ライフサイエンスコーパス: RANKL

1 RANKL activities in SR900 and control groups were close

2 RANKL and its receptor RANK are downstream effectors of

3 RANKL binding to LGR4 activates the Galphaq and GSK3-bet

4 RANKL can be produced by a variety of hematopoietic (e.g

5 RANKL expression by MSCs decreased after propranolol adm

6 RANKL is the osteoclast differentiating factor and dimin

7 RANKL was significantly different (P <0.05) only for non

8 RANKL-induced signaling in macrophages and the different

9 RANKL-mediated suppression of RNF146 results in the stab

10 When cocultured with THP-1, RANKL released by PGE2-stimulated HMOBs is adequate to d

11 her molecules - including IL-1, IL-6, IL-17, RANKL, OPG, and CCL2 - modulate probiotic action.

12 dy, we aimed to investigate whether OP3-4, a RANKL-binding peptide, promotes BMP-2-induced bone forma

13 ion between younger age at onset of RA and a RANKL promoter SNP that conferred an elevated promoter a

14 ole for IL-33 in exacerbating bone loss in a RANKL-dependent manner in the context of bacterial infec

15 pression than donor-matched ABCs, yielding a RANKL/OPG ratio of 41:1 (ABCs:DPCs).

16 Moreover, LGR4-ECD therapeutically abrogated RANKL-induced bone loss in three mouse models of osteopo

17 ockout mice than in the wild-type mice after RANKL injection.

18 ZH2 was recruited to the IRF8 promoter after RANKL stimulation to deposit the negative histone mark H

19 expression, and decreased MMP-3, MMP-13 and RANKL expressions in cartilage, increased BMD, BV/TV, an

20 expression but stimulates MMP-3, MMP-13 and RANKL production by chondrocytes through ERK1/2 and PKA

21 ecrosis factor-alpha, interleukin-1beta, and RANKL in the gingival tissue compared with the control s

22 ced neutrophil recruitment, reduced IL-6 and RANKL, and less bone resorption.

23 f IL-1beta, tumor necrosis factor alpha, and RANKL was significantly reduced.

24 bone expressed higher levels of beta2-AR and RANKL; norepinephrine stimulation further increased thei

25 ion of DJ-1 in mouse models of arthritis and RANKL-induced bone disease leads to an increase in the n

26 of RANKL-treated WT versus Cox2 KO BMMs, and RANKL induced Saa3 protein secretion only from WT BMMs.

27 ous bone under physiological conditions, and RANKL production by B lymphocytes is required for the bo

28 therefore attenuated the number of M-CSF and RANKL-derived osteoclasts in vitro.

29 st (JNJ7777120), the gene expression H4R and RANKL was determined by real-time PCR.

30 4 hours and then collected to assess MMP and RANKL production by immunoblotting.

31 stimulated the production of MMP1, MMP8, and RANKL in a dose- and time-dependent manner; blocking EDN

32 promoting the protein expression of MMPs and RANKL via the phospholipase C pathway.

33 recans, matrix metalloproteinases (MMPs) and RANKL by chondrocytes were evaluated.

34 iectomized-induced bone loss mouse model and RANKL-injection-induced bone resorption model, we found

35 re three lines of evidence that HS, OPG, and RANKL form a stable ternary complex.

36 Sclerostin, OPG, and RANKL levels were measured by enzyme-linked immunosorben

37 Middle T (MMTV-PyMT), which mimics RANK and RANKL expression patterns seen in human breast adenocarc

38 on and increased the expression of RANKL and RANKL/OPG ratio by mesenchymal stem cells at 2 h.

39 teoclastogenesis, osteoclast resorption, and RANKL-induced signaling pathway using both in vitro and

40 the main postnatal source of sclerostin and RANKL (receptor activator of NF-kB ligand), two regulato

41 l-autonomous increase in SOST/sclerostin and RANKL/OPG ratio in the setting of unloading.

42 -inflammatory cytokines upregulated SOX5 and RANKL expression in both primary RA SF and the rheumatoi

43 paration, osteoclast number and surface, and RANKL expression.

