ライフサイエンスコーパス: RANK

1 RANK and its ligand RANKL play important roles in the de

2 RANK and RANKL, the key regulators of osteoclast differe

3 RANK expression is associated with poor prognosis in bre

4 RANK has a cytoplasmic (535)IVVY(538) (IVVY) motif that

5 RANK ligand (RANKL), a TNF-related molecule, is essentia

6 RANK ligand (RANKL), by mechanisms unknown, directly act

7 RANK overexpression in tumor cells with nonfunctional BR

8 RANK overexpression under the control of the mouse mamma

9 RANK present in EVs may function by competitively inhibi

10 RANK was constitutively expressed in the liver and was n

11 RANK was significantly expressed in ovariectomized rats

12 RANK was strongly expressed in hepatocytes and very weak

13 RANK, the receptor for RANKL, contains an IVVY(535-538)

14 RANK-Fc doses of 100 or 500 microg had no detectable eff

15 RANK-Fc doses of 100 or 500 microg were tested in a mous

16 RANK-Fc inhibition of RANKL has antiosteoclast activity

17 RANK-rich EVs may also take advantage of the RANK/RANKL

18 RANK/RANKL signaling pathway is critical for OCL differe

19 Moreover, the presence of 5 RANK(+) CTCs in the blood of patients undergoing targete

20 in reduced expression of iNOS, MMP-1 and -8, RANK, and RANKL and increased BMP-2 and OPG levels in th

21 demonstrated the superiority of denosumab, a RANK-ligand antagonist, compared to zoledronic acid in t

22 culture system suggests a role for aberrant RANK signaling during breast tumorigenesis.

23 eir collaboration, alphavbeta3 and activated RANK coprecipitate, but only in the presence of c-Src.

24 c-Src binds activated RANK via its Src homology 2 (SH2) domain and alphavbeta3

25 Thus, activated RANK prompts two distinct signaling pathways; one promot

26 During chronic immune activation, RANK ligand on activated immune cells likewise drives pa

27 expressed in primary lung tumors, an active RANK pathway correlates with decreased survival, and pha

28 VPS35 loss of function altered RANK ligand (RANKL)-induced RANK distribution, enhanced

29 enesis, reveal a cross talk between A2AR and RANK signaling in osteoclastogenesis, and uncover an unr

30 nd metastatic tumors revealed that ABCB5 and RANK subpopulations are more common among CTCs than in t

31 Whereas CD40 and RANK represent key examples, interplay between these rec

32 ependent upon both miR-142-3p expression and RANK-signaling, with no harmful effects detected in the

33 thereby limiting crosstalk between ITAM and RANK/TNFR signaling and allowing fine tuning of osteocla

34 e tumor xenografts reduced proliferation and RANK expression while maintaining EGFR expression.

35 s implicated the TNF family members RANK and RANK-Ligand (RANKL) in the development of Aire-expressin

36 subsets of luminal progenitors (RANK(+) and RANK(-)) in histologically normal tissue of BRCA1-mutati

37 aspects of the interactions between TLR and RANK signaling and provide a new model for understanding

38 resses the activation of both RANK-TRAF6 and RANK-FcRgamma/Syk signaling pathways because of activati

39 Denosumab, an anti-RANK ligand monoclonal antibody, significantly increases

40 aimed to investigate the effects of the anti-RANK ligand antibody denosumab in postmenopausal, aromat

41 KL and its receptor TNFRSF11A (also known as RANK) contribute to mammary tumorigenesis, we investigat

42 receptors and heterologous receptors such as RANK, and they identify a mechanism by which IL-10 can s

43 eceptor activator of nuclear factor kappa B (RANK) ligand, with zoledronic acid in delaying or preven

44 eceptor activator of nuclear factor-kappa B (RANK)-RANK ligand (RANKL)-osteoprotegerin (OPG) axis.

