| Name | CD95 |
|---|---|
| Synonyms | ALPS1A; APT1; FAS; APO 1; APO 1 cell surface antigen; APO1; Apo 1 Fas; Apo 1 antigen… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. Treatment with cycloheximide during CD40 activation prevents up-regulation of those c-FLIP isoforms and sensitizes ALL cells toward CD95-mediated apoptosis. |
86(1,1,1,6) | Details |
| 19553664 | Sommerfeld A, Reinehr R, Haussinger D: Bile acid-induced epidermal growth factor receptor activation in quiescent rat hepatic stellate cells can trigger both proliferation and apoptosis. J Biol Chem. 2009 Aug 14;284(33):22173-83. Epub 2009 Jun 24. When, however, a JNK signal was induced by coadministration of cycloheximide or peroxide (H2O2), activated EGFR associated with CD95 and triggered EGFR-mediated CD95- phosphorylation and subsequent formation of the death-inducing signaling complex. |
81(1,1,1,1) | 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. |
65(0,2,2,5) | Details |
| 19751723 | Lajmanovich A, Ribeyron JB, Florin A, Fournier A, Pasquier MA, Duley S, Chauvet M, Plumas J, Bonnefoix T, Gressin R, Leroux D, Callanan MB: Identification, characterisation and regulation by CD40 activation of novel CD95 splice variants in CD95-apoptosis-resistant, human, B-cell non-Hodgkin's lymphoma. Exp Cell Res. 2009 Nov 15;315(19):3281-93. Epub 2009 Sep 12. This, in conjunction with treatment by the protein synthesis inhibitor, cycloheximide, could sensitise a subset of B-NHLr to CD95 apoptosis. |
37(0,1,1,7) | Details |
| 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. 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. |
36(0,1,1,6) | Details |
| 18281499 | Herrmann T, Grosse-Hovest L, Otz T, Krammer PH, Rammensee HG, Jung G: Construction of optimized bispecific antibodies for selective activation of the death receptor CD95. Cancer Res. 2008 Feb 15;68(4):1221-7. The presence of sensitizing reagents such as cycloheximide and various cytostatic drugs further enhanced antibody-mediated killing of the tumor cells. |
6(0,0,0,6) | 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. |
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. 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. |
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. |
2(0,0,0,2) | Details |
| 17950288 | Bojic L, Petelin A, Stoka V, Reinheckel T, Peters C, Turk V, Turk B: cathepsins are not involved in Fas/CD95 signalling in primary skin fibroblasts. FEBS Lett. 2007 Nov 13;581(27):5185-90. Epub 2007 Oct 12. The potential role of cathepsins, especially cathepsin B, in Fas/CD95-induced apoptosis was investigated using wild-type and cathepsin B-deficient primary skin fibroblasts. Apoptosis was induced with an anti-Fas/CD95 antibody in the presence of cycloheximide and no difference was observed between the two genotypes. |
1(0,0,0,1) | Details |
| 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. Fas ligand (FasL/CD95L/TNFSF6), a member of the tumor necrosis factor family, initiates apoptosis in lymphoid and nonlymphoid tissues by binding to its receptor Fas (CD95/TNFRSF6). HSS1 chromatin remodeling preceded detectable TNFSF6 mRNA accumulation and was blocked by cycloheximide that also prevented TNFSF6 transcription. |
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. The goal of our study was to characterize the apoptotic response of herpes simplex virus (HSV)-infected, human epithelial HEp-2 cells to extrinsic treatments through the Fas receptor. 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. |
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. OBJECTIVES: To investigate the effect of poly (ADP- polymerase 1 (PARP-1) suppression on CD95/Apo-1 (Fas)-induced apoptosis in fibroblast-like synoviocytes (FLS) from RA patients. |
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. Apoptosis by the combination treatment occurred independently from CD95/Fas receptor stimulation. 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. |
1(0,0,0,1) | Details |
| 15701649 | Golks A, Brenner D, Fritsch C, Krammer PH, Lavrik IN: c-FLIPR, a new regulator of death receptor-induced apoptosis. J Biol Chem. 2005 Apr 15;280(15):14507-13. Epub 2005 Feb 8. Impor-/tantly, c-FLIP (R) is recruited to the CD95 (Fas/APO-1) death-inducing signaling complex upon CD95 stimulation. |
1(0,0,0,1) | 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. |
1(0,0,0,1) | 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. Particular interest has been focused on the mechanisms that protect neoplastic cells from deletion by the cytotoxic effects induced by death ligands (TNF-alpha, CD95/APO-1/FasL, TRAIL). |
1(0,0,0,1) | Details |
| 16465293 | Belloc F, Cotteret S, Labroille G, Schmit V, Jaloustre C, Dumain P, Durrieu F, Reiffers J, Boisseau MR, Bernard P, Lacombe F: Bcr-abl translocation can occur during the induction of multidrug resistance and confers apoptosis resistance on myeloid leukemic cell lines. Cell Death Differ. 1997 Dec;4(8):806-14. Apoptosis was studied in parental and mdr-1 expressing U937, HL60 and K562 myeloid leukemic cell lines using mdr unrelated inducers of apoptosis such as Ara-C, cycloheximide, serum deprivation, monensin and UV irradiation. |
0(0,0,0,0) | Details |