44 cells, which leads to elevated TNFalpha and RANKL signaling and enhanced osteoclastogenesis.

45 xpressing higher levels of both TNFalpha and RANKL, BgnFmod KO derived osteoblasts cannot retain thes

46 fferences in the RANKL/OPG Axis in vivo, and RANKL-induced maturation of osteoclast-precursors in vit

47 uccessfully used as immunogen to induce anti-RANKL immune response.

48 nome-wide expression analyses show that anti-RANKL therapy promotes lactogenic differentiation of tum

49 uperfamily member 11 (TNFSF11; also known as RANKL) is a key paracrine effector of progesterone signa

50 uperfamily member 11 (TNFSF11, also known as RANKL) regulates multiple physiological or pathological

51 osteolytic and osteoblastic factors such as RANKL (receptor activator of NFkappaB ligand) and parath

52 n and Fmod directly bind TNFalpha as well as RANKL in a dose dependent manner and that despite expres

53 MMD1 protein expression by hypoxia augmented RANKL-induced expression of inflammatory and E2F1 target

54 LGR4 competes with RANK to bind RANKL and suppresses canonical RANK signaling during ost

55 oluble LGR4 extracellular domain (ECD) binds RANKL and inhibits osteoclast differentiation in vivo.

56 P-mAb also inhibited pit formation caused by RANKL-stimulated bone marrow cells.

57 a3 secretion from preosteoclasts, induced by RANKL in a Cox2-dependent manner, inhibits PTH-stimulate

58 In BMMs committed to become osteoclasts by RANKL treatment, Saa3 expression peaked prior to appeara

59 timulation of RANK on osteoclast surfaces by RANKL similar to osteoprotegerin.

60 To mimic an inflamed condition, RANKL upregulation in human mandibular osteoblast-like c

61 1(-/-) and WT mice were cultured with M-CSF, RANKL and/or MCP-1.

62 proof of concept, an inter-species cytokine RANKL was successfully used as immunogen to induce anti-

63 -dependent metabolic pathway by the cytokine RANKL.

64 asma OPN levels, and significantly decreased RANKL levels.

65 way, and it helps in restoring the decreased RANKL/OPG ratio in adult mice.

66 silencing SOX5 gene significantly diminished RANKL positive cells and bone erosion in CIA mice.

67 OC development and activation by disrupting RANKL-induced localization of TRAF6 and c-SRC into lipid

68 T-cell reconstitution elicits RANKL and TNFalpha production by B cells and/or T cells,

69 Furthermore, IL-3 enhances RANKL expression in mesenchymal stem cells of wild-type

70 Excessive RANKL signaling leads to superfluous osteoclast formatio

71 e established that chondrocytes also express RANKL/OPG and support osteoclast formation.

72 tients despite increased osteocyte-expressed RANKL.

73 ingival tissues and T lymphocytes expressing RANKL in the cervical draining lymph nodes were higher i

74 steoclast differentiation through expressing RANKL/OPG cytokines.

75 production of the cancer cell motile factor RANKL.

76 sts that secrete the osteoclastogenic factor RANKL upon binding of galectin-8.

77 ability of the pro-osteoclastogenic factors RANKL and insulin-like growth factor 1 (IGF-1) to induce

78 ed an enhanced osteolytic response following RANKL injection over the calvaria of NLRP12-deficient ch

79 ted IFN-gamma reduced the mRNAs encoding for RANKL, TRAP, and Cathepsin K.

80 a, and IL-1beta; immunostaining increase for RANKL and TRAP; reduction of OPG and leukocytosis, which

81 hondrial SIRT3 is an intrinsic inhibitor for RANKL-mediated osteoclastogenesis.

82 OPG is a decoy receptor for RANKL, thereby increasing BMD.

83 , also called GPR48) is another receptor for RANKL.

