| Name | FLIP |
|---|---|
| Synonyms | CASH; CASP8 and FADD like apoptosis regulator; CASP8 and FADD like apoptosis regulator precursor; CASP8AP1; CFLAR; CLARP; Caspase homolog; Caspase like apoptosis regulatory protein… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. |
38(0,1,1,8) | 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. |
34(0,1,1,4) | 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. |
8(0,0,0,8) | 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. |
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. |
2(0,0,0,2) | 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 |
| 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. |
1(0,0,0,1) | Details |
| 17118471 | Marin-Vinader L, van Genesen ST, Lubsen NH: mRNA made during heat shock enters the first round of translation. Biochim Biophys Acta. 2006 Nov-Dec;1759(11-12):535-42. Epub 2006 Oct 24. Using fluorescence loss in photobleaching (FLIP) we show that cytoplasmic EGFP-CBP20 is immobile in heat shocked cells. |
1(0,0,0,1) | Details |
| 18202809 | Hofmanova J, Vaculova A, Hyzd'alova M, Kozubik A: Response of normal and colon cancer epithelial cells to TNF-family apoptotic inducers. Oncol Rep. 2008 Feb;19(2):567-73. We studied apoptosis with regard to the changes at the receptor level (DR, DcR and FLIP) and at the level of mitochondria (Bid protein cleavage, Apo2.7 protein expression and caspase-9 activation). Two different approaches were used to sensitize the cells to TRAIL-induced apoptosis: inhibition of protein synthesis (cycloheximide, CHX) and inhibition of the pro-survival MEK/ERK pathway (U0126). |
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. It has been suggested that the presence of the cleaved form of FLIP (L)-p43 at the DISC prevents caspase-8 cleavage. |
1(0,0,0,1) | 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. |
0(0,0,0,0) | 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. 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. |
0(0,0,0,0) | 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. 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. |
0(0,0,0,0) | 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. |
0(0,0,0,0) | 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. Cycloheximide reduced the expression of FLIP in the resistant cells. |
164(2,2,2,4) | 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. 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. |
83(1,1,1,3) | 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. Treatment with cycloheximide during CD40 activation prevents up-regulation of those c-FLIP isoforms and sensitizes ALL cells toward CD95-mediated apoptosis. |
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. |
82(1,1,1,2) | 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). |
82(1,1,1,2) | Details |
| 16077198 | Pajak B, Gajkowska B, Orzechowski A: Cycloheximide-mediated sensitization to TNF-alpha-induced apoptosis in human colorectal cancer cell line COLO 205; role of FLIP and metabolic inhibitors. J Physiol Pharmacol. 2005 Jun;56 Suppl 3:101-18. |
81(1,1,1,1) | Details |