ライフサイエンスコーパス: trance

1 and TNF-related activation-induced cytokine (TRANCE).

2 F-kappaB ligand; also known as OPGL, ODF, or TRANCE).

3 anner that likely requires local delivery of TRANCE.

4 r (TNF)-related activation-induced cytokine (TRANCE), a member of the TNF family expressed on activat

5 r (TNF)-related activation-induced cytokine (TRANCE), a member of the TNF family, is a dendritic cell

6 KL)/TNF-related activation-induced cytokine (TRANCE), a primarily T-cell restricted TNF family member

7 r (TNF)-related activation-induced cytokine (TRANCE), a TNF family member, before immunization enhanc

8 factor-related, activation-induced cytokine (TRANCE), a tumor necrosis factor family member, mediates

9 TRANCE, a TNF family member, and its receptor, TRANCE-R,

10 We recently demonstrated that TRANCE activates Akt via a mechanism involving TRANCE re

11 These results define a mechanism by which TRANCE activates Src family kinases and PKB and provide

12 Here, we demonstrate that TRANCE activates the antiapoptotic serine/threonine kina

13 a), TNF-related activation-induced cytokine (TRANCE, also referred to as osteoprotegerin ligand), and

14 ppaB, and its ligand RANKL (initially termed TRANCE, also termed ODF and OPGL), are a TNF superfamily

15 TRANCE and CD40L-mediated Akt activation is defective in

16 , myeloma cell lines stimulate expression of TRANCE and inhibit expression of OPG by stromal cells.

17 Thus, we propose that both TRANCE and LTalphabeta regulate the colonization and clu

18 subjects were writing, in both dissociative trance and non-trance states.

19 Our data identify TRANCE and OPG as key cytokines whose deregulation promo

20 factor-related activation-induced cytokine (TRANCE) and decrease in its decoy receptor, osteoprotege

21 of TNF-related activation-induced cytokine (TRANCE) and receptor activator of NF-kappaB (RANK) was c

22 factor-related activation-induced cytokine (TRANCE), and its receptors, receptor activator of nuclea

23 Unlike soluble OPG receptors, which preclude TRANCE binding to RANK, OP3-4 shows the ability to modul

24 mplications for the functional regulation of TRANCE by potentially more than one protease.

25 rotein and of a peptide corresponding to the TRANCE cleavage site by TACE occurs at the same site tha

26 A recombinant soluble form of TRANCE composed of the entire ectodomain induced c-Jun N

27 Moreover, TRANCE cooperates with CD40 ligand or TNF-alpha to furth

28 We report the skeletal phenotype of TRANCE-deficient mice and its rescue by the TRANCE trans

29 c overexpression of TRANCE in lymphocytes of TRANCE-deficient mice rescued osteoclast development in

30 TRANCE-deficient mice showed severe osteopetrosis, with

31 that subjects produced complex content in a trance dissociative state suggests they were not merely

32 TRANCE does not induce the proliferation of or increase

33 We propose that the TRANCE ectodomain is released from cells by TACE or a re

34 cells; and (iv) that in vitro cleavage of a TRANCE ectodomain/CD8 fusion protein and of a peptide co

35 In sharp contrast, TRANCE expression by stromal cells was completely indepe

36 In addition, TRANCE expression is restricted to lymphoid organs and T

37 sis, the functional consequence of increased TRANCE expression, is counteracted by addition of a reco

38 factor-related activation-induced cytokine (TRANCE) expression.

39 The TRANCE gene encodes a type II membrane protein of 316 am

40 rane by a metalloprotease; (ii) that soluble TRANCE has potent dendritic cell survival and osteoclast

41 TRANCE, however, does not exert any significant effect o

42 is an important component of the function of TRANCE in bone and immune homeostasis.

43 ests a potential role for ADAM19 in shedding TRANCE in cells where both molecules are highly expresse

44 In addition, expression of TRANCE in ILF was concentrated just beneath the follicle

45 Transgenic overexpression of TRANCE in lymphocytes of TRANCE-deficient mice rescued o

46 is not required for shedding of TNFalpha and TRANCE in mouse embryonic fibroblasts, its overexpressio

47 vertase (TACE) can cleave immunoprecipitated TRANCE in vitro in a fashion that mimics the cleavage ob

48 constant at all time points, suggesting that TRANCE-induced MITF, not PU.1 expression, is one of the

49 sion by PU.1/MITF is further enhanced by the TRANCE-induced MKK6/p38 signaling cascade.

