 May;48(5):483-9. Epub 2009 Feb 19. Fas-associated via death domain (FADD), pro-caspase-8, Fas, c-Fas-associated death domain-like IL-1b-converting enzyme-inhibitory protein (FLIP) expression, and AKT and GSK phosphorylation were analysed by western blot. |
1(0,0,0,1) | Details |
| 16546965 | Lane D, Cote M, Grondin R, Couture MC, Piche A: Acquired resistance to TRAIL-induced apoptosis in human ovarian cancer cells is conferred by increased turnover of mature caspase-3. Mol Cancer Ther. 2006 Mar;5(3):509-21. Cleavage of caspase-8 and caspase-3 occurred in both TRAIL-resistant and TRAIL-sensitive cells. Pretreatment with cycloheximide showed that active caspase-3 fragments have a high turnover rate in OVCAR3 R350 cells. |
1(0,0,0,1) | Details |
| 16508982 | D'Osualdo A, Ferlito F, Prigione I, Obici L, Meini A, Zulian F, Pontillo A, Corona F, Barcellona R, Di Duca M, Santamaria G, Traverso F, Picco P, Baldi M, Plebani A, Ravazzolo R, Ceccherini I, Martini A, Gattorno M: Neutrophils from patients with TNFRSF1A mutations display resistance to tumor necrosis factor-induced apoptosis: pathogenetic and clinical implications. Arthritis Rheum. 2006 Mar;54(3):998-1008. Neutrophils were isolated from heparinized blood by dextran sedimentation and incubated with and without cycloheximide (CHX) and TNFalpha. Cell apoptosis was assessed by human annexin V binding, and caspase 8 activation was assessed by flow cytometry. |
1(0,0,0,1) | 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. Cycloheximide completely attenuated 3-NF-induced cell death. Activation of caspase-8, -9, and -3 were observed. |
1(0,0,0,1) | Details |
| 16569452 | Sakurai T, Itoh K, Higashitsuji H, Nonoguchi K, Liu Y, Watanabe H, Nakano T, Fukumoto M, Chiba T, Fujita J: Cirp protects against tumor necrosis factor-alpha-induced apoptosis via activation of extracellular signal-regulated kinase. Biochim Biophys Acta. 2006 Mar;1763(3):290-5. Epub 2006 Mar 20. In BALB/3T3 cells treated with tumor necrosis factor (TNF)-alpha and cycloheximide, the down-shift in temperature from 37 degrees C to 32 degrees C increased the expression of Cirp and suppressed the apoptosis. Activation of caspase-8 was suppressed, and the level of phosphorylated extracellular signal-regulated kinase (ERK) was increased. |
1(0,0,0,1) | Details |
| 19952118 | Ballot C, Kluza J, Martoriati A, Nyman U, Formstecher P, Joseph B, Bailly C, Marchetti P: Essential role of mitochondria in apoptosis of cancer cells induced by the marine alkaloid Lamellarin D. Mol Cancer Ther. 2009 Dec;8(12):3307-17. Epub . However, lamellarin D killed efficiently mutated p53 or p53 null cancer cells, and sensitivity to lamellarin D was abrogated neither by cycloheximide nor in enucleated cells. Moreover, leukemia cells deficient in caspase-8 or Fas-associated protein with death domain underwent apoptosis through the typical mitochondrial apoptotic cascade, indicating that cell death induced by lamellarin D was independent of the extrinsic apoptotic pathway. |
1(0,0,0,1) | Details |
| 16581346 | Tamai M, Kawakami A, Tanaka F, Miyashita T, Nakamura H, Iwanaga N, Izumi Y, Arima K, Aratake K, Huang M, Kamachi M, Ida H, Origuchi T, Eguchi K: Significant inhibition of TRAIL-mediated fibroblast-like synovial cell apoptosis by IFN-gamma through JAK/STAT pathway by translational regulation. J Lab Clin Med. 2006 Apr;147(4):182-90. As disruption of mitochondrial transmembrane potential (DeltaPsim), --His-Asp ase (IETD ase) activity, and the appearance of hypodiploid DNA + cells were markedly suppressed in IFN-gamma-treated FLS in response to TRAIL, IFN-gamma-induced suppression was supposed to achieve at upstream of caspase-8. Janus kinase (JAK)-induced phosphorylation of STAT1/3/6, which acts at translational regulation, seemed to be crucial because chemical inhibition of JAK as well as cycloheximide (CHX) abolished both the phosphorylation of STAT1/3/6 and the IFN-gamma-induced inhibitory effect. |
1(0,0,0,1) | Details |
