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 OPG concentrations were estimated in peri-impl

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 gene transcription was robustly induced by the pro

6 RANKL increased and OPG decreased in P group and 100 mg/

7 RANKL inhibition increases the anti-tumor effect of immu

8 RANKL is the osteoclast differentiating factor and dimin

9 RANKL mediated signaling utilizes reactive oxygen specie

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

11 RANKL-induced signaling in macrophages and the different

12 RANKL-mediated suppression of RNF146 results in the stab

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

14 2, Jagged 1, Hes 1, Hey 1, TNF-alpha, IL-17, RANKL, and OPG) was determined by reverse transcriptase

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

16 iators in the gingiva (IL-6, IL-17A, IL-17F, RANKL, IL-10, TGF-beta and GITR; P < 0.05), and the prol

17 elevated osteocyte TNF-alpha, interleukin-6, RANKL, OPG, and sclerostin corresponded with higher oste

18 with nitrogen-containing bisphosphonates, a RANKL inhibitor, antiangiogenic agents, or mTOR inhibito

19 e/cartilage interface support VAOs through a RANKL-RANK signalling mechanism.

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

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

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

23 In turn a neutralizing Ab against RANKL, denosumab improves bone strength in osteoporosis.

24 ilitates binding of OPG to membrane-anchored RANKL.

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

26 nt increase of Notch 2, TNF-alpha, IL-17 and RANKL and a significant decrease of Notch 1 and Jagged 1

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

28 Notch 2 and RANKL were also overexpressed in CP group compared to co

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

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

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

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

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

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

35 17, or T regulatory-associated cytokines and RANKL, as well as the periodontal bacterial load, were q

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

37 D <=4.5 mm; PIMP: BOP >0.25%, PD >4.5 mm and RANKL <=19.9 pg/site; PIM: BOP >0.25%, PD >4.5 mm, and R

38 .9 pg/site; PIM: BOP >0.25%, PD >4.5 mm, and RANKL >19.9 pg/site.

39 4 hours and then collected to assess MMP and RANKL production by immunoblotting.

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

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

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

43 used a decrease in the osteoclast number and RANKL/OPG ratio in periodontal lesions.

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

45 and PR, binding of PR and MED12 to PRBS, and RANKL gene expression are significantly higher in LM con

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

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

48 inhibitor of tumor necrosis factor (TNF) and RANKL trimerization, we identified four compounds (1b, 3

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

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

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

52 ent with CCL3, beta-catenin inhibitors, anti-RANKL or bisphosphonates as potential combination therap

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

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

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

56 C-PC attenuated RANKL stimulated ROS.

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

58 eceptor activator of nuclear factor-kappa B (RANKL) and of osteoprotegerin (OPG) were evaluated by im

59 eceptor activator of nuclear factor kappa-B (RANKL) and osteoprotegerin (OPG) to diagnose healthy per

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

61 OPG is incapable of binding to HS but binds RANKL normally.

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

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

64 y reduced the autophagic response induced by RANKL in osteoclast precursors (OCPs) derived from bone

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

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

67 In conclusions, RANKL deteriorates, while its inhibitor improves, muscle

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

69 1(-/-) and WT mice were cultured with M-CSF, RANKL and/or MCP-1.

70 -dependent metabolic pathway by the cytokine RANKL.

71 0 mg/kg luteolin increased OPG and decreased RANKL levels significantly.

72 clinical trials for breast cancer, decreased RANKL and M-CSF, and subsequently RANKL and M-CSF-depend

73 apoptosis of bystander osteocytes, decreased RANKL secretion, reduced osteoclast recruitment and bone

74 asma OPN levels, and significantly decreased RANKL levels.

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

76 orbing osteoclasts through osteocyte-derived RANKL is well defined, little is known about the regulat

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

78 ed bone loss was associated with a dismissed RANKL expression, decreased Th1- and Th17-type of cytoki

79 Enhanced RANKL protein expression caused by D3 and DEX was absent

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

81 tients despite increased osteocyte-expressed RANKL.

82 production of the cancer cell motile factor RANKL.

