| Name | Fas Ligand |
|---|---|
| Synonyms | APT1LG1; FAS; APTL; Apoptosis (APO 1) antigen ligand 1; Apoptosis antigen ligand; Apoptosis antigen ligand 1; CD178; CD178 antigen… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16595663 | Castellano R, Vire B, Pion M, Quivy V, Olive D, Hirsch I, Van Lint C, Collette Y: Active transcription of the human FASL/CD95L/TNFSF6 promoter region in T lymphocytes involves chromatin remodeling: role of DNA methylation and protein acetylation suggest distinct mechanisms of transcriptional repression. J Biol Chem. 2006 May 26;281(21):14719-28. Epub 2006 Apr 4. HSS1 chromatin remodeling preceded detectable TNFSF6 mRNA accumulation and was blocked by cycloheximide that also prevented TNFSF6 transcription. |
88(1,1,1,8) | Details |
| 19960225 | Vinken M, Decrock E, De Vuyst E, De Bock M, Vandenbroucke RE, De Geest BG, Demeester J, Sanders NN, Vanhaecke T, Leybaert L, Rogiers V: Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death. Cell Mol Life Sci. 2010 Mar;67(6):907-18. Epub 2009 Dec 4. Primary hepatocyte cultures were exposed to Fas ligand and cycloheximide, and modifications in connexin32 expression and localization, and gap junction functionality were studied. |
6(0,0,1,1) | 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. |
6(0,0,1,1) | Details |
| 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. |
6(0,0,0,6) | Details |
| 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. |
6(0,0,1,1) | Details |
| 15802531 | Baumann S, Dostert A, Novac N, Bauer A, Schmid W, Fas SC, Krueger A, Heinzel T, Kirchhoff S, Schutz G, Krammer PH: Glucocorticoids inhibit activation-induced cell death (AICD) via direct DNA-dependent repression of the CD95 ligand gene by a glucocorticoid receptor dimer. Blood. 2005 Jul 15;106(2):617-25. Epub 2005 Mar 31. |
3(0,0,0,3) | Details |
| 18252892 | McKenzie MD, Carrington EM, Kaufmann T, Strasser A, Huang DC, Kay TW, Allison J, Thomas HE: Proapoptotic BH3-only protein Bid is essential for death receptor-induced apoptosis of pancreatic beta-cells. Diabetes. 2008 May;57(5):1284-92. Epub 2008 Feb 5. RESEARCH DESIGN AND METHODS: We isolated islets from mice lacking Bid, Bax, or Bak and those overexpressing Bcl-2 and exposed them to Fas ligand, tumor necrosis factor (TNF)-alpha, and proinflammatory cytokines or cytotoxic stimuli that activate the mitochondrial apoptotic pathway (staurosporine, etoposide, gamma-radiation, tunicamycin, and thapsigargin). Bid-deficient islets were also resistant to apoptosis induced by TNF-alpha plus cycloheximide and were partially resistant to proinflammatory cytokine-induced death. |
2(0,0,0,2) | Details |
| 15611255 | Cousens LP, Goulette FA, Darnowski JW: JAK-mediated signaling inhibits Fas ligand-induced apoptosis independent of de novo protein synthesis. J Immunol. 2005 Jan 1;174(1):320-7. Surprisingly, these antiapoptotic effects of IFN-alpha-2a were independent of de novo protein synthesis, because they occurred in both the absence and the presence of cycloheximide. |
2(0,0,0,2) | Details |
| 15749881 | Monari C, Pericolini E, Bistoni G, Casadevall A, Kozel TR, Vecchiarelli A: Cryptococcus neoformans capsular glucuronoxylomannan induces expression of fas ligand in macrophages. J Immunol. 2005 Mar 15;174(6):3461-8. |
2(0,0,0,2) | 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. 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. |
2(0,0,0,2) | Details |
| 15653751 | Bosque A, Pardo J, Martinez-Lorenzo MJ, Iturralde M, Marzo I, Pineiro A, Alava MA, Naval J, Anel A: Down-regulation of normal human T cell blast activation: roles of APO2L/TRAIL, FasL, and c- FLIP, Bim, or Bcl-x isoform expression. J Leukoc Biol. 2005 Apr;77(4):568-78. Epub 2005 Jan 14. A systematic study was undertaken to characterize the role of APO 2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (APO2L/TRAIL) and Fas ligand (FasL) together with the expression of several anti- or proapoptotic proteins in the down-regulation of normal human T cell responses. Cell death was only observed in the presence of cycloheximide or after a pulse through CD3 or CD59, correlating with a net reduction in cellular Fas-associated death domain-like IL-1beta-converting enzyme-inhibitory protein long (c-FLIPL) and c-FLIPS expression. |
1(0,0,0,1) | Details |
| 17545621 | Ivanov VN, Zhou H, Hei TK: Sequential treatment by ionizing radiation and arsenite dramatically accelerates TRAIL-mediated apoptosis of human melanoma cells. Cancer Res. 2007 Jun 1;67(11):5397-407. We show in the present study that gamma-irradiation, as well as alpha-particle exposure, dramatically increases the susceptibility of melanoma cells to recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis via up-regulation of surface TRAIL-receptor 1/receptor 2 (DR4/DR5) levels and to Fas ligand-mediated apoptosis via up-regulation of surface Fas levels. |
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. The selected resistant cells were cross-resistant to Fas ligand but remained sensitive to drug-induced apoptosis. Pretreatment with cycloheximide showed that active caspase-3 fragments have a high turnover rate in OVCAR3 R350 cells. |
1(0,0,0,1) | 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. In contrast to Fas ligand stimulation, the general caspase inhibitor barely prevented the mitochondrial release of these pro-apoptotic proteins in Ac-CHX-treated cells, suggesting that caspase-8 activity is dispensable for triggering the mitochondrial pathway in Ac-CHX-induced apoptosis. |
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. The membrane receptor Fas (Apo-1/CD95) is an important initiator of programmed cell death induced by anti-Fas antibody or Fas ligand. 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 |
| 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. OBJECTIVE: Binding of Fas ligand or agonistic anti-Fas antibody to the death receptor Fas can activate a caspase-cascade resulting in apoptosis. |
1(0,0,0,1) | Details |
| 17523868 | Morton ER, Blaho JA: Herpes simplex virus blocks Fas-mediated apoptosis independent of viral activation of NF-kappaB in human epithelial HEp-2 cells. J Interferon Cytokine Res. 2007 May;27(5):365-76. We found the following: (1) Treatment of HEp-2 cells with anti-Fas antibody or Fas ligand (FasL) alone did not induce apoptosis. (2) In addition, these inducers did not activate NF-kappaB in these cells. (3) The addition of cycloheximide (CHX) during these treatments caused a dramatic increase in programmed cell death. (4) HEp-2 cells infected with HSV for 6 h prior to anti-Fas plus CHX treatment were nonapoptotic, and (5) these cells possessed nuclear NFkappaB. (6) HSV blocked anti-Fas or FasL plus CHX-induced apoptosis in HEp-2 cells that stably expressed a dominant-negative form of IkappaBalpha. |
0(0,0,0,0) | Details |