84 K) is considered to be the sole receptor for RANKL.

85 alyses demonstrate that Shp2 is required for RANKL-induced formation of giant multinucleated OCs by u

86 RESV reduced expression of messenger RNA for RANKL in animals receiving CSI (P <0.05).

87 CM from RANKL-stimulated BMMs with Saa3 knockdown did not inhibi

88 Conditioned medium (CM) from RANKL-treated WT, but not KO, BMMs blocked PTH-stimulate

89 SIRT3 expression from RANKL induction depended on the transcription coactivato

90 The global RANKL/OPG ratio in the spine after 8 months of steroid a

91 se-3-dependent apoptosis, and express higher RANKL (TNFSF11) and sclerostin levels than osteocytes in

92 However, RANKL did not regulate the expression or activation of S

93 he crystal structure of the complex of human RANKL and its rodent counterpart receptor RANK.

94 prevent undesirable side-effects, the human RANKL was mutated based on the crystal structure of the

95 gs mouse survival by disengaging the Shh-IL6-RANKL signaling network in stromal cells in the tumor mi

96 ion in BRCA1-mutation carriers and implicate RANKL blockade as a promising strategy in the prevention

97 ssue homeostasis, the role of these cells in RANKL regulation remains unknown.

98 nsal microbiota induces sustained changes in RANKL-mediated osteoclastogenesis.

99 n osteogenic gene expression, a reduction in RANKL expression and osteoclast activity, and an increas

100 ed by growth factors and cytokines including RANKL and BMPs, in osteoclastogenesis and bone resorptio

101 signal to neighboring osteocytes to increase RANKL expression, which, in turn, increases osteoclastog

102 eactive oxygen species (ROS), which increase RANKL-mediated signaling in osteoclast (OC) precursor bo

103 r of alveolar bone osteoclasts and increased RANKL expression after P. gingivalis infection.

104 ast lineage cells, which expressed increased RANKL and produced an abnormal resorption-stimulating bo

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

106 of SOX5 resulted in significantly increased RANKL levels, while knockdown of SOX5 resulted in dimini

107 PGE2 significantly increased RANKL messenger RNA (mRNA) and protein in HMOBs in a dos

108 The increased RANKL expression by IL-3 induces mononuclear osteoclasts

109 J osteoarthritisis associated with increased RANKL secretion by MSCs.

110 We found that IL-3 increases RANKL expression at both the transcriptional and transla

111 osteal/endosteal cell cultures by increasing RANKL.

112 stimulated bone formation but did not induce RANKL, suggesting that intracellular signaling activated

113 Sclerostin is suggested to induce RANKL expression in osteocytes.

114 X5 is an important regulator of IL-6-induced RANKL expression in RA SF.

115 We now report that CFZ inhibits PTH-induced RANKL expression and secretion without affecting PTH inh

116 s proved to contain molecule(s) that induced RANKL expression.

117 last formation (p < 0.0001) in inflammatory (RANKL+TNF) and noninflammatory (RANKL) conditions.

118 sorption by its additional effect to inhibit RANKL-mediated IkappaB degradation and NF-kappaB activat

119 Furthermore, IL-3 inhibited RANKL-induced osteoclast differentiation less effectivel

120 Additionally, ASCs inhibited RANKL-induced osteoclastogenesis in the presence of proi

121 We found that STAT5 overexpression inhibited RANKL-induced osteoclastogenesis.

122 of transcription 5 (STAT5) by IL-3 inhibits RANKL-induced osteoclastogenesis through the induction o

123 differentiation, interleukin (IL)-3 inhibits RANKL-induced osteoclastogenesis.

124 e function of OPG and affect how it inhibits RANKL.

125 ultured in a transwell system to investigate RANKL-driven THP-1 osteoclastic activity.

126 Mice lacking RANKL in osteocytes were protected from the increase in

127 Receptor-activator of NF-kappaB, its ligand RANKL, and the soluble decoy receptor osteoprotegerin ar

128 activator of nuclear factor-kappa B ligand (RANKL) activation was analyzed in the mandible samples s

129 activator of nuclear factor-kappa B ligand (RANKL) activity.

130 activator of nuclear factor kappa B ligand (RANKL) and thus bone metabolism.