| 15809706 | Chaturvedi R, Srivastava RK, Hisatsune A, Shankar S, Lillehoj EP, Kim KC: Augmentation of Fas ligand-induced apoptosis by MUC1 mucin. . Int J Oncol. 2005 May;26(5):1169-76. Following treatment with 50 nM FasL, apoptosis, caspase-8 activity, and cell surface Fas receptor were measured by cytosolic nucleosome ELISA, colorimetric enzyme assay, and immunofluorescence analysis, respectively. Our results showed that (i) treatment with FasL increased caspase-8 activity (maximum at 4 h) and apoptosis (maximum at 8 h) in both MUC1 (+) and MUC1 (-) cells, (ii) FasL-induced caspase-8 activity and apoptosis were significantly greater in MUC1 (+) cells compared with MUC1 (-) cells, (iii) FasL treatment increased cell surface expression of Fas receptor in MUC1 (+) cells to a greater extent compared with MUC1 (-) cells, (iv) increased cell surface expression of Fas in MUC1 (+) cells was not blocked by an inhibitor of protein synthesis (cycloheximide), but was completely abrogated by brefeldin A, an inhibitor of post-translational protein trafficking to the cell surface, and (v) brefeldin A inhibited the increased sensitivity of MUC1 (+) cells to FasL-induced apoptosis. |
1(0,0,0,1) | 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. Caspase-8 on average was activated 45-600 min after TRAIL/cycloheximide addition. |
85(1,1,1,5) | 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. |
82(1,1,1,2) | Details |
| 19777442 | Pucci B, Indelicato M, Paradisi V, Reali V, Pellegrini L, Aventaggiato M, Karpinich NO, Fini M, Russo MA, Farber JL, Tafani M: ERK-1 MAP kinase prevents TNF-induced apoptosis through bad phosphorylation and inhibition of Bax translocation in HeLa Cells. J Cell Biochem. 2009 Dec 1;108(5):1166-74. The caspase-8 inhibitor IETD-FMK and the mitochondrial membrane permeabilization inhibitor bongkrekic acid (BK), partially prevented cell death by TNF + CHX. |
1(0,0,0,1) | Details |
| 15608694 | Inoue S, MacFarlane M, Harper N, Wheat LM, Dyer MJ, Cohen GM: Histone deacetylase inhibitors potentiate TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in lymphoid malignancies. Cell Death Differ. 2004 Dec;11 Suppl 2:S193-206. HDAC inhibitors sensitized resistant cells to TRAIL-induced apoptosis by facilitating formation of an active death-inducing signalling complex (DISC), leading to the rapid activation of caspase-8. |
1(0,0,0,1) | Details |
| 15924153 | Jeon YK, Kim H, Park SO, Choi HY, Kim YA, Park SS, Kim JE, Kim YN, Kim CW: Resistance to Fas-mediated apoptosis is restored by cycloheximide through the downregulation of cellular FLIPL in NK/T-cell lymphoma. Lab Invest. 2005 Jul;85(7):874-84. Interestingly, cotreatment of Hank-1 with cycloheximide, a protein synthesis inhibitor, markedly sensitized cells to Fas-mediated apoptosis along with caspase 8 activation and c-FLIP (L) (cellular FLICE inhibitory protein long form) downregulation. |
82(1,1,1,2) | Details |
| 16888780 | Wieckowski E, Atarashi Y, Stanson J, Sato TA, Whiteside TL: FAP-1-mediated activation of NF-kappaB induces resistance of head and neck cancer to Fas-induced apoptosis. J Cell Biochem. 2007 Jan 1;100(1):16-28. In the presence of cycloheximide, the selected SCCHN sublines become susceptible to CH-11 Ab, and showed cleavage of caspase-8, suggesting that apoptosis resistance was mediated by an inhibitory protein (s) acting upstream of caspase-8. |
81(1,1,1,1) | Details |
| 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. |
1(0,0,0,1) | 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. DFMO decreased caspase-8 activity and procaspase-8 content, an apical caspase essential for TNF-induced apoptosis. |
1(0,0,0,1) | Details |
| 15614529 | Brooks AD, Sayers TJ: Reduction of the antiapoptotic protein cFLIP enhances the susceptibility of human renal cancer cells to TRAIL apoptosis. Cancer Immunol Immunother. 2005 May;54(5):499-505. Epub 2004 Dec 22. In contrast to a previous study, a rapid and dramatic decrease in levels of cellular FLICE (Fas-associated death domain-like IL-1beta-converting enzyme) inhibitory protein (cFLIP) following cycloheximide treatment was observed in all RCCs studied. |
62(0,2,2,2) | 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 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. |
33(0,1,1,3) | 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. LPS-induced apoptosis in TBBEC was hallmarked by the activation of caspase 3, caspase 6, and caspase 8 after the stimulation of LPS, followed by poly (ADP- polymerase cleavage and lactate dehydrogenase release. |