45 eceptor activator of nuclear factor kappa-B (RANK) ligand on osteoblasts drives OC differentiation by

46 racytoplasmic sequestration of FHL2 to blunt RANK activation and as a component of a transcription co

47 DJ-1 suppresses the activation of both RANK-TRAF6 and RANK-FcRgamma/Syk signaling pathways beca

48 IKKalpha activation by RANK ligand (RANKL/TNFSF11) inhibits Maspin expression i

49 clear abundance is specifically increased by RANK ligand (RANKL).

50 The effect of RANKL inhibition by RANK-Fc on osteoclast function was determined by inhibit

51 Induction of effective osteoclastogenesis by RANK (receptor activator of NF-kappaB) requires costimul

52 acid phosphatase (TRAP) activity produced by RANK-L-stimulated osteoclast precursors.

53 TNFRSF11A (also called RANK) is considered to be the sole receptor for RANKL.

54 RANK to bind RANKL and suppresses canonical RANK signaling during osteoclast differentiation.

55 s indicate that VPS35 critically deregulates RANK signaling, thus restraining increased formation of

56 NK Venus reporter mice, we identify distinct RANK(+) subsets that reside within both the mTEC(hi) and

57 id organ formation and organization, express RANK and undergo hyperproliferation, which is abrogated

58 differentiation of myeloid cells expressing RANK, we assessed the capacity of wild-type T cells and

59 Flow cytometry analysis showed fewer RANK-expressing cells in the marrow of Col2a1-Opg mice,

60 Overexpression of RANK (FL-RANK) in a panel of tumoral and normal human mammary cel

61 ates NF-kappaB and AP-1 activation following RANK ligand (RANKL) stimulation.

62 We show that B cells deficient for RANK undergo normal development and do not show any obvi

63 Taken together, PLCgamma2 is essential for RANK signaling, and its deficiency leads to defective ly

64 ew rapidly induced costimulatory pathway for RANK signaling that is dependent on TREM-2 and mediated

65 tion of M-CSF signaling that is required for RANK expression.

66 2-dependent calcium signals are required for RANK-mediated activation of calcium/calmodulin-dependent

67 These data uncover a direct role for RANK in lung cancer and may explain why female sex hormo

68 ocarcinomas, suggesting additional roles for RANK signaling beyond its hormone-dependent function.

69 trolling the differentiation of M cells from RANK-expressing intestinal epithelial precursor cells.

70 Furthermore, RANK(369-373) is the only one of six putative TRAF bindi

71 Using newly generated RANK Venus reporter mice, we identify distinct RANK(+) s

72 es not stimulate NK reactivity, we generated RANK-Fc fusion proteins with modified Fc moieties.

73 thologic grade and proliferation index; high RANK/RANKL expression was significantly associated with

74 However, RANK expression is enriched in hormone receptor negative

75 the current study, we sought to determine if RANK and RANKL were important in the hepatic response to

76 tact site on the TNFR is partly conserved in RANK.

77 ed osteoclastogenesis and bone resorption in RANK-deficient mice.

78 Indeed, RANK signalling in mammary carcinoma cells that overexpr

79 -leukemia reactivity of NK cells and induced RANK expression, and NK cells of AML patients displayed

80 function altered RANK ligand (RANKL)-induced RANK distribution, enhanced RANKL sensitivity, sustained

81 IL-10 inhibited RANK-induced osteoclastogenesis and selectively inhibite

82 Mechanisms that inhibited RANK expression were down-regulation of RANK transcripti

83 ow that when PGE(2) production is inhibited, RANK-L production is decreased.

84 Osteoprotegerin (OPG) inhibits RANK signaling by sequestering RANKL.

85 FN-beta upregulation, which in turn inhibits RANK signaling and facilitates AIRE expression in mTECs.

86 t, with CD40 upregulation induced by initial RANK signaling subsequently controlling proliferation wi

87 iation of early mesenchymal progenitors into RANK-expressing pre-osteoclasts.

88 receptor activator of nuclear factor kappaB (RANK) ligand but attach to substrate and migrate poorly,

89 receptor activator of nuclear factor kappab (RANK) ligand-expressing proT2-cells induce changes in bo

90 receptor activator of nuclear factor kappaB (RANK) signaling, providing an explanation for AMPK-media

91 receptor activator of nuclear factor kappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) we

92 receptor activator of nuclear factor kappaB (RANK)-mediated osteoclastogenesis.

