ライフサイエンスコーパス: TRAF5

1 0, and are either sufficient or deficient in TRAF5.

2 rotypic association of TRAF1-TRAF2 and TRAF3-TRAF5.

3 s blocked by dominant-negative TRAF2 but not TRAF5.

4 e complex of Act1 and the adaptors TRAF2 and TRAF5, activation of mitogen-activated protein kinases (

5 , these data provide the first evidence that TRAF5 acts as a negative regulator of TLR signaling.

6 of selected mRNA species through Act1, TRAF2-TRAF5 and the RNA-binding protein SF2 (ASF).

7 lved the adaptor Act1, the adaptors TRAF2 or TRAF5 and the splicing factor SF2 (also known as alterna

8 -associated factors TRAF1, TRAF2, TRAF3, and TRAF5 and the TNFR-associated death domain proteins TRAD

9 re only 25% identity, yet both interact with TRAF5 and TRAF2.

10 tail (CD40ct) with much higher affinity than TRAF5 and TRAF6 and that TRAF2 and TRAF3 bind to differe

11 and cellular responses to stress, and TRAF2, TRAF5 and TRAF6 have been demonstrated to mediate activa

12 ed removal of Lys63-linked ubiquitination in TRAF5 and TRAF6 mediated by the adaptor Act1.

13 d the association of USP25 with the adaptors TRAF5 and TRAF6, and USP25 induced removal of Lys63-link

14 Dominant negative forms of TRAF2, TRAF5, and TRAF6 and an endogenous inhibitor of TRAF2, T

15 or of NF-kappaB (RANK) interacts with TRAF2, TRAF5, and TRAF6 and that its overexpression activates N

16 ere we show that TANK synergized with TRAF2, TRAF5, and TRAF6 but not with TRAF3 in SAPK activation.

17 deletion analysis, we determined that TRAF2, TRAF5, and TRAF6 interact with RANK at its C-terminal 85

18 The in vivo locations of TRAF1, TRAF2, TRAF5, and TRAF6 were determined in human and mouse tiss

19 rminal center B cells, whereas TRAF2, TRAF3, TRAF5, and TRAF6 were relatively unchanged.

20 family proteins (TRAF1, TRAF2, TRAF3, TRAF4, TRAF5, and TRAF6), whereas the TD of SPOP interacts weak

21 RAF) family proteins including TRAF2, TRAF3, TRAF5, and TRAF6, as well as Jak3, have been implicated

22 s) have identified positive roles for TRAF2, TRAF5, and TRAF6, but not TRAF3, in canonical (p50-depen

23 ed factor (TRAF) family, specifically TRAF1, TRAF5, and TRAF6, but not with TRAF2, TRAF3, or TRAF4.

24 ruit several TRAF proteins, including TRAF2, TRAF5, and TRAF6, through distinct TRAF-binding motifs.

25 in the steady-state levels of TRAF1, TRAF2, TRAF5, and TRAF6.

26 c tail of TRANCE-R with TRAF1, TRAF2, TRAF3, TRAF5, and TRAF6.

27 NA damage was normal in TNF-R1-/-, TRAF2-/-, TRAF5-/- and FADD-/- fibroblasts or when de novo protein

28 TRAF5(-/-) animals are viable and have normal developmen

29 eptor (TNFR)-associated factor 2 (TRAF2) and TRAF5 are adapter proteins involved in TNFalpha-induced

30 Our results identify TRAF5 as a negative regulator of the IL-6 receptor signa

31 Collectively, these studies identify TRAF5 as an important positive signaling element that en

32 e show that hCD40-P227A binds more TRAF3 and TRAF5, as well as certain associated proteins, than wild

33 Following TLR stimulation, TRAF5 associated in a complex with the TLR adaptor prote

34 This study shows that TRAF5 associated strongly with the viral oncogenic CD40

35 several regions N-terminal to the TRAF2 and TRAF5 association sites.

36 ivation can occur independently of TRAF2 and TRAF5 association.

37 omain of RANK, we demonstrate that TRAF2 and TRAF5 bind to consensus TRAF binding motifs located in t

38 nding region (340-358), but not the TRAF2 or TRAF5-binding region, is necessary and sufficient for RA

39 1, TRAF2, TRAF3, and TRAF6, but not TRAF4 or TRAF5, bound directly to the CD40 cytoplasmic domain.

40 blocked JNK activation directed by TRAF2 or TRAF5 but had no effect on JNK activation directed by TR

41 RAF) family, namely TRAF1, TRAF2, TRAF3, and TRAF5, but not to TRAF6.

42 Co-expression of ATAR with TRAF5, but not TRAF2, results in synergistic activation

43 The site also binds TRAF2 and TRAF5, but not TRAF6.

44 gomers interacted with CD40, indicating that TRAF5 can be indirectly recruited to the CD40 cytoplasmi

45 rminal TRAF domain, of the highly homologous TRAF5 can functionally replace the corresponding domains

46 These results suggest that TRAF5 can limit the induction of Th2 responses, and that

47 mit the induction of Th2 responses, and that TRAF5 can play a role in modulating responses driven by

48 aB and JNK by LIGHT was normal in RIP-/- and TRAF5-/- cells.

