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1. |
Opiate addiction in humans is associated with an altered balance between p-Ser194 FADD (increased) and total FADD (decreased) in brain, which may favor its neuroplastic actions. |
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2. |
Report specific reduction of fas-associated protein with death domain (FADD) in clear cell renal cell carcinoma. |
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3. |
existence of differential pathways directing FADD nuclear export and cytoplasmic trafficking and subcellular compartmentalization of FADD as a novel regulatory mechanism in death receptor signaling. |
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4. |
results present the earliest conservation analysis and biophysical characterization of the Fas-associated death domain |
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5. |
the disordered C-terminus of RTN3 is able to interact with FADD via a novel mode previously unobserved for FADD. |
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6. |
a phi-value analysis of the pathway of folding |
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7. |
human Fas-FADD death domain complex 2.7 A crystal structure |
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8. |
an apoptotic inhibitory complex comprised of DR5, FADD, caspase-8, and c-FLIP(L) exists in MCF-7 cells, and the absence of c-FLIP(L) from this complex induces DR5- and FADD-mediated caspase-8 activation in the death inducing signaling complex |
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9. |
the simultaneous downregulation of uPAR and MMP-9 induces apoptosome-mediated apoptosis through FADD-associated protein RIP and caspase 9 |
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10. |
the interaction between human papillomavirus type 16 and FADD is mediated by a novel E6 binding domain |
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11. |
These results illustrate that JEV infection triggers caspase cascades involving the initiators caspase-8 and -9, probably through FADD-independent but mitochondrion-dependent pathways. |
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12. |
Implication of FGF3 and FADD in human craniofacial disease. |
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13. |
Increased expression and activation of Fas in beta-cells could constitute a molecular event common to the pathogenesis of both type 1 and type 2 diabetes. |
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14. |
Observational study of gene-disease association. (HuGE Navigator) |
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15. |
cancer cells expressing high levels of the Ser(194) phosphorylated isoform of FADD are sensitive to Taxol-induced cell cycle arrest |
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16. |
Transgenic FADD/caspase-8 play an essential role in maintaining S6 kinase activity during T cell cycle progression. |
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17. |
The expression of Fas-associated death domain (FADD) in peripheral blood mononuclear cells was significantly decreased in SLE patients. |
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18. |
Reduced expression of the proapoptotic proteins FADDor overexpression of Bcl-2 improved myoblast transplantation survival. |
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19. |
Endoplasmic reticulum, ER-bound RTN3 protein recruited endogenous FADD to the ER membrane and subsequently initiated caspase-8 cascade, including activation of caspase-8, processing of Bid and release of cytochrome c from mitochondria. |
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20. |
dominant negative form inhibits cytochrome c release in response to TRAIL receptor 2 or CD95 |
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21. |
binding of Fas-associated death domain (FADD) to the tumor necrosis factor-related apoptosis-inducing ligand receptor DR5 is regulated by the death effector domain of FADD |
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22. |
acid sphingomyelinase activation within rafts involves a Fas-mediated mechanism dependent upon caspase 8 and FADD |
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23. |
Apoptosis and NF-kappa B: the FADD connection. |
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24. |
The ability of MHC class II to modulate activation of the pro-apoptotic receptor Fas by blocking the accessory molecule FADD and to delay apoptosis induction could allow for cytokine secretion by H pylori-infected gastric epithelial cells. |
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25. |
Phosphorylation of FADD by casein kinase Ialpha is a crucial event during mitosis. |
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26. |
FADD self-associates through a conserved RXDLL motif in the death effector domain |
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27. |
expression blocks keratinocyte apoptosis and vesication induced by sulfur mustard |
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28. |
absolute requirement for the C-terminal tail of TRAIL for FADD binding and signaling |
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29. |
taxol induces FADD-dependent apoptosis primarily through activation of caspase-10 but independently of death receptors |
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30. |
alteration associated with nodal metastasis in non-small cell lung cancer |
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31. |
Truncated receptor-interacting serine-threonine kinase 3 may function upstream of FADD to induce apoptosis in TNFR-1 signaling pathway |
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32. |
dispensability for apoptotic function of Hid |
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33. |
HLA class II signals sensitize B lymphocytes to apoptosis, in part, by increasing FADD recruitment to activated Fas |
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34. |
evidence for caspase-8-ganglioside interaction in T cells |
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35. |
caspase-8 and FADD are obligatory for TNF-mediated apoptosis but are not recruited to a TNF-induced membrane-bound receptor signaling complex; they must be activated elsewhere within the cell |
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36. |