93 receptor activator of nuclear factor kappaB (RANK).

94 receptor activator of nuclear factor-kappaB (RANK) are integrated by TAK1 in DCs, which in turn media

95 receptor activator of nuclear factor-kappaB (RANK) in calcified aortic valves.

96 receptor activator of nuclear factor-kappaB (RANK) ligand (RANKL) and inhibited osteoclast formation.

97 receptor activator of nuclear factor-kappaB (RANK) ligand (RANKL) and lymphotoxin.

98 receptor activator of nuclear factor-kappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) si

99 receptor activator of nuclear factor-kappaB (RANK), RANK-ligand (RANKL), osteoprotegerin (OPG), and o

100 receptor activator of nuclear factor-kappaB (RANK), soluble RANK ligand (sRANKL), osteoprotegerin (OP

101 in RANKL or receptor activator of NF-kappaB (RANK) also lead to strong B cell defects in mice and hum

102 c domain of receptor activator of NF-kappaB (RANK) and is an essential component of the signaling com

103 Receptor activator of NF-kappaB (RANK) and its ligand (RANKL) are essential for osteoclas

104 eraction of receptor activator of NF-kappaB (RANK) and its ligand (RANKL) promotes NF-kappaB activati

105 Activating receptor activator of NF-kappaB (RANK) and TNF receptor (TNFR) promote osteoclast differe

106 is context, receptor activator of NF-kappaB (RANK) ligand (RANKL) plays a pivotal role in lymphoid ti

107 ntly of the receptor activator of NF-kappaB (RANK) ligand (RANKL), others demonstrated that TNF-media

108 equires the receptor activator of NF-kappaB (RANK) ligand (RANKL).

109 Receptor activator for NF-kappaB (RANK) ligand stimulation results in IFN-beta upregulatio

110 f M-CSF and receptor activator of NF-kappaB (RANK) ligand.

111 ing through receptor activator of NF-kappaB (RANK) pathway mediates the expansion of mammary epitheli

112 Receptor activator of NF-kappaB (RANK) plays a critical role in osteoclastogenesis, an es

113 tion of the receptor activator of NF-kappaB (RANK) signaling pathway, which is critical for OC develo

114 endently of receptor activator of NF-kappaB (RANK) signaling.

115 omplex with receptor activator of NF-kappaB (RANK), the tyrosine phosphatase, SHP-1, and the adapter

116 pression of receptor activator of NF-kappaB (RANK), thereby making precursor cells refractory to the

117 ness of the receptor activator of NF-kappaB (RANK), which is central for mTEC differentiation, defici

118 mediated by receptor activator of NF-kappaB (RANK)-ligand in the bone microenvironment.

119 Both the receptor activator for NF-kappaB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) axis and

120 ctivated by receptor activator of NF-kappaB (RANK/TNFRSF11A), in mammary epithelial proliferation dur

121 271, and receptor activator of NF-kappabeta (RANK) in individual circulating tumor cells (CTCs) from

122 the receptor activator of nuclear factor-kB (RANK), the key regulator of osteoclastogenesis, is frequ

123 blockade of the receptor activator of NF-kB (RANK)-RANK ligand and B cell-activating factor-APRIL (a

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

125 activator of nuclear factor kappa B ligand (RANK-L) due to pro-inflammatory cytokines, and the simul

126 The receptor activator of NF-kappaB ligand (RANK-L) also failed to induce the expression of Cyp1 enz

127 Receptor activator of NF-kappaB ligand (RANK-L) and prostaglandin E(2) (PGE(2)) are two such mol

128 r activator of nuclear factor kappaB-ligand (RANK-L).

129 rdinated cross talks between the RANK ligand/RANK and IRF7/IFN-beta/IFNAR/STAT1 pathways are essentia

130 rgy between cross-linking B7-DC and ligating RANK was observed.