1(0,0,0,1) | Details |
| 17492827 | Chung MJ, Liu T, Ullenbruch M, Phan SH: Antiapoptotic effect of found in inflammatory zone (FIZZ) 1 on mouse lung fibroblasts. J Pathol. 2007 Jun;212(2):180-7. FIZZ1 treatment also inhibited the apoptotic agent-induced activities of caspase-3 and caspase-8. |
1(0,0,0,1) | Details |
| 16158257 | Martinet W, De Meyer GR, Herman AG, Kockx MM: Amino acid deprivation induces both apoptosis and autophagy in murine C2C12 muscle cells. Biotechnol Lett. 2005 Aug;27(16):1157-63. Starvation eliminated multiple pro-apoptotic proteins, but upregulated caspase-8, and rendered starved C2C12 cells much more susceptible to TNF-alpha/cycloheximide-induced apoptosis than non-starved cells. |
6(0,0,1,1) | Details |
| 15863130 | Hougardy BM, van der Zee AG, van den Heuvel FA, Timmer T, de Vries EG, de Jong S: Sensitivity to Fas-mediated apoptosis in high-risk HPV-positive human cervical cancer cells: relationship with Fas, caspase-8, and Bid. Gynecol Oncol. 2005 May;97(2):353-64. |
6(0,0,0,6) | 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. TRAIL and Fas receptor death-inducing signaling complex (DISCs) formation are similar and involve ligand-dependent recruitment of FADD and caspase-8. |
6(0,0,0,6) | Details |
| 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. |
0(0,0,0,0) | Details |
| 15639338 | Hofmanova J, Vaculova A, Kozubik A: Polyunsaturated fatty acids sensitize human colon adenocarcinoma HT-29 cells to death receptor-mediated apoptosis. Cancer Lett. 2005 Jan 31;218(1):33-41. The higher amount of floating cells, subG0/G1 population and apoptotic cells detected in pre-treated cells was potentiated by cycloheximide. |
0(0,0,0,0) | Details |
| 15928597 | Pajak B, Orzechowski A: [FLIP--an enemy which might lose the battle against the specific inhibitors of translation]. Postepy Hig Med Dosw. 2005;59:140-9. In in vitro studies, such activity is exerted by cycloheximide or bisindolylmaleimide, either of which, at a low, non-toxic concentration, totally abrogates FLIP protein expression or, in turn, sensitizes cancer cells to death ligands. |
0(0,0,0,0) | Details |
| 16478887 | Mitchell JW, Baik N, Castellino FJ, Miles LA: Plasminogen inhibits TNFalpha-induced apoptosis in monocytes. . Blood. 2006 Jun 1;107(11):4383-90. Epub 2006 Feb 14. Plasminogen treatment also markedly reduced internucleosomal DNA fragmentation and reduced levels of active caspase 3, caspase 8, and caspase 9 induced by TNFalpha or by cycloheximide. |
31(0,1,1,1) | 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. |
8(0,0,0,8) | Details |
| 19115040 | Albrecht EA, Sarma JV, Ward PA: Activation by C5a of endothelial cell caspase 8 and cFLIP. Inflamm Res. 2009 Jan;58(1):30-7. |
5(0,0,0,5) | Details |
| 18289527 | Ogura H, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Ectodomain shedding of TNF receptor 1 induced by protein synthesis inhibitors regulates TNF-alpha-mediated activation of NF-kappaB and caspase-8. Exp Cell Res. 2008 Apr 1;314(6):1406-14. Epub 2008 Feb 6. It has been established that the protein synthesis inhibitor cycloheximide (CHX) sensitizes many types of cells to tumor necrosis factor (TNF)-alpha-induced apoptosis, mainly due to its ability to block de novo synthesis of cellular FLICE-inhibitory protein (c-FLIP). |
4(0,0,0,4) | Details |
| 20005201 | Sengupta R, Billiar TR, Kagan VE, Stoyanovsky DA: and thioredoxin type 1 modulate the activity of caspase 8 in HepG2 cells. Biochem Biophys Res Commun. 2010 Jan 1;391(1):1127-30. Epub 2009 Dec 11. |
3(0,0,0,3) | Details |
| 16036110 | Zhang L, Zhu H, Teraishi F, Davis JJ, Guo W, Fan Z, Fang B: Accelerated degradation of caspase-8 protein correlates with TRAIL resistance in a DLD1 human colon cancer cell line. Neoplasia. 2005 Jun;7(6):594-602. |
6(0,0,0,6) | Details |
| 19214542 | Capper D, Gaiser T, Hartmann C, Habel A, Mueller W, Herold-Mende C, von Deimling A, Siegelin MD: Stem-cell-like glioma cells are resistant to TRAIL/Apo2L and exhibit down-regulation of caspase-8 by promoter methylation. Acta Neuropathol. 2009 Apr;117(4):445-56. Epub 2009 Feb 12. |
3(0,0,0,3) | Details |
| 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. |
3(0,0,0,3) | Details |
