ライフサイエンスコーパス: receptor activator of NF-kappaB ligand

1 ts, a response dependent on increased RANKL (receptor activator of NF-kappaB ligand).

2 f TNFalpha expression by IL-1, TNFalpha, and receptor activator of NF-kappaB ligand.

3 ption and bone loss in response to high-dose receptor activator of NF-kappaB ligand.

4 and reducing the production of IL-17 and the receptor activator of NF-kappaB ligand.

5 tiation and activity even in the presence of receptor activator of NF-kappaB ligand.

6 d by osteoclasts expressed FoxP3, CTLA4, and receptor activator of NF-kappaB ligand.

7 f cytokines including type I and II IFNs and receptor activator of NF-kappaB ligand.

8 T-PCR) for OPG (osteoprotegerin); and RANKL (receptor activator of NF-kappaB ligand); 3) signaling pa

9 e tumor necrosis factor family member RANKL (receptor activator of NF-kappaB ligand), a critical bone

10 ce of signaling events elicited by M-CSF and receptor activator of NF-kappaB ligand, acting on their

11 tumor necrosis factor-related factor, RANKL (receptor activator of NF-kappaB ligand; also known as OP

12 s derived from Xid mice were stimulated with receptor activator of NF-kappaB ligand, an osteoclast di

13 n the concerted action of osteoblast-derived receptor activator of NF-kappaB ligand and colony-stimul

14 environment also regulated to expression of receptor activator of NF-kappaB ligand and osteoproteger

15 cantly inhibit in vivo production of TNF and receptor activator of NF-kappaB ligand, and block joint

16 tiation assays by stimulating with M-CSF and receptor activator of NF-kappaB ligand bone marrow cells

17 by macrophage-colony stimulating factor and receptor activator of NF-kappaB ligand, both of which ar

18 in production of osteoprotegerin to that of receptor activator of NF-kappaB ligand by B cells, and w

19 om SHIP1 null mice respond to M-CSF, but not receptor activator of NF-kappaB ligand, by increasing Ak

20 triol, phosphorus, alkaline phosphatase, and receptor activator of NF-kappaB ligand concentrations, a

21 ith macrophage-colony stimulating factor and receptor activator of NF-kappaB ligand cytokines, DAP12

22 ate-resistant acid phosphatase 5 (TRAP) with receptor activator of NF-kappaB ligand-evoked OC lineage

23 BMP-2 stimulates receptor activator of NF-kappaB ligand expression.

24 RANKL (receptor activator of NF-kappaB ligand) expression is si

25 required for mechanical repression of RANKL (receptor activator of NF-kappaB ligand) expression, the

26 TF4 phosphorylation and thus increase RANKL (receptor activator of NF-kappaB ligand) expression, whic

27 Finally, IL-1/TNFalpha and receptor activator of NF-kappaB ligand fail to stimulate

28 s the macrophage colony-stimulating factor-1-receptor activator of NF-kappaB ligand formation of mult

29 , and hypersensitivity to macrophage CSF and receptor activator of NF-kappaB ligand in BM-derived ost

30 presence of colony stimulating factor-1 and receptor activator of NF-kappaB ligand in the presence o

31 oproteinases (MMP9, -13, and -14) and RANKL (receptor activator of NF-kappaB ligand) in the hypertrop

32 , independent of PLCgamma1, was required for receptor activator of NF-kappaB ligand-induced (RANKL-in

33 We revealed that C/EBPalpha is important for receptor activator of NF-kappaB ligand-induced Akt activ

34 ppressed TNF-induced invasion, and inhibited receptor activator of NF-kappaB ligand-induced osteoclas

35 gents and inhibited TNF-induced invasion and receptor activator of NF-kappaB ligand-induced osteoclas

36 We show here that IL-4 inhibits receptor activator of NF-kappaB ligand-induced osteoclas

37 icient (Mfge8(-/-)) mice underwent increased receptor activator of NF-kappaB ligand-induced osteoclas

38 istently, exogenously added MFG-E8 inhibited receptor activator of NF-kappaB ligand-induced osteoclas

39 factor-induced cellular invasion, abrogated receptor activator of NF-kappaB ligand-induced osteoclas

40 steoclast monocyte precursors and facilitate receptor activator of NF-kappaB ligand-induced osteoclas

41 critical transcription factor downstream of receptor activator of NF-kappaB-ligand-induced calcium s

42 monocyte/macrophage cells, in the absence of receptor activator of NF-kappaB ligand, induces expressi

43 This was associated with an inhibition of receptor activator of NF-kappaB ligand levels and osteoc

44 oprotegerin (OPG) without inducing change in receptor activator of NF-kappaB ligand levels, whereas t

45 osteoblasts, treatment with Vit D increased receptor activator of NF-kappaB ligand mRNA by 17-, 19-,

46 In WT cells, Vit D and IL-1 stimulated receptor activator of NF-kappaB ligand mRNA expression b

47 The latter prevents signaling by receptor activator of NF-kappaB ligand needed for osteoc

48 ing OPG production and restoring a favorable receptor activator of NF-kappaB ligand/OPG ratio, in add