131 Mechanistically, RANK rewires energy homeostasis in human and murine lung

132 h its role as a suppressor of TRAF6-mediated RANK signaling, TRAF6/RANK association is enhanced in FH

133 t work has implicated the TNF family members RANK and RANK-Ligand (RANKL) in the development of Aire-

134 s-Polyoma Middle T (MMTV-PyMT), which mimics RANK and RANKL expression patterns seen in human breast

135 -function (mouse mammary tumour virus (MMTV)-RANK transgenic mice) and loss-of function (pharmacologi

136 cultures of primary mammary cells from MMTV-RANK mice with RANKL results in increased proliferation

137 mmary tumour formation were observed in MMTV-RANK transgenic mice after multiparity or treatment with

138 only in hormone- and carcinogen-treated MMTV-RANK and wild-type mice, but also in the MMTV-neu transg

139 Moreover, RANK signaling in tumor cells negatively regulates the e

140 the aegis of two critical cytokines, namely RANK ligand and M-CSF.

141 stablishment of the family Euctenizidae (NEW RANK); (2) establishment of the subfamily Apomastinae wi

142 es implicated in osteoclastogenesis (NFATc1, RANK, costimulatory receptors, and immunoreceptor tyrosi

143 These data suggest that RANK(+) and not RANK(-) progenitors are a key target population in these

144 t occurs during pregnancy, and activation of RANK pathway promotes mammary tumorigenesis in mice.

145 Osteoclastogenesis requires activation of RANK signaling as well as costimulatory signals from imm

146 e, inhibited the RANKL-induced activation of RANK-dependent signaling in RAW 264.7 cells but had no e

147 In vitro, the activation of RANK-dependent signals is enhanced in DJ-1-deficient BMM

148 evaluation was combined with the analysis of RANK/RANKL loop activation in the leukemic clone, given

149 cular level, XN disrupted the association of RANK and TRAF6, resulted in the inhibition of NF-kappaB

150 Concentrations of RANK, sRANKL, OPG, and sclerostin were significantly inc

151 Depletion of RANK-rich EVs relieved the ability of osteoclast-derived

152 nant cells could be blocked by disruption of RANK-RANKL interaction with denosumab.

153 A single dose of RANK-Fc > or =100 microg suppressed elevation of serum c

154 e osteoclasts were depleted by high doses of RANK-Fc (500 and 1000 microg) or 100 microg of OPG-Fc.

155 is mediates this effect by downregulation of RANK and c-Fms, the receptors for the essential osteocla

156 ly inhibited calcium signaling downstream of RANK by inhibiting transcription of TREM-2.

157 tivation of signaling pathways downstream of RANK were measured by immunoblotting.

158 MAP kinase signaling pathways downstream of RANK, a receptor that plays a central role in the differ

159 crophages and their activation downstream of RANK.

160 ated with IFN-gamma to inhibit expression of RANK and of the CSF1R gene that encodes c-Fms, and to sy

161 of NFATc1, down-regulated the expression of RANK and triggering receptor expressed on myeloid cells

162 cts were mediated by enhancing expression of RANK in osteoclast progenitor cells and by upregulating

163 Expression of RANK, TRAP, cathepsin K, calcitonin receptor, matrix met

164 osteoclast differentiation and expression of RANK.

165 Although the signaling and function of RANK have been investigated extensively, much less is kn

166 Mammary glands of RANK- and RANKL-deficient mice develop normally during s

167 c1-driven osteoclastogenesis, independent of RANK ligand, which disrupts normal bone homeostasis lead

168 ore, ATF4 was crucial for M-CSF induction of RANK expression on BMMs, and lack of ATF4 caused a shift

169 Similar but less robust inhibition of RANK expression was observed in murine cells.

170 s demonstrate that therapeutic inhibition of RANK signaling drastically reduces the cancer stem cell

171 Inhibition of RANK using the approved drug denosumab may be a therapeu

172 In this work, we studied the involvement of RANK-RANKL interaction in NK cell-mediated immunosurveil

173 eta-blocker propranolol, and by knockdown of RANK expression in MDA-231 cells.