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

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

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

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

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

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

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

90 SIRT3 expression from RANKL induction depended on the transcription coactivato

91 Furthermore, RANKL could induce the phosphorylation of Bcl-2, subsequ

92 Furthermore, RANKL expression was detected on a fraction of the ILC1s

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

94 nist R5020, leading to a dramatically higher RANKL expression in LM compared to adjacent myometrial (

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

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

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

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

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

100 ntagonist) mRNA expression and a decrease in RANKL (receptor activator of nuclear factor kappa-Beta l

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

102 ssue and characterized ILC subsets including RANKL expression in single-cell suspensions using flow c

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

104 Increased RANKL expression was seen at the orthodontic tooth movem

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

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

110 Sclerostin is suggested to induce RANKL expression in osteocytes.

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

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

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

114 , 3b, 4a, and 4c) that selectively inhibited RANKL-induced osteoclastogenesis in a dose-dependent man

115 TRAF3 limits bone destruction by inhibiting RANKL-induced NF-kappaB signaling in osteoclast precurso

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

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

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

119 The receptor activator of NF-kappaB (RANKL) was recently identified as a novel progesterone/P

120 Using fluorescently labeled RANKL, we showed that, within this time frame, S100A9 in

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

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

123 activator of nuclear factor kappa B ligand (RANKL) and its antagonist osteoprotegerin (OPG) were mea

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

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

126 activator of nuclear factor kappa-B ligand (RANKL), a cytokine crucial for osteoclast differentiatio

127 activator of nuclear factor-kappa B ligand (RANKL), increased osterix(+) osteoblastic cells, and dec

128 activator of nuclear factor kappa B ligand (RANKL), macrophage colony-stimulating factor (M-CSF) and

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

130 ceptor activator of nuclear factor B ligand (RANKL), plays an essential role in regulating bone resor

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

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

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

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

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

136 tivator of nuclear factor kappa-Beta ligand (RANKL) and sclerostin (SOST) levels, osteoclastogenesis

137 tivator of nuclear factor kappa-Beta ligand (RANKL) induced osteoclastogenesis to model MGC formation

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

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

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

141 r activator of nuclear factor-kappaB ligand (RANKL) constitutes the master mediator of osteoclastogen

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

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

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

145 e to receptor activator of NF-kappaB ligand (RANKL) or the combination of RANKL and TNF.

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

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

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

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

150 r activator of nuclear factor kappaB ligand (RANKL), and osteoprotegerin (OPG) were determined by imm

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

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

153 r activator of nuclear factor kappaB ligand (RANKL), which is responsible for osteoclast differentiat

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

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

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

157 for receptor activator of NF-kappaB ligand (RANKL)-induced osteoclastogenesis.

158 activator for nuclear factor-kappaB ligand (RANKL).

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

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

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

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

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

164 Receptor activator of Nfkb ligand (RANKL) activates, while osteoprotegerin (OPG) inhibits,

165 ceptor activator of NF-kappaB (RANK) ligand (RANKL) in the presence or absence of S100A9.

166 OPG] and receptor activator of NF-KB ligand [RANKL]).

167 erminant of osteolytic activity, while a low RANKL/OPG ratio is often observed in inactive lesions.

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

169 etwork that affects progesterone/PR-mediated RANKL gene expression, with an important role in activat

170 H4R mediates RANKL expression and osteoclast differentiation induced

171 sis to examine the role of NEMO in mediating RANKL-induced signaling in mouse bone marrow macrophages

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

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

174 Proinflammatory cytokines directly modulate RANKL/OPG expression and consequently drive lesion progr

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

176 t the DMR and distal PRBS constitute a novel RANKL distal regulatory element that actively regulates

177 to, and inhibits, the receptor activator of RANKL (TNFSF11) and might affect breast cancer biology,

178 -kappaB ligand (RANKL) or the combination of RANKL and TNF.

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

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

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

182 We investigated the effects of RANKL inhibitors on muscle in osteoporotic women and mic

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

184 mber of osteoclasts and higher expression of RANKL indicated increased bone resorption in irisin lack

185 periodontitis and concomitant expression of RANKL on a fraction of the ILC1 population suggest that

186 trontium ranelate showed lower expression of RANKL than the estrogen-deficient group (P < 0.05).

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

188 teoblasts, including increased expression of RANKL, M-CSF, and osteoprotegerin (OPG).

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

190 SM-164 also inhibited expression of RANKL, which mediates interactions between metastatic BC

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

192 nitiates osteoclastogenesis independently of RANKL.