131 activator of nuclear factor kappa-B ligand (RANKL) resulted in a robust formation of large, multinuc

132 receptor for nuclear factor kappa-B ligand (RANKL) were significantly different between obese- and n

133 -activator of nuclear factor kappa B ligand (RANKL) were significantly elevated in the gingival tissu

134 activator of nuclear factor-kappa B ligand (RANKL), osteoprotegerin (OPG), and tartrate-resistant ac

135 activator for nuclear factor kappa-B ligand (RANKL), osteoprotegerin, osteocalcin, and osteopontin as

136 activator of nuclear factor-kappa B ligand (RANKL), sclerostin, and Dickkopf Wnt signaling pathway i

137 activator of nuclear factor kappa-B ligand (RANKL), which, in turn, promotes the periodontal bone lo

138 activator of nuclear factor kappa-B ligand (RANKL)-RANK-osteoprotegerin (OPG) signaling associated w

139 activator of nuclear factor-kappa B ligand (RANKL); 2) osteoprotegerin (OPG); 3) interleukin (IL)-6;

140 uble receptor activator of NF-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF)

141 n of receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) signaling in osteocytes

142 r activator of nuclear factor-kappaB ligand (RANKL) and released enzymes such as matrix metalloprotei

143 r activator of nuclear factor-kappaB ligand (RANKL) and tartrate resistant acid phosphatase were sign

144 Receptor activator of NF-kappab ligand (RANKL) and Xanthine/Xanthine Oxidase induced TRAP mRNA e

145 n of receptor activator of NF-kappaB ligand (RANKL) coupled with decline in osteoprotegerin correlate

146 and receptor activator of NF-kappaB ligand (RANKL) expression is increased with unloading in mice.

147 ctor receptor activator of NF-kappaB ligand (RANKL) in osteoblasts.

148 r activator of nuclear factor-kappaB ligand (RANKL) in osteocytes and mouse calvarial explants and pr

149 r activator of nuclear factor-kappaB ligand (RANKL) in the gingival crevicular fluid (GCF) of patient

150 tes expressing nuclear factor kappaB ligand (RANKL) in the gingival tissues and T lymphocytes express

151 r activator of nuclear factor kappaB ligand (RANKL) in the osteoblastic lineage cells, which then cau

152 r activator of nuclear factor kappaB ligand (RANKL) is critically involved in bone erosion of rheumat

153 g of receptor activator of NF-kappaB ligand (RANKL) to its receptor RANK on osteoclast (OC) precursor

154 n of receptor activator of NF-kappaB ligand (RANKL), an essential cytokine for bone resorption by ost

155 r activator of nuclear factor-kappaB ligand (RANKL), an essential cytokine for osteoclast differentia

156 r activator of nuclear factor-kappaB ligand (RANKL), and alkaline phosphatase activity.

157 les, receptor activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) that modulate bone hom

158 r activator of nuclear factor kappaB ligand (RANKL), osteoprotegerin (OPG), and tartrate-resistant ac

159 r activator of nuclear factor-kappaB ligand (RANKL), osteoprotegerin (OPG), tartrate-resistant acid p

160 r activator of nuclear factor-kappaB ligand (RANKL), osteoprotegerin (OPG), wingless (WNT) 10b, dickk

161 ated receptor activator of NK-kappaB ligand (RANKL), tartrate-resistant acid phosphatase (TRAP), and

162 and receptor activator of NF-kappaB ligand (RANKL), two ligands associated with diabetes, induce NIK

163 r activator of nuclear factor kappaB ligand (RANKL), which plays a central role in promoting osteocla

164 s of receptor activator of NF-kappaB ligand (RANKL)-activated murine bone marrow macrophage (BMM) cul

165 r activator of nuclear factor kappaB ligand (RANKL)-binding peptide promotes osteoblast differentiati

166 r activator of nuclear factor-kappaB ligand (RANKL)-evoked signaling; its role in osteoclastogenesis

167 activator of nuclear factor- kappab ligand (RANKL)-induced osteoclastogenesis in bone marrow-derived

168 ited receptor activator of NF-kappaB ligand (RANKL)-induced osteoclastogenesis in both a contact-depe

169 r activator of nuclear factor kappaB ligand (RANKL).

