| Name | FADD |
|---|---|
| Synonyms | FADD; FADD protein; FAS associating protein with death domain; FAS associating death domain containing protein; Fas (TNFRSF6) associated via death domain; GIG 3; GIG3; MORT 1… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. Knockdown of Fas-associated death domain protein (FADD) by either siRNA or overexpression of a truncated version of FADD that lacks the N-terminal death effector domain (FADD (DN)) increases the sensitivity of HUVECs to LPS plus cycloheximide-mediated death. |
32(0,1,1,2) | 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. TRAIL and Fas receptor death-inducing signaling complex (DISCs) formation are similar and involve ligand-dependent recruitment of FADD and caspase-8. |
2(0,0,0,2) | 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 |
| 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. |
1(0,0,0,1) | 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. |
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. With regard to TNF-alpha R1, FLIP binds to FADD when DISC is formed and redirects the death signal to cell survival, with subsequent activation of NF-kappaB. |
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. 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 |
| 17097066 | Lee TJ, Lee JT, Park JW, Kwon TK: Acquired TRAIL resistance in human breast cancer cells are caused by the sustained cFLIP (L) and XIAP protein levels and ERK activation. Biochem Biophys Res Commun. 2006 Dec 29;351(4):1024-30. Epub 2006 Nov 7. The selected TRAIL-resistant cells were cross-resistant to TNF-alpha/cycloheximide but remained sensitive to DNA-damage drugs such as oxaliplatin and etoposide. |
0(0,0,0,0) | 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. |
31(0,1,1,1) | Details |