49 ormally linked with TNFR signaling pathways, TRAF5 constitutively associated with a cytoplasmic regio

50 However, TRAF5 could be recruited to wild-type CD40 in a TRAF3-de

51 s T cell intrinsic and not due to effects of TRAF5 deficiency on APCs.

52 TLR stimulation of TRAF5-deficient B cells did not affect cell survival, pr

53 the presence of interleukin 6 (IL-6), naive TRAF5-deficient CD4(+) T cells showed an enhanced abilit

54 1 that prevents binding of TRAF2, TRAF3, and TRAF5 does not affect NF-kappaB-activating potential.

55 tion is believed to be impaired in TRAF2 and TRAF5 double knockout (T2/5 DKO) cells.

56 DeltaR at a physiological level in TRAF2 and TRAF5 double knockout (TRAF2/5 DKO) cells almost complet

57 can activate IKK in the absence of TRAF2 and TRAF5 expression and receptor-interacting protein 1 ubiq

58 Full-length TRAF3 and TRAF5 formed hetero-oligomers, presumably through their

59 inity appeared to be in the order of TRAF2 > TRAF5 > TRAF6.

60 TRAF5 has been shown to be a positive regulator of a num

61 A clear role for TRAF5 has yet to emerge.

62 ng protein TNF receptor-associated factor 5 (TRAF5) has been implicated in several biological roles i

63 TRAF3-TRAF5 hetero-oligomers interacted with CD40, indicating

64 However, a clear connection between in vivo TRAF5 immune cell functions and specific signaling pathw

65 with these data, exogenous overexpression of TRAF5 in B cells inhibited TLR-mediated cytokine and Ab

66 However, the potential importance of TRAF5 in cellular immune responses to infection or in T

67 ng potentially different roles for TRAF2 and TRAF5 in post-receptor signaling.

68 first report showing a major requirement for TRAF5 in signaling by a specific receptor both in vitro

69 anine impaired the IL-17-mediated Act1-TRAF2-TRAF5 interaction and gene expression.

70 eletion mutants suggested that the TRAF2 and TRAF5 interaction sites were restricted to the C-termina

71 first time that another TRAF family member, TRAF5, is a negative regulator of TLR signaling.

72 signaling in a cell-specific manner, because TRAF5(-/-) macrophages and dendritic cells showed less d

73 lso called A20) and positive (CARD11, TRAF2, TRAF5, MAP3K7 (TAK1) and TNFRSF11A (RANK)) regulators of

74 Thus, in contrast to CD40, TRAF5 may have an important nonredundant role as a posit

75 B lymphocytes from TRAF5(-/-) mice produced more IL-6, IL-12p40, IL-10, TNF

76 ability remained intact, CD8(+) T cells from TRAF5(-/-) mice were more sensitive to apoptosis and wer

77 y controlled by OX40, was more pronounced in TRAF5(-/-) mice, characterized by higher levels of Th2 c

78 alomyelitis (EAE) was greatly exaggerated in Traf5(-/-) mice.

79 0 Ab resulted in enhanced Th2 development in TRAF5(-/-) mice.

80 Furthermore, TRAF5 negatively regulated the association of TAB2 with

81 TRAF5 negatively regulated TLR signaling in a cell-speci

82 The effect of TRAF5 on CD8(+) T cell expansion was T cell intrinsic an

83 N-kappa-Ras, DN-AKT and DN-IKK but not by DN-TRAF5 or DN-TRAF6.

84 2 and TRAF3, direct binding of TRAF1, TRAF4, TRAF5, or TRAF6 to CD40 was not detected.

85 Results revealed that TRAF5 plays a critical role in LMP1-mediated c-Jun kinas

86 In sum, our studies indicate that TRAF5 plays a crucial role in GITR-induced signaling pat

87 OX40 (CD134) interacts with TRAF5, suggesting that this pathway could be involved in

88 In tissue culture, OX40 stimulation of TRAF5(-/-) T cells resulted in a pronounced Th2 phenotyp

89 imulatory effects of GITR were diminished in TRAF5-/- T cells.

90 as functionally interchangeable with that of TRAF5, the TRAF domain of TRAF3 was not.

91 is due to an inability of the TRAF domain of TRAF5 to bind the TIM of Cardif.

92 with the specific binding of TRAF3, but not TRAF5, to the previously reported TRAF3 binding motif in

93 IL-17 promoted the formation of complexes of TRAF5-TRAF2, Act1 and SF2 (ASF).

94 mutants of TNF receptor-associated factor 5 (TRAF5), TRAF6, NF-kappaB-inducing kinase (NIK), and Ikap

95 s, examples exhibited abnormal expression of TRAF5, TRAF6, and cIAP1 after IR, suggesting increased N

96 ed as complexes that contained TRAF2, TRAF3, TRAF5, TRAF6, and the inhibitor of apoptosis protein (c-

97 ALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-, and IKK-dependent pathway.

98 TRAF5 was necessary for optimal T cell expansion followi

99 We report in this study that TRAF5 was required for optimal CD8(+) T cell responses f

100 ptor-associated factor 2 (TRAF2), TRAF3, and TRAF5, was not required for NF-kappa B activation.

101 TRAF2 and TRAF5 were necessary for IL-17 to signal the stabilizati