50 -/-) mice developed normally, but CD40L- and TRANCE-induced survival and IL-12 production was abolish

51 In DCs, TRANCE induces the expression of proinflammatory cytokin

52 However, TRANCE induction is significantly suppressed when cells

53 is counteracted by addition of a recombinant TRANCE inhibitor, RANK-Fc, to marrow/myeloma cocultures.

54 TRANCE inhibits apoptosis of mouse bone marrow-derived D

55 Therefore, TRANCE is a new DC-restricted survival factor that media

56 TRANCE is an immediate early gene up-regulated by TCR st

57 TRANCE is most highly expressed in thymus and lymph node

58 CE occurs at the same site that is used when TRANCE is shed from cells into the supernatant.

59 TNF-related activation-induced cytokine (TRANCE) is a member of the TNF family recently identifie

60 r (TNF)-related activation-induced cytokine (TRANCE) is a TNF family member essential for osteoclast

61 such as dancing) or through reverie (such as trance), it is usually the temporal qualities of the mus

62 In this report we demonstrate (i) that TRANCE, like TNF-alpha, is made as a membrane-anchored p

63 , and OSCAR in TRANCE-treated (RAW 264.7) or TRANCE/M-CSF-treated cells (primary osteoclasts) reveal

64 ition of Src family kinase inhibitors blocks TRANCE-mediated PKB activation in osteoclasts.

65 Thus, TRANCE-mediated regulation of the skeleton is complex, a

66 Transgenic TRANCE-mediated restoration of LN development requires L

67 nstrate that the defective LN development in TRANCE(-/)- mice correlates with a significant reduction

68 Transgenic TRANCE overexpression in TRANCE(-/)- mice results in selective restoration of thi

69 fate of CD45(+)CD4(+)CD3(-) cells similar to TRANCE(-/)- mice.

70 Upon TCR/CD3 stimulation, TRANCE mRNA and surface protein expression are rapidly u

71 We report here that TRANCE mRNA is constitutively expressed in memory, but n

72 The TNF-family molecule RANK-L (RANK-L, TRANCE, ODF) and its receptor RANK are key regulators of

73 These findings suggest that TRANCE on stromal cells contributes to the differentiati

74 s indicate that in vivo, deregulation of the TRANCE-OPG cytokine axis occurs in myeloma, but not in t

75 erstand complex biological functions of RANK-TRANCE-OPG receptors and also can be used as a platform

76 g of the tumor necrosis factor family member TRANCE/OPGL in different cell types.

77 ces osteoclast survival in response to RANKL/TRANCE/OPGL, providing evidence that Src family kinases

78 Transgenic TRANCE overexpression in TRANCE(-/)- mice results in sel

79 ex with TRAF6-binding peptides from CD40 and TRANCE-R (also known as RANK), members of the TNFR super

80 Here, we show that TRANCE-R and CD40 recruit TRAF6, Cbl family-scaffolding

81 ed competition between TRAF proteins for the TRANCE-R and the possibility of a TRAF-independent NF-ka

82 Signaling by TRANCE-R appears to be dependent on TNF receptor-associa

83 Here, we show that high levels of TRANCE-R are detected on mature dendritic cells (DCs) bu

84 motif, which is present not only in CD40 and TRANCE-R but also in the three IRAK adapter kinases for

85 utants revealed that multiple regions of the TRANCE-R can mediate NF-kappaB activation.

86 Furthermore, transfection experiments with TRANCE-R deletion mutants revealed that multiple regions

87 Analysis of TRANCE-R deletion mutants suggested that the TRAF2 and T

88 The recruitment of Cbl-b and c-Cbl to TRANCE-R is dependent upon the activity of Src-family ki

89 and TRAF6 interact with each other and with TRANCE-R upon receptor engagement.