| 18603835 | Matsuda F, Inoue N, Goto Y, Maeda A, Cheng Y, Sakamaki K, Manabe N: cFLIP regulates death receptor-mediated apoptosis in an ovarian granulosa cell line by inhibiting procaspase-8 cleavage. J Reprod Dev. 2008 Oct;54(5):314-20. Epub 2008 Jul 7. Cellular FLICE-like inhibitory protein (cFLIP), a homologue of procaspase-8 (also called FLICE), is an intracellular anti-apoptotic protein. |
2(0,0,0,2) | Details |
| 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. Furthermore, a caspase-8 inhibitor completely abolished caspase-3 activation, Bid cleavage, and subsequent DNA fragmentation by Compound K. 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. |
2(0,0,0,2) | Details |
| 18078929 | Brumatti G, Yon M, Castro FA, Bueno-da-Silva AE, Jacysyn JF, Brunner T, Amarante-Mendes GP: Conversion of CD95 (Fas) Type II into Type I signaling by sub-lethal doses of cycloheximide. Exp Cell Res. 2008 Feb 1;314(3):554-63. Epub 2007 Nov 17. One involves a direct activation of caspase-3 by large amounts of caspase-8 generated at the DISC (Type I cells). |
2(0,0,0,2) | Details |
| 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. Here we show that cytosolic 2-cysPrx suppresses the TNF-alpha-induced apoptosis of human cervical cancer cells in a caspase-8-dependent manner. 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. |
2(0,0,0,2) | Details |
| 16325265 | Sylte MJ, Kuckleburg CJ, Leite FP, Inzana TJ, Czuprynski CJ: Tumor necrosis factor-alpha enhances Haemophilus somnus lipooligosaccharide-induced apoptosis of bovine endothelial cells. Vet Immunol Immunopathol. 2006 Apr 15;110(3-4):303-9. Epub 2005 Dec 1. Haemophilus somnus lipooligosaccharide (LOS)-induced apoptosis of bovine pulmonary artery endothelial cells has been shown previously to be dependent on caspase-8 activation. However, blocking de novo protein synthesis by addition of cycloheximide significantly enhanced apoptosis of bovine endothelial cells by TNF-alpha, LOS or TNF-alpha and LOS in combination. |
2(0,0,0,2) | Details |
| 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. |
2(0,0,0,2) | 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. The activation of caspase-2, caspase-8, caspase-9 and effector caspase-3 was investigated by caspase assay plates and Western blots. 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. |
1(0,0,0,1) | Details |
| 17376892 | Troeger A, Schmitz I, Siepermann M, Glouchkova L, Gerdemann U, Janka-Schaub GE, Schulze-Osthoff K, Dilloo D: Up-regulation of c-FLIPS+R upon CD40 stimulation is associated with inhibition of CD95-induced apoptosis in primary precursor B-ALL. Blood. 2007 Jul 1;110(1):384-7. Epub 2007 Mar 21. We show that this apoptosis resistance involves the selective up-regulation of the short isoforms of the caspase-8 inhibitor c-FLIP acting directly at the CD95 receptor level. Treatment with cycloheximide during CD40 activation prevents up-regulation of those c-FLIP isoforms and sensitizes ALL cells toward CD95-mediated apoptosis. |
1(0,0,0,1) | Details |
| 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. In Jurkat T cells transfected with the caspase-8 modulator FLIP (L), E-73 still induced activation of procaspase-3 and subsequent apoptosis, suggesting that the caspase-8 activity is dispensable for apoptosis. |
1(0,0,0,1) | 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. Specific caspase inhibitors revealed that caspase-3, caspase-6, caspase-8, and caspase-9 were primarily involved in apoptosis induction. |
1(0,0,0,1) | Details |
| 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. The proapototic proteins Bid and caspase-8, however, were higher expressed in GLC4-Adr. Both lines were resistant to anti-Fas antibody, but plus the protein synthesis inhibitor cycloheximide anti-Fas antibody induced 40% apoptosis in GLC4-Adr. |
2(0,0,0,2) | Details |
| 19372210 | Li TW, Zhang Q, Oh P, Xia M, Chen H, Bemanian S, Lastra N, Circ M, Moyer MP, Mato JM, Aw TY, Lu SC: and inhibit cellular FLICE inhibitory protein expression and induce apoptosis in colon cancer cells. Mol Pharmacol. 2009 Jul;76(1):192-200. Epub 2009 Apr 16. Inhibiting caspase 8 activity or overexpression of cFLIP protected against apoptosis, whereas supplementing with polyamines did not. |
1(0,0,0,1) | Details |