49 the metaphysis indicated that, although the receptor activator of NF-kappaB ligand/osteoprotegerin a

50 bone resorption, consistent with the reduced receptor activator of NF-kappaB ligand/osteoprotegerin r

51 ted osteoclastogenesis is independent of the receptor activator of NF-kappaB ligand pathway and uses

52 The receptor activator of NF-kappaB ligand (RANK-L) also fai

53 Receptor activator of NF-kappaB ligand (RANK-L) and pros

54 Receptor activator of NF-kappaB ligand (RANKL) activates

55 izing that activated T cells express surface receptor activator of NF-kappaB ligand (RANKL) and can i

56 tenin signaling leading to induction of both receptor activator of NF-kappaB ligand (RANKL) and its r

57 nflammation and bone metabolism and that the receptor activator of NF-kappaB ligand (RANKL) and its r

58 We show here that estrogen can suppress receptor activator of NF-kappaB ligand (RANKL) and macro

59 efects secondary to diminished production of receptor activator of NF-kappaB ligand (RANKL) and macro

60 monocytic precursor cells in the presence of receptor activator of NF-kappaB ligand (RANKL) and macro

61 cultured in media supplemented with soluble receptor activator of NF-kappaB ligand (RANKL) and macro

62 However, the quantification of receptor activator of NF-kappaB ligand (RANKL) and osteo

63 is induced by 1,25(OH)2D3 without modulating receptor activator of NF-kappaB ligand (RANKL) and osteo

64 tumor necrosis factor-alpha (TNF-alpha), and receptor activator of NF-kappaB ligand (RANKL) and suppo

65 The receptor activator of NF-kappaB ligand (RANKL) and the p

66 steoclast precursors were hyperresponsive to receptor activator of NF-kappaB ligand (RANKL) and TNF-a

67 ated the possibility of a cross-talk between receptor activator of NF-kappaB ligand (RANKL) and tumor

68 ast formation and bone resorption induced by receptor activator of NF-kappaB ligand (RANKL) and tumor

69 han cells from WT littermates in response to receptor activator of NF-kappaB ligand (RANKL) and was a

70 Receptor activator of NF-kappab ligand (RANKL) and Xanth

71 elevation in the expression and secretion of receptor activator of NF-kappaB ligand (RANKL) by hepara

72 unosuppression-mediated B-cell production of receptor activator of NF-kappaB ligand (RANKL) coupled w

73 row cells or osteoclasts formed from them by receptor activator of NF-kappaB ligand (RANKL) different

74 oss with reduced mechanical stimulation, and receptor activator of NF-kappaB ligand (RANKL) expressio

75 by decreased collagen type I alpha1 mRNA and receptor activator of NF-kappaB ligand (RANKL) expressio

76 response to osteotropic factors by inducing receptor activator of NF-kappaB ligand (RANKL) expressio

77 Recently, receptor activator of NF-kappaB ligand (RANKL) has been

78 nd up-regulating the pro-osteoclastic factor receptor activator of NF-kappaB ligand (RANKL) in osteob

79 recursors with the osteoclastogenic cytokine receptor activator of NF-kappaB ligand (RANKL) increases

80 blockade of receptor activator of NF-kappaB/receptor activator of NF-kappaB ligand (RANKL) interacti

81 Receptor activator of NF-kappaB ligand (Rankl) is a TNF-

82 Receptor activator of NF-kappaB ligand (RANKL) is a tran

83 Receptor activator of NF-kappaB ligand (RANKL) is a tumo

84 Receptor activator of NF-kappaB ligand (RANKL) is an ess

85 Receptor activator of NF-kappaB ligand (RANKL) is essent

86 Receptor activator of NF-kappaB ligand (RANKL) is expres

87 Gene deletion studies have shown that receptor activator of NF-kappaB ligand (RANKL) is one of

88 The TNF superfamily member receptor activator of NF-kappaB ligand (RANKL) is select

89 sive to limiting concentrations of M-CSF and receptor activator of NF-kappaB ligand (RANKL) levels.

90 Ethanol increased receptor activator of NF-kappaB ligand (RANKL) mRNA expr

91 , but increased expression in these cells of receptor activator of NF-kappaB ligand (RANKL) mRNA, whe

92 The transmembrane receptor activator of NF-kappaB ligand (RANKL) of osteob

93 ormed osteoclasts in vitro without exogenous receptor activator of NF-kappaB ligand (RANKL) or MCSF.