170 s of receptor activator of NF-kappaB ligand (RANKL)/osteoprotegerin (OPG), tumor necrosis factor alph

171 f nuclear factor-kappa B (NF-kappaB) ligand (RANKL), a potent osteoclast-stimulating factor, by human

172 r activator of nuclear factor kappaB-ligand (RANKL)-stimulated differentiation into osteoclasts.

173 ctivator of nuclear factor kappaBeta ligand (RANKL)/osteoprotegerin (OPG) (2.5 +/- 0.7-fold, p < 0.00

174 Receptor activator of NF-kB ligand (RANKL) generates intracellular reactive oxygen species (

175 ermal receptor activator of NFkappaB ligand (RANKL) is critical for the induction of anti-viral CD8(+

176 okine receptor activator of NFkappaB ligand (RANKL) produced by osteocytes is essential for osteoclas

177 activator for NF-kappaB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) axis and expression of the

178 ceptor activator of NF-kappaB (RANK) ligand (RANKL) plays a pivotal role in lymphoid tissue formation

179 DPCs yielded ~20-fold lower RANKL expression but >2-fold higher osteoprotegerin (OPG

180 Because osteocytes are major RANKL producers, we hypothesized that apoptotic osteocyt

181 of SOX5 resulted in diminished IL-6 mediated RANKL upregulation in MH7A cells.

182 H4R mediates RANKL expression and osteoclast differentiation induced

183 Moreover, IL-3 increases membrane RANKL by activating the JAK2/STAT5 pathway.

184 by reducing ectodomain shedding of membrane RANKL through downregulation of metalloproteases mainly

185 nflammatory (RANKL+TNF) and noninflammatory (RANKL) conditions.

186 murine preosteoclast cells in the absence of RANKL stimulation compared to ground based (Xg) cultures

187 expressed gene in a microarray comparison of RANKL-treated WT versus Cox2 KO BMMs, and RANKL induced

188 Salivary concentrations of RANKL, osteocalcin, and osteopontin were higher, and ost

189 ture mononuclear OCs, in primary cultures of RANKL-stimulated bone marrow cells.

190 P) showed approximately 3-fold enrichment of RANKL-specific DNA in anti-SOX5 immunoprecipitate in IL-

191 stimulation and increased the expression of RANKL and RANKL/OPG ratio by mesenchymal stem cells at 2

192 Expression of RANKL by hPDL cells significantly increased after IL-12

193 Expression of RANKL was evaluated at mRNA and protein levels.

194 osteoblasts display increased expression of RANKL, the central osteoclastogenic cytokine.

195 erentially regulates two functional forms of RANKL through metalloproteases and the JAK2/STAT5 pathwa

196 nitiates osteoclastogenesis independently of RANKL.

197 Furthermore, inhibition of RANKL in a Brca1-deficient mouse model substantially cur

198 r-alpha (ERalpha) or selective inhibition of RANKL in hematopoietic vs. mesenchymal cells, in conjunc

199 Inhibition of RANKL signaling by treatment with denosumab in three-dim

200 o the remarkable IL-3-mediated inhibition of RANKL-induced osteoclastogenesis by activating Id genes

201 Salivary levels of RANKL, osteoprotegerin, osteocalcin, osteopontin, and se

202 lls expressed significantly higher levels of RANKL.

203 umented by FDG uptake and with the number of RANKL + cells present in the circulating blood.

204 berant osteoclastogenesis in the presence of RANKL, a response that correlates with NLRP3 abundance a

205 astogenesis through osteoblast production of RANKL and IL6.

206 T-cell response and resultant production of RANKL was affected by anti-DC-STAMP-mAb.

207 tion and activity by increasing the ratio of RANKL/OPG in osteoblasts.

208 hat NFATc1 is the sole critical regulator of RANKL/RANK-dependent osteoclast activation.

209 Secretion of RANKL by galectin-8-treated osteoblasts can be attribute

210 Immunohistochemical staining of RANKL and osteoclast activity were significantly lower i

211 HDAC4 and HDAC5, whereas PTH stimulation of RANKL, a stimulator of bone resorption, requires CRTC2.

212 d by lack of ERalpha-mediated suppression of RANKL expression in bone lining cells.

