ライフサイエンスコーパス: Fas-associated death domain protein

1 EPEC NleB1, and SseK2 glycosylated the FADD (Fas-associated death domain protein).

2 e inhibitors or transduced dominant-negative Fas-associated death domain protein.

3 between the action of RIP and FADD/MORT-1, a Fas-associated death domain protein.

4 Kv1.3 stimulation required the expression of Fas-associated death domain protein and activation of ca

5 tures seen in mice deficient in caspase 8 or Fas-associated death domain protein and are not resistan

6 ould induce cell death, the requirements for Fas-associated death domain protein and caspase-9 were d

7 fs are also critical to TRADD for recruiting Fas-associated death domain protein and receptor-interac

8 complex (DISC) formed by Fas receptor, FADD (Fas-associated death domain protein) and caspase 8 is a

9 nduced recruitment of large amounts of FADD (FAS-associated death domain protein) and procaspase 8, l

10 of the death receptor adaptor protein FADD (Fas-associated death domain protein) and used these vect

11 s the TNFR1-associated death domain protein, Fas-associated death domain protein, and caspase-8.

12 K1 induced a modest reduction in levels of Fas-associated death domain protein, and procaspase 8 re

13 NFR-associated death domain protein (TRADD), Fas-associated death domain protein, and receptor-intera

14 TRADD-Fas-associated death domain protein apoptotic pathway.

15 levels of Fas signaling molecules including Fas-associated death domain protein, caspase 8, and casp

16 ane and subsequently induced cytosolic TRADD-Fas-associated death domain protein complex.

17 ell development to a lesser extent than does Fas-associated death domain protein deficiency or anothe

18 ells, as well as caspase-8-, caspase-9-, and Fas-associated death domain protein-deficient Jurkat cel

19 s lacking casp8 or its adaptor protein FADD (Fas-associated death domain protein) develop a hyperauto

20 nteractive protein) triggers apoptosis via a FAS-associated death domain protein (FADD) and caspase 8

21 ptosis through MyD88 via a pathway involving Fas-associated death domain protein (FADD) and caspase 8

22 Fas-associated death domain protein (FADD) and caspase-8

23 -8 appeared sufficient, inadequate levels of Fas-associated death domain protein (FADD) and DAP3 may

24 ein preferentially associated with cytosolic Fas-associated death domain protein (FADD) and localized

25 ector domain present in the adaptor molecule Fas-associated death domain protein (FADD) and the initi

26 Knockdown of Fas-associated death domain protein (FADD) by either siR

27 Fas-associated death domain protein (FADD) constitutes a

28 cking the CD95 death receptor pathway with a Fas-associated death domain protein (FADD) dominant-nega

29 f death domains (SODD) and dominant-negative FAS-associated death domain protein (FADD) efficiently i

30 tive and survival defects as T cells lacking Fas-associated death domain protein (FADD) function.

31 he expression of a dominant-negative form of FAS-associated death domain protein (FADD) in a number o

32 The pivotal discovery that Fas-associated death domain protein (FADD) interleukin-1

33 Fas-associated death domain protein (FADD) is an adaptor

34 th receptor pathway (WT) and a corresponding Fas-associated death domain protein (FADD) KO cell line

35 Furthermore, the dominant negative Fas-associated death domain protein (FADD) protein block

36 Signal transduction mediated by Fas-associated death domain protein (FADD) represents a

37 cloheximide (FasL/Chx), or overexpression of Fas-associated death domain protein (FADD) result in inc

38 TNFR1 signaling factors TRADD and Fas-associated death domain protein (FADD) were also fou

39 So far, only Fas-associated death domain protein (FADD), another deat

40 Fas-associated death domain protein (FADD), caspase-8-re

41 oteins involved in LPS signaling such as the Fas-associated death domain protein (FADD), IkappaB kina

42 gous missense mutation in FADD, encoding the Fas-associated death domain protein (FADD), in the patie

43 Two of the genes identified, Dbs and Fas-associated death domain protein (FADD), previously i

44 the activation of caspases 3, 8, and 9, the Fas-associated death domain protein (FADD), reactive oxy

45 this study we investigated death receptors, FAS-associated death domain protein (FADD), the activati

46 ssion of a dominant negative mutated form of Fas-associated death domain protein (FADD), which blocks

47 re protein does not interfere with the TRADD-Fas-associated death domain protein (FADD)-procaspase-8

48 We show that the Fas-associated death domain protein (FADD)/caspase-8 pat

49 Fas-associated death domain protein (FADD)/mediator of r

50 Fas-associated death domain protein (FADD)/MORT1 is a 23

51 The Fas-associated death domain protein (FADD)/Mort1 is a si

52 ive mutant of the cell death adaptor protein Fas-associated death domain protein (FADD/MORT1), which

53 volving dephosphorylation and aggregation of Fas-associated death domain protein followed by death re

54 Along with Fas-associated death domain protein, it is also essentia

55 ecoy receptors 1 and 2, Bax, cellular FLICE (Fas-associated death domain protein-like IL-1-converting

56 protein (IAP), IAP1, Bcl-x(L), A1/Bfl-1 and Fas-associated death domain protein-like IL-1beta-conver

57 strate that expression of HHV8-encoded viral Fas-associated death domain protein-like IL-1beta-conver

58 F receptor-associated factor 1, and cellular Fas-associated death domain protein-like interleukin-1be

59 NF receptor-associated factor-1 (TRAF1), and Fas-associated death domain protein-like interleukin-1be

60 urkat cells by a mechanism that requires the Fas-associated Death Domain Protein-mediated activation

61 RIP1 participates in the Fas-associated death domain protein-mediated recruitment

62 s was completely inhibited in caspase-8- and Fas-associated death domain protein-negative Jurkat cell

63 Expression of dominant-negative mutant of Fas-associated death domain protein or a caspase-8 inhib

64 Jurkat cell variants lacking Fas-associated death domain protein or procaspase-8 were

65 ptosis does not involve the adaptor proteins Fas-associated death domain protein or tumor necrosis fa

66 onstrate that signals initiated by regulated Fas-associated death domain protein overexpression in ra

67 er crmA or a dominant-negative mutant of the Fas-associated death domain protein prevented TNFalpha-

68 converting enzyme) inhibitory protein, FADD (Fas-associated death domain protein), procaspase 8, and

69 Moreover, Fas-associated death domain protein recruitment to the d

70 Knock down of CD95 or Fas-associated death domain protein suppressed drug comb

71 In contrast, the fact that Fas-associated death domain protein was recruited to the

72 p-fluoromethyl ketone, and dominant negative Fas-associated death domain protein, we found that delet