94 sible for sustained giant cell formation via receptor activator of NF-kappaB ligand (RANKL) paracrine

95 Receptor activator of NF-kappaB ligand (RANKL) plays a c

96 ace, which was associated with a decrease in receptor activator of NF-kappaB ligand (RANKL) productio

97 mor necrosis factor (TNF) superfamily member receptor activator of NF-kappaB ligand (RANKL) regulates

98 oclastogenesis is controlled by the ratio of receptor activator of NF-kappaB ligand (RANKL) relative

99 e to colony-stimulating factor-1 (CSF-1) and receptor activator of NF-kappaB ligand (RANKL) signaling

100 Binding of receptor activator of NF-kappaB ligand (RANKL) to its re

101 ctivate the central osteoclastogenic pathway receptor activator of NF-kappaB ligand (RANKL) to promot

102 ivated by c-Fos and NF-kappaB in response to receptor activator of NF-kappaB ligand (RANKL) treatment

103 M-1 mRNA is down-regulated by treatment with receptor activator of NF-kappaB ligand (RANKL), a cytoki

104 s in human periodontal lesions bear abundant receptor activator of NF-kappaB ligand (RANKL), a major

105 The receptor activator of NF-kappaB ligand (RANKL), a recent

106 ng, in part, by modulating the expression of receptor activator of NF-kappaB ligand (RANKL), an essen

107 heddase releasing non-ECM substrates such as receptor activator of NF-kappaB ligand (RANKL), an osteo

108 ntified matrix metalloproteinase 13 (MMP13), receptor activator of NF-kappaB ligand (RANKL), and inte

109 e marrow (BM) plasma levels of the catabolic receptor activator of NF-kappaB ligand (RANKL), and its

110 regulation of osteoblast-specific molecules, receptor activator of NF-kappaB ligand (RANKL), and oste

111 In vitro, additional MCSF, but not receptor activator of NF-kappaB ligand (RANKL), complete

112 ophage-colony-stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL), cytokine

113 d/or protein expression of VCAM-1, IL-6, and receptor activator of NF-kappaB ligand (RANKL), enhancin

114 e quantitative RT-PCR analysis revealed that receptor activator of NF-kappaB ligand (RANKL), interleu

115 the TCR signal can elicit the expression of receptor activator of NF-kappaB ligand (RANKL), TNF-alph

116 med increased numbers of OCLs in response to receptor activator of NF-kappaB ligand (RANKL), tumor ne

117 TNF and receptor activator of NF-kappaB ligand (RANKL), two liga

118 f the tumor necrosis factor-related protein, receptor activator of NF-kappaB ligand (RANKL), we condi

119 CaP cells produced a soluble form of receptor activator of NF-kappaB ligand (RANKL), which ac

120 cytes in periodontal disease lesions express receptor activator of NF-kappaB ligand (RANKL), which in

121 Microarray analysis of receptor activator of NF-kappaB ligand (RANKL)-activated

122 Recently, a receptor activator of NF-kappaB ligand (RANKL)-blocking

123 e was observed in LC-ablated mice, including receptor activator of NF-kappaB ligand (RANKL)-expressin

124 tamic acids instigates spontaneous bona fide receptor activator of NF-kappaB ligand (RANKL)-independe

125 pendent on the ability of TGF-beta to enable receptor activator of NF-kappaB ligand (RANKL)-induced c

126 e observed that ASCs significantly inhibited receptor activator of NF-kappaB ligand (RANKL)-induced o

127 This alteration of the receptor activator of NF-kappaB ligand (RANKL)-induced o

128 we have investigated the cross talk between receptor activator of NF-kappaB ligand (RANKL)-induced o

129 Interleukin 4 (IL-4) inhibits receptor activator of NF-kappaB ligand (RANKL)-induced o

130 The absence of Lyn enhances receptor activator of NF-kappaB ligand (RANKL)-mediated

131 To clarify the role of calpain in the receptor activator of NF-kappaB ligand (RANKL)-supported

132 on of the osteoclast differentiation factor, receptor activator of NF-kappaB ligand (RANKL).

133 last differentiation induced by the cytokine receptor activator of NF-kappaB ligand (RANKL).

134 cytokines from the cell membrane, including receptor activator of NF-kappaB ligand (RANKL).

135 e monocyte/macrophage lineage in response to receptor activator of NF-kappaB ligand (RANKL).

136 nificantly increased, whereas expressions of receptor activator of NF-kappaB ligand (RANKL)/osteoprot

137 been characterized as a second receptor for receptor activator of NF-kappaB ligand (RANKL)/TNF-relat

138 gand 20 (CCL20), IL-23 receptor (IL-23R) and receptor activator of NF-kappaB ligand (RANKL, also call

139 y stimulating factor-1 (CSF-1, or M-CSF) and receptor activator of NF-kappaB ligand (RANKL, or TRANCE

140 The TNF superfamily member receptor activator of NF-kappaB ligand (RANKL, TNFSF11)

141 lation by osteoclastogenic cytokines such as receptor activator of NF-kappaB-ligand (RANKL, also know

142 of macrophage colony-stimulating factor and receptor activator of NF-kappaB ligand significantly ind

143 ibits macrophage colony-stimulating factor-1-receptor activator of NF-kappaB ligand-stimulated osteoc

144 n the anabolic effects of PTH in addition to receptor activator of NF-kappaB ligand stimulation to in

145 is factor-related apoptosis-inducing ligand, receptor activator of NF-kappaB ligand, syndecan-1, and

146 heterozygosity expressed the OPG receptors, receptor activator of NF-kappaB ligand, syndecan-1, and

147 consequence of an imbalance in the ratio of receptor activator of NF-kappaB ligand, the key osteocla

148 ression of the osteoclast-stimulating factor receptor activator of NF-kappaB ligand was also reduced.