213 We found that treatment of RANKL-stimulated primary bone marrow-derived macrophage

214 These results support the use of RANKL inhibitors to reduce recurrence and metastasis in

215 e, and their differentiation is dependent on RANKL, a member of the TNF family of cytokines.

216 possible effects of M1 and M2 macrophages on RANKL-induced osteoclastogenesis.

217 versed the effect of epithelial mediators on RANKL expression.

218 NA expression in mouse macrophages, but only RANKL also induced TRAP activity in mouse lung slices.

219 at HS plays an active role in regulating OPG-RANKL interaction and osteoclastogenesis.

220 DD had significant decreases in baseline OPG/RANKL ratio and in plasma OPN levels.

221 etamine significantly increased both the OPG/RANKL ratio and plasma OPN levels, and significantly dec

222 ass through sequestration of TNFalpha and/or RANKL, thereby adjusting their bioavailability in order

223 eting ILC3 or neutralizing CCL21, CXCL13, or RANKL was sufficient to decrease lymph node metastasis.

224 f bone mass, bone loss caused by hormonal or RANKL perturbations is significantly reduced in Nlrp3 de

225 sustained exposure to parathyroid hormone or RANKL.

226 Although murine models lacking RANK or RANKL show defects in B cell number, the role of the RAN

227 Reconstitution of TNFalpha- or RANKL-null T-cells and pharmacological TNFalpha antagoni

228 did not prevent the increase in osteoblastic RANKL.

229 crease in osteocyte apoptosis and osteocytic RANKL expression.

230 cyte apoptosis leads to increased osteocytic RANKL.

231 OX and IL6 were acting in concert to promote RANKL-dependent osteoclast differentiation, thereby crea

232 Vitamin D3 significantly promoted RANKL expression in ABCs and OPG in DPCs.

233 inflammation-the osteoprotegerin (OPG)-RANK-RANKL system or osteopontin (OPN)-play a role in the bon

234 We conclude that the OPG-RANK-RANKL system and the OPN system play important roles in

235 The OPG-RANK-RANKL system plays the principal role in determining the

236 RANK/RANKL signaling pathway is critical for OCL differentiat

237 ation was combined with the analysis of RANK/RANKL loop activation in the leukemic clone, given recen

238 rich EVs may also take advantage of the RANK/RANKL interaction to target RANK-rich EVs to RANKL-beari

239 by Denosumab-mediated disruption of the RANK/RANKL loop.

240 It can be concluded that SR can reduce RANKL activity and osteoclast numbers, as well as ABL.

241 Reduced RANKL immunolabeling and fewer TRAP-positive multinuclea

242 KCa3.1(-/-) reduced RANKL+/-TNF-stimulated phosphorylation of CREB and expre

243 ATV reduced RANKL and DKK-1 and increased OPG, WNT10b, and beta-cate

244 concurrently with PGE2 stimulation, reduced RANKL, but not OPG, expression.

245 yte precursors, but it was linked to reduced RANKL-driven osteoclast formation.

246 in part through mechanisms linked to reduced RANKL-mediated osteoclastogenesis.

247 ith HMOBs by releasing IFN-gamma to regulate RANKL expression and contribute to osteoclastogenesis.

248 LPS P. gingivalis and Pam2 also up-regulated RANKL and osteoclastic genes in vivo, resulting in an in

249 scavenging protein DJ-1 negatively regulates RANKL-driven OC differentiation, also called osteoclasto

250 Mechanistically, SMURF2 regulates RANKL expression by disrupting the interaction between S

251 Interestingly, IL-3 restores RANKL expression in adult mice by enhancing bone-specifi

252 unae were present in root dentin with robust RANKL and OPG expression.

253 The sclerostin/OPG and sclerostin/RANKL ratios were significantly lower in healthy individ

254 Therefore, LGR4 acts as a second RANKL receptor that negatively regulates osteoclast diff

255 ing bone-specific RANKL and decreasing serum RANKL.

256 Interestingly, IL-3 decreases soluble RANKL by reducing ectodomain shedding of membrane RANKL

257 Gene expression levels of soluble RANKL, osteoprotegerin, tumor necrosis factor alpha, and

258 ion in adult mice by enhancing bone-specific RANKL and decreasing serum RANKL.