174 ng also suppressed mRNA expression levels of RANK and c-fms in bone upon unloading.

175 ues showed significantly increased levels of RANK and cathepsin-K in mucositis.

176 High levels of RANK in untransformed MCF10A cells induce changes associ

177 High levels of RANK were found in human primary breast adenocarcinomas

178 osteoblasts will express increased levels of RANK-L and PGE(2).

179 als from this cell promote the maturation of RANK-expressing CD80(-)Aire(-) mTEC progenitors into CD8

180 hich also stimulated pulmonary metastasis of RANK(+) human breast cancer cells.

181 e dose of 0, 10, 100, 500, or 1000 microg of RANK-Fc; 100 microg of OPG-Fc; or 5 microg of zoledronat

182 Overexpression of RANK (FL-RANK) in a panel of tumoral and normal human ma

183 Collectively, our study defines patterns of RANK expression within the thymus medulla, and it shows

184 ent initiation showed that the percentage of RANK(+) CTCs significantly increased in the patients und

185 itory factors by AML cells and prevention of RANK signaling into NK cells.

186 ereby osteoblasts regulate the production of RANK-L during infection.

187 ited RANK expression were down-regulation of RANK transcription, and inhibition of M-CSF signaling th

188 ith Traf6, a critical cytosolic regulator of RANK-L-regulated osteoclast development.

189 Here, to explore the role of RANK signaling once tumors have developed, we use the mo

190 gery or at reperfusion to assess the role of RANK/RANKL signaling during I/R injury.

191 In addition, spheroids of RANK overexpressing MCF10A cells display disrupted acina

192 competitively inhibiting the stimulation of RANK on osteoclast surfaces by RANKL similar to osteopro

193 teopetrosis with severity similar to that of RANK or RANKL deficient mice.

194 +)Aire(+) mTECs, and that transplantation of RANK-deficient thymic stroma into immunodeficient hosts

195 bone inflammation-the osteoprotegerin (OPG)-RANK-RANKL system or osteopontin (OPN)-play a role in th

196 We conclude that the OPG-RANK-RANKL system and the OPN system play important role

197 The OPG-RANK-RANKL system plays the principal role in determinin

198 tasis could be mediated by regulation of OPG/RANK/RANKL/MMP-9 signaling, resulting in the inhibition

199 Our findings introduce Fc-optimized RANK-Ig fusion proteins as attractive tools to neutraliz

200 The osteoclastogenesis triggered by BaP or RANK-L was reduced in Ahr(-/-) cells, consistent with th

201 t formation in vivo in mice lacking RANKL or RANK when the mice also lacked NF-kappaB p100, and TNF-T

202 tion was observed by adding osteoprotegerin, RANK:Fc, TNFalpha, or interleukin-8 or by blocking the L

203 s with decreased survival, and pharmacologic RANK inhibition reduces tumor growth in patient-derived

204 entified two subsets of luminal progenitors (RANK(+) and RANK(-)) in histologically normal tissue of

205 r activator of nuclear factor-kappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) signaling

206 r activator of nuclear factor kappaB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) were also

207 r activator of nuclear factor-kappaB (RANK), RANK-ligand (RANKL), osteoprotegerin (OPG), and osteocal

208 r activator of nuclear factor-kappa B (RANK)-RANK ligand (RANKL)-osteoprotegerin (OPG) axis.

209 de of the receptor activator of NF-kB (RANK)-RANK ligand and B cell-activating factor-APRIL (a prolif

210 the receptor activator for NF-kappaB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) axis and expre

211 tor of nuclear factor kappa-B ligand (RANKL)-RANK-osteoprotegerin (OPG) signaling associated with bon

212 dicates that the cognate receptor for RANKL, RANK, is expressed in prostate cancer cells, suggesting

213 We therefore examined whether RANKL, RANK and IKK-alpha are also involved in mammary/breast c

214 RANKL-RANK signaling regulates numerous physiologic processes

215 osis and suggest that the targeting of RANKL-RANK can be used in conjunction with the therapeutic eli

216 of the negative regulatory circuit of RANKL-RANK signaling in osteoclastogenesis and that the augmen

217 ce and human patients, suggesting that RANKL-RANK inhibition could interfere with B cell physiology a

218 hese data point to a novel role of the RANKL-RANK axis in the regulation of B cell homeostasis and hi

219 ects in B cell number, the role of the RANKL-RANK axis on B physiology is still a matter of debate.