The association of FADD with ABCA1 provides an unexpected link between high density lipoprotein metabolism and an adaptor molecule mainly described in death receptor signal transduction. |
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37. |
This is the first report of FADD gene mutation in gastrointestinal cancers, and data suggest that the FADD gene is rarely mutated in human colon and stomach cancers. |
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38. |
Hypoxia-induced apoptosis was not affected by lack of caspase-8 or FADD. |
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39. |
DeltaDD-decoy receptors act as dominant-negative receptors exerting local inhibition, while avoiding systemic neutralization of apoptosis ligands, and might have therapeutic potential in hepatitis. |
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40. |
The mechanism controlling PEA-15 binding to ERK/MAPK or FADD, and its subsequent role in cell proliferation and apoptosis is reported. |
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41. |
JNK-mediated phosphorylation of FADD plays an important role in the negative regulation of cell growth and metastasis, independent of the ER status of a breast cancer |
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42. |
induction of NF-kappaB activity and its effects on cell-cycle progression may represent a molecular basis underlying the aggressive tumor behavior associated with elevated p-FADD expression in lung adenocarcinoma |
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43. |
binding of FADD and caspase-8 to molluscum contagiosum virus MC159 v-FLIP is not sufficient for its antiapoptotic function |
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44. |
FADD death domain has an expanded binding surface responsible for interaction with CD95/Fas |
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45. |
The majority of Langerhans cell histiocytosis cells express FADD. |
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46. |
Regulation of FADD expression by UV may serve to enhance death receptor-mediated keratinocyte death. |
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47. |
Functional assays using mutants of Fas-associated death domain revealed that this basic region influences binding and recruitment of caspase-8 and cellular FLICE inhibitor protein to the DISC. |
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48. |
FADD uses a Tube-like surface in each of its death motifs to engage its binding partners, either CD95 or TRADD. |
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49. |
study showed a significant decrease in the percentage of FADD-immunoreactive dopaminergic (DA) neurons in the substantia nigra pars compacta of patients with Parkinson's disease |
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50. |
Caspase-10 is recruited to and activated at the native death-inducing signalling complexes in a FADD-dependent manner. |
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51. |
c-FLIPL is recruited to death receptor 5 independent of Fas-associated protein with death domain (FADD) |
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52. |
Extensive regions of the FADD death domain are required for binding to the TRAIL receptor DR5. |
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53. |
Transfection of the human papillomavirus (HPV) 16 E6 oncogene into HCT116 cells provides protection from tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-mediated apoptosis. |
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54. |
results suggest that autophagy 5-like Atg5 plays a crucial role in interferon-gamma-induced autophagic cell death by interacting with Fas-associated protein with death domain (FADD) |
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55. |
FADD dominant-negative transgenic mice are resistant to experimental autoimmune encephalomyelitis; FADD therefore serves as an enhancer of autoimmune encephalomyelitis. |
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56. |
FADD does not play an essential role in NF-kappaB activation, suggesting an alternative route by which this adaptor promotes the clonal expansion of T cells |
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57. |
TRAIL-R1 and TRAIL-R2 recruit FADD which then interacts with procaspase-8. This results in the assembly of FADD and procaspase-8 into DISC and initiates the cascacde to apoptosis. |
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58. |
A deficiency in FADD sensitises Jurkat T cells to TNF-alpha-dependent necrosis during activation-induced cell death . |
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59. |
This review suggests that levels of phosphorylated FADD may be used as a prognostic biomarker for predicting survival of lung cancer patients. |
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60. |
the death effector domain of FADD is involved in interaction with Fas. |
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61. |
FADD is present in both the cytoplasm and the nucleus of cells; its nuclear localization relies on strong nuclear localization and nuclear export signals (NLS and NES, respectively) that reside in the death-effector domain. |
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62. |
C-FADD may affect apoptosis sensitivity of cells by interfering with cell cycle progression and not only by binding to death receptors. |
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63. |
FADD may play a role in regulating genome surveillance |
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64. |
FADD/caspase-8 pathway induces apoptosis through p53 in human pre-malignant and malignant cells |
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65. |
These findings reveal that prolonged ERK1-2/MAPK stimulation results in FADD-independent caspase 8 activation and cell death. |
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66. |
We propose an alternative architecture for the FADD signaling complex in which FADD acts as a molecular bridge to stitch together an array of activated death receptors. |
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67. |
The identification of a procaspase-specific binding surface on the FADD DED suggests a preferential interaction with one, but not both, of the DEDs of procaspase-8 in a perpendicular arrangement. |