259 tingly, assessment of the osteocyte-specific RANKL/OPG ratio showed that the steroid-induced osteopor

260 Histamine, IL-17, and IL-22 stimulated RANKL expression in RA monocytes and JNJ7777120 reduced

261 onists HKLM, FSL1, Pam2, and Pam3 stimulated RANKL in osteoblasts and parietal bone resorption.

262 sis in its late progressive phase stimulates RANKL expression in osteocytes.

263 formation and bone resorption by stimulating RANKL in osteoblasts via TLR2.

264 rived from oral epithelial cells, suppressed RANKL expression at both the mRNA and protein level, res

265 n of M1 macrophages significantly suppressed RANKL-induced osteoclastogenesis compared to nonstimulat

266 Therefore, targeting RANKL or its signaling pathway has been a promising and

267 effector of progesterone signaling and that RANKL and its receptor TNFRSF11A (also known as RANK) co

268 ken together, these results demonstrate that RANKL expressed by osteocytes is required for the bone l

269 Here, we have provided evidence that RANKL controls the expression of 3BP2, an adapter protei

270 We found that RANKL represses the transcription of the E3 ubiquitin li

271 Given that RANKL is an important paracrine mediator of hormonal sig

272 The RANKL/OPG ratio was significantly lower in healthy indiv

273 The RANKL/RANK pathway is critical for both osteoclast forma

274 ed link between IL-10 CD40 signaling and the RANKL pathway.

275 2) clastic cell fusion and activation by the RANKL/RANK/OPG and ATP-P2RX7-IL1 pathways; and (3) regul

276 evealed that Saa3 was secreted only from the RANKL-stimulated B220(-) CD3(-)CD11b(-/low) CD115(+) pre

277 Differences in the RANKL/OPG Axis in vivo, and RANKL-induced maturation of

278 These data point to a novel role of the RANKL-RANK axis in the regulation of B cell homeostasis

279 ow defects in B cell number, the role of the RANKL-RANK axis on B physiology is still a matter of deb

280 n in RA monocytes and JNJ7777120 reduced the RANKL expression.

281 the sheep model of osteoporosis to study the RANKL/OPG ratio correlation to the method of osteoporosi

282 Targeting the RANKL pathway by osteoprotegerin administration abrogate

283 lerostin level may be more reliable than the RANKL/OPG ratio as a diagnostic and prognostic marker of

284 preventing the osteoclast activation via the RANKL-OPG axis, without interfering with bone anabolism.

285 the differentiation by interfering with the RANKL-induced expression of PGC-1beta.

286 nephrine stimulation further increased their RANKL expression and pro-osteoclastic function.

287 e osteoclastogenic cytokines TNFalpha (TNF), RANKL, and IL-17 in the small intestine and the BM.

288 RANKL interaction to target RANK-rich EVs to RANKL-bearing cells for the delivery of other regulatory

289 the regulation of SOX5 levels in relation to RANKL expression in RA synovial fibroblasts (SF) and the

290 owers the inhibitory threshold of OPG toward RANKL.

291 lacking osteoprotegerin or by adding TRANCE (RANKL, Tnfsf11).

292 hat TRAM-34 pretreatment decreased transient RANKL-induced Ca(2+) amplitudes in BMMs by approximately

293 rs with CXCL12-gamma fibroblasts upregulated RANKL (receptor activator of nuclear factor-kappaB ligan

294 kinase-dependent pathway and 2) upregulates RANKL by a different pathway.

295 Activation via RANKL prevents Langerhans cell apoptosis, thus leading t

296 Stronger OPG immunolabeling and weaker RANKL immunolabeling were observed in the SRP/SA group a

297 P2 groups than in the control group, whereas RANKL, osteocalcin, and osteopontin were not related wit

298 Here, we examined whether RANKL produced by osteocytes is also required for the bo

299 ype (WT) bone marrow macrophages (BMMs) with RANKL, TAK1 deficiency in these cells leads to increased

300 cantly more OCs when they were cultured with RANKL and M-CSF.