220 Our data indicate that ablation of the RANKL-RANK pathway has no direct adverse effect on B cell phys

221 In addition to the RANKL-RANK-OPG signaling axis, other factors produced by osteo

222 tions linking hIFN-gamma+ Th1 cells to RANKL-RANK/OPG signaling for periodontal osteoclastogenesis in

223 ss this key question--that is, whether RANKL-RANK signaling affects B cell physiology directly or the

224 amounts of RANKL, thereby activating a RANKL/RANK autocrine loop that determines sustained giant cell

225 CT-R+ cathepsin-k+ functional OC in a RANKL/RANK-dependent manner.

226 of RelB-expressing FAE enterocytes by RANKL/RANK induces the EMT-regulating transcription factor Slu

227 osteoclastogenic potential upstream of RANKL/RANK signaling, suggesting that immature CD11c+ DC can i

228 ATc1 is the sole critical regulator of RANKL/RANK-dependent osteoclast activation.

229 teoprotegerin (OPG) signaling pathway (RANKL/RANK/OPG signaling) is implicated in the osteolysis asso

230 Our data provide direct evidence that RANKL/RANK/OPG signaling is modulated in patients with CN and

231 The RANKL/RANK pathway is critical for both osteoclast formation a

232 st differentiation, independent of the RANKL/RANK signaling axis.

233 stic cell fusion and activation by the RANKL/RANK/OPG and ATP-P2RX7-IL1 pathways; and (3) regulatory

234 an RANKL and its rodent counterpart receptor RANK.

235 RANKL and its receptor RANK are downstream effectors of the progesterone signal

236 of NF-kappaB ligand (RANKL) and its receptor RANK are the key regulators for bone remodeling and for

237 RANKL and its receptor RANK control the proliferation of mammary lobuloalveolar

238 erentiation by interaction with its receptor RANK on OC precursors.

239 of NF-kappaB ligand (RANKL) to its receptor RANK on osteoclast (OC) precursors up-regulates c-Fos an

240 l transduction including RANKL, its receptor RANK, and the downstream remodeling enzyme cathepsin K (

241 of NF-kappaB ligand (RANKL) and its receptor RANK.

242 rvival through interaction with its receptor RANK.

243 examination of HER2 and NF-kappaB receptor (RANK) coexpression revealed increased levels of both pro

244 L-suppression of its own signaling receptor (RANK) in the mammary epithelium.

245 tes osteoclastogenesis through its receptor, RANK, and the signaling adaptor TRAF6.

246 r NF-kappaB ligand (RANKL) and its receptors RANK and osteoprotegerin are key regulators of bone remo

247 Furthermore, CYLD negatively regulated RANK signaling by inhibiting TRAF6 ubiquitination and ac

248 Immunogold labeling showed RANK was enriched in 1 in every 32 EVs isolated from ost

249 tor of nuclear factor-kappaB (RANK), soluble RANK ligand (sRANKL), osteoprotegerin (OPG), cathepsin-K

250 osteopetrosis--we generated B cell-specific RANK knockout mice.