90 interactions between the cytoplasmic tail of TRANCE-R with TRAF1, TRAF2, TRAF3, TRAF5, and TRAF6.

91 The TRANCE receptor (TRANCE-R), recently identified as receptor activator of

92 fter interaction with its putative receptor (TRANCE-R).

93 t via a mechanism involving TRANCE receptor (TRANCE-R)/RANK, TRAF6, and c-Src.

94 ANCE, a TNF family member, and its receptor, TRANCE-R, are critical regulators of dendritic cell and

95 ting protein (TRIP), substantially inhibited TRANCE-R-mediated NF-kappaB activation, suggesting a rol

96 ignal transducers as important components of TRANCE-R-mediated NF-kappaB activation.

97 tor receptor (TNFR) family members (GITR and TRANCE-R/RANK) in Treg biology, the improved understandi

98 ed osteoclast activation that occurs through TRANCE-RANK causes osteopenic disorders such as osteopor

99 lts demonstrate that CD40L(-/-) mice use the TRANCE-RANK costimulatory pathway to promote IL-12 produ

100 ng mice lacking osteoprotegerin or by adding TRANCE (RANKL, Tnfsf11).

101 n osteoclast differentiation and activation, TRANCE/RANKL also functions to augment T-cell dendritic

102 onstrated that the degree of bone erosion in TRANCE/RANKL knockout mice was dramatically reduced comp

103 cal scoring, was comparable in wild-type and TRANCE/RANKL knockout mice.

104 n was present in both control littermate and TRANCE/RANKL knockout mice.

105 , we generated inflammatory arthritis in the TRANCE/RANKL knockout mouse using a serum transfer model

106 r activator of nuclear factor-kappaB ligand (TRANCE/RANKL) is an essential factor for osteoclast diff

107 The TRANCE receptor (TRANCE-R), recently identified as recep

108 ANCE activates Akt via a mechanism involving TRANCE receptor (TRANCE-R)/RANK, TRAF6, and c-Src.

109 alters the biological functions of the RANK-TRANCE receptor complex by facilitating a defective rece

110 High levels of TRANCE receptor expression are found on mature dendritic

111 Here, we show that in vivo treatment with a TRANCE receptor fusion protein results in a decrease in

112 ow that activated T and B cells also express TRANCE receptor, but only at low levels.

113 s some properties with RANK, the first RANKL/TRANCE receptor, we discuss how the balance between RANK

114 of TNF-related activation-induced cytokine (TRANCE)-receptor activator of NF-kappaB (RANK) interacti

115 One of the TRANCE sheddases is induced by the tyrosine phosphatase

116 At least two TRANCE shedding activities emerged, both of which are di

117 in COS-7 cells results in strongly increased TRANCE shedding.

118 NK, OP3-4 shows the ability to modulate RANK-TRANCE signaling pathways and alters the biological func

119 writing, in both dissociative trance and non-trance states.

120 ber TNF-related activation-induced cytokine (TRANCE) that are produced by osteoblasts/stromal cells i

121 tor activator of NF-kappaB ligand (RANKL, or TRANCE, TNFSF11) to carry out bone resorption.

122 egulatory T cells (Treg), whereas 4-1BBL and TRANCE together can stimulate T cells and dendritic cell

123 TRANCE-deficient mice and its rescue by the TRANCE transgene specifically expressed in lymphocytes.

124 plate defects were largely unimproved by the TRANCE transgene.

125 ression patterns of MITF, PU.1, and OSCAR in TRANCE-treated (RAW 264.7) or TRANCE/M-CSF-treated cells

126 TRANCE (tumor necrosis factor [TNF]-related activation-i

127 TRANCE upregulates Bcl-xL expression, suggesting a poten

128 stensibly transforming during initiation and trance, violating folk-intuitions of humanness to assure

129 E was mapped to chromosome 13q14 while mouse TRANCE was located to the portion of mouse chromosome 14

130 Human TRANCE was mapped to chromosome 13q14 while mouse TRANCE

131 sis factor (TNF) cytokine family, designated TRANCE, was cloned during a search for apoptosis-regulat

132 g psychography compared to their normal (non-trance) writing.