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

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

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

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

197 the most potent and less toxic inhibitors of RANKL-induced osteoclastogenesis, we synthesized a focus

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

199 lls expressed significantly higher levels of RANKL.

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

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

202 astogenesis through osteoblast production of RANKL and IL6.

203 Production of RANKL and its competitive antagonist osteoprotegerin (OP

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

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

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

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

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

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

210 nergistic interactions between DEX and D3 on RANKL and osteoclast formation were present in BMC from

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

212 lay among effector cells and their impact on RANKL/OPG balance and lesion outcome.

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

214 versed the effect of epithelial mediators on RANKL expression.

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

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

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

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

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

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

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

222 sustained exposure to parathyroid hormone or RANKL.

223 tivator of NF-kappaB ligand/osteoprotegerin (RANKL/OPG) ratio as the primary determinant of osteolyti

224 rotic women and mice that either overexpress RANKL (HuRANKL-Tg+), or lack Pparb and concomitantly dev

225 breast volume at the beginning of pregnancy, RANKL and OPG appeared to influence breast volume with a

226 ing breast volume at the start of pregnancy, RANKL, OPG, and other factors was used to predict breast

227 activated NF-kappaB RelA and RelB to promote RANKL expression and enhance bone destruction.

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

229 l tumor microenvironment, and PD-L1 promoted RANKL-induced osteoclastogenesis through JNK activation

230 fsf11, encoding the osteoclastogenic protein RANKL) in cultured osteoblasts and osteocytes from Notch

231 eptor activator of NF-kappaB ligand protein (RANKL), numbers of osteoclasts on plastic, and pit forma

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

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

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

235 RANK/RANKL signaling pathway is critical for OCL differentiat

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

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

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

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

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

241 Similarly, in vitro N2-NRR Ab reduced RANKL-induced osteoclastogenesis in PAR1 KO cells to WT

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

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

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

245 l regulatory element that actively regulates RANKL expression.

246 JNK1 regulates RANKL-induced osteoclastogenesis via activation of a nov

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

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

249 ntified lysine (K)270 as a target regulating RANKL signaling as K270A substitution results in exubera

250 nesis to model MGC formation, here we report RANKL cellular programming requires extracellular argini

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

252 ANK signaling activation in tumors and serum RANKL levels at baseline predict these immune-modulatory

253 ing bone-specific RANKL and decreasing serum RANKL.

254 elated with a significant reduction in serum RANKL levels.

255 dKO-Hom mice are correlated with lower serum RANKL and higher SOST levels that resulted in dysregulat

256 determinants of host response switch, since RANKL imprint a tolerogenic phenotype in DCs, described

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

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

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

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

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

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

263 decreased RANKL and M-CSF, and subsequently RANKL and M-CSF-dependent osteoclastogenesis of murine b

264 Despite preclinical evidence suggesting RANKL inhibition might delay bone metastasis or disease

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

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

267 discover small-molecule inhibitors targeting RANKL trimer formation.

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

269 We demonstrated that RANKL specifically upregulates LSC proliferation through

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

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

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

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

274 7/Treg imbalance could eventually arrest the RANKL-mediated alveolar bone loss.

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 Linking the RANKL/RANK/OPG pathway with breast volume changes suppor

279 PR-binding site (PRBS) 87 kb upstream of the RANKL transcription start site.

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

283 These RANKL-selective inhibitors are an excellent starting poi

284 atory (Treg) lymphocyte activity favors this RANKL overexpression.

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

286 factor superfamily [TNFSF] members TNFSF11 [RANKL], TNFSF13B [BAFF], and TNFSF14 [LIGHT]) produced b

287 of OPG, which is responsible for binding to RANKL, the exact biological functions of the three C-ter

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

289 e expression of type I IFN response genes to RANKL stimulation and thus inhibits osteoclastogenesis v

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

291 ns to limit Notch2 signaling in responses to RANKL and TNF and moderates osteoclastogenic response to

292 clast lineage cells were hyper-responsive to RANKL and showed elevated ex vivo osteoclast number and

293 ng osteoclast lineage cell responsiveness to RANKL and coupling to bone formation.

294 owers the inhibitory threshold of OPG toward RANKL.

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

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

297 inactive can originate from an unanticipated RANKL immunoregulatory feedback, involving the induction

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

299 Here, we used RANKL as a representative gene to investigate how steroi

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

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