251 ANKL and epidermal LC expressed cell surface RANK.

252 tage of the RANK/RANKL interaction to target RANK-rich EVs to RANKL-bearing cells for the delivery of

253 egulation of osteoclastogenesis that targets RANK expression and limits bone resorption during infect

254 We demonstrate in this paper that RANK trafficking, signaling, and function are regulated

255 Here we show that RANK and RANKL are expressed within normal, pre-malignan

256 Together, our findings show that RANK promotes tumor initiation, progression, and metasta

257 Here, we show that RANK protein expression is strictly regulated in a spati

258 e of BRCA1-mutation carriers and showed that RANK(+) cells are highly proliferative, have grossly abe

259 These results suggest that RANK expression in primary breast cancer associates with

260 Our data suggest that RANK in EVs may be mechanistically linked to the inhibit

261 These data suggest that RANK(+) and not RANK(-) progenitors are a key target pop

262 The data suggest that RANK/RANKL may be a viable therapeutic target in acute l

263 udy provide evidence for the first time that RANK-L mRNA and protein and PGE(2) expression are upregu

264 The RANK IVVY motif, which has been previously shown to comm

265 The RANK receptor for RANKL is expressed by epithelial cells

266 The infection alters the RANK/RANKL/OPG signalling dynamics that regulates osteob

267 , we found that expression of TFAP2B and the RANK inhibitor, OPG, in human breast cancer correlate an

268 mporally coordinated cross talks between the RANK ligand/RANK and IRF7/IFN-beta/IFNAR/STAT1 pathways

269 Fos, partly via C/EBPalpha regulation by the RANK (535)IVVY(538) motif.

270 e pathology arising due to imbalances in the RANK/RANKL/OPG molecular pathway, and due to the progres

271 her the c-Src SH2 or SH3 domain obviates the RANK/alphavbeta3 association.

272 othesis, SH2(N+C) abrogated formation of the RANK-Gab2 complex, which mediates NF-kappaB and AP-1 act

273 unravel a previously unknown function of the RANK-RANKL molecule system in AML pathophysiology as wel

274 options are likely to have regulation of the RANK-RANKL-OPG axis as their goal.

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

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

277 els, manipulated to induce activation of the RANK/RANKL pathway in the absence of strict hormonal con

278 Recent findings indicate that the RANK and NF-kappaB pathways are aberrantly activated in

279 evious data to human cells and show that the RANK pathway promotes the development of mammary stem ce

280 can promote lung cancer progression via the RANK pathway.

281 pro-apoptotic mechanism activated within the RANK signalosome.

282 An enhancement of osteoclastogenesis through RANK-RANKL signaling results in an expansion of the TBI,

283 teoclastogenesis and bone resorption through RANK/TRAF6 signaling pathways.

284 these results suggest that signaling through RANK not only promotes proliferation but also inhibits t

285 , TRAF2, TRAF5, MAP3K7 (TAK1) and TNFRSF11A (RANK)) regulators of NF-kappaB.

286 or with denosumab (a monoclonal antibody to RANK ligand) reduces risk for skeletal events in men wit

287 aB ligand (RANKL) that blocks its binding to RANK, inhibiting the development and activity of osteocl

288 inhibits TNF-alpha-induced activity bound to RANK ligand (RANKL).

289 ,5) abundance and desensitizes precursors to RANK ligand-stimulated differentiation.

290 orylation, and modulated GAB2 recruitment to RANK.

291 nerates preosteoclasts that are resistant to RANK downregulation and committed to osteoclast formatio

292 layed no changes in p65*(536) in response to RANK-L, but levels rapidly increased after the cells wer

293 ssor of TRAF6-mediated RANK signaling, TRAF6/RANK association is enhanced in FHL2-/- osteoclasts.

294 a exhibited low levels of Cathepsin K, TRAP, RANK, and tumor necrosis factor receptor-associated fact

295 tial formation of Aire(+) mTECs depends upon RANK signaling, continued mTEC development to the involu

296 patients displayed significantly upregulated RANK expression compared with healthy controls.

297 epwise process of mTEC development, in which RANK is a master player in controlling the availability

298 RANKL induces c-Src to associate with RANK(369-373) in an alphavbeta3-dependent manner.

299 LGR4 competes with RANK to bind RANKL and suppresses canonical RANK signali

300 cell proliferation in vitro correlated with RANK expression and was impaired by Denosumab-mediated d

301 ry signals are regulated and integrated with RANK signaling.