ライフサイエンスコーパス: osteoclast differentiation

1 lation of MITF at Ser-307 by p38 MAPK during osteoclast differentiation.

2 proteins, we determined the role of EPAC in osteoclast differentiation.

3 steoblasts, HDAC4 is a critical regulator of osteoclast differentiation.

4 miR-34a is downregulated during osteoclast differentiation.

5 (Ki16425, Debio0719, and VPC12249) inhibited osteoclast differentiation.

6 or osteoclast precursors, suggesting altered osteoclast differentiation.

7 pathways are utilized at different stages of osteoclast differentiation.

8 from NF-kappaB activated LNCaP cells induce osteoclast differentiation.

9 ts as a negative regulator of RANKL-mediated osteoclast differentiation.

10 mechanisms employed by BMP signaling during osteoclast differentiation.

11 p family protein that is up-regulated during osteoclast differentiation.

12 t miR-29 controls the tempo and amplitude of osteoclast differentiation.

13 n and function of different FcgammaRs during osteoclast differentiation.

14 egative regulatory factors in RANKL-mediated osteoclast differentiation.

15 oblasts that can control both osteoblast and osteoclast differentiation.

16 itrullination of vimentin was induced during osteoclast differentiation.

17 role of A(2A) receptor in the regulation of osteoclast differentiation.

18 predominant bioenergetic pathway to support osteoclast differentiation.

19 iptional repressors such as IRF-8 that block osteoclast differentiation.

20 tf, a transcription factor, is necessary for osteoclast differentiation.

21 ectin-induced inhibition in RANKL-stimulated osteoclast differentiation.

22 aB ligand) expression, which then stimulates osteoclast differentiation.

23 xpression program leading to cell fusion and osteoclast differentiation.

24 little is known about the role HDACs play in osteoclast differentiation.

25 loid differentiation factor 88 in modulating osteoclast differentiation.

26 gnaling, and an increase in apoptosis during osteoclast differentiation.

27 a direct and novel role of Tie2 signaling in osteoclast differentiation.

28 ctional disruption of Notch signaling during osteoclast differentiation.

29 tion in promoting macrophage recruitment and osteoclast differentiation.

30 ovide a new mechanism of inhibition of human osteoclast differentiation.

31 ) in osteoblasts and subsequently potentiate osteoclast differentiation.

32 ng, which, in turn, inhibited RANKL-mediated osteoclast differentiation.

33 cts as a negative regulator of RANKL-induced osteoclast differentiation.

34 ds to defective lymph node organogenesis and osteoclast differentiation.

35 lusively demonstrate that osteoblasts direct osteoclast differentiation.

36 ited myeloma cell-induced tube formation and osteoclast differentiation.

37 r, member 2 (SLC4A2), is up-regulated during osteoclast differentiation.

38 exhibited severe osteopetrosis and impaired osteoclast differentiation.

39 d the critical interaction of these genes in osteoclast differentiation.

40 (Ctsk) and acid phosphatase 5 (Acp5) during osteoclast differentiation.

41 s at the promoters during terminal stages of osteoclast differentiation.

42 of NF-kappaB ligand (RANKL) signaling during osteoclast differentiation.

43 ed kinase 1 and IKK and to cause spontaneous osteoclast differentiation.

44 like cells were treated with RANKL to induce osteoclast differentiation.

45 eoclastogenic cytokine, causes the increased osteoclast differentiation.

46 ed by Flt-1, which was down-regulated during osteoclast differentiation.

47 NFATc1 in human beta3 integrin expression in osteoclast differentiation.

48 ice are osteopenic with evidence of enhanced osteoclast differentiation.

49 oth in vivo and in vitro and plays a role in osteoclast differentiation.

50 appaB (RANK) and TNF receptor (TNFR) promote osteoclast differentiation.

51 ion of bone matrix remodeling enzymes during osteoclast differentiation.

52 ay and provide a mechanism for BMP-2-induced osteoclast differentiation.

53 al role in transducing signals from RANKL in osteoclast differentiation.

54 MITF in the absence of signals required for osteoclast differentiation.

55 H) receptor (TSHR), TSH negatively regulates osteoclast differentiation.

56 one microenvironment to promote specifically osteoclast differentiation.

57 ession of the CaR plays an important role in osteoclast differentiation.

58 bined with RANKL had no additional effect on osteoclast differentiation.

59 c proteins (BMPs) are important mediators of osteoclast differentiation.

60 AMPs for the NLRP3 inflammasome and regulate osteoclast differentiation.

61 n cxcr3.2 prevent macrophage recruitment and osteoclast differentiation.

62 d positive regulators, NFATc1 and miR182, of osteoclast differentiation.

63 r LTB4R1 (BLT1) in synovial inflammation and osteoclast differentiation.

64 axis to drive metabolic reprogramming during osteoclast differentiation.

65 ed that MYO10 is also expressed early during osteoclast differentiation.

66 nflammation, angiogenesis, tumor growth, and osteoclast differentiation.

67 ress from inflamed sites and is required for osteoclast differentiation.

68 the expression or activation of STAT5 during osteoclast differentiation.

69 role of STAT5 in IL-3-mediated inhibition of osteoclast differentiation.

70 d suppresses canonical RANK signaling during osteoclast differentiation.

71 aB ligand (RANKL), an essential cytokine for osteoclast differentiation.

72 on using antisense oligonucleotides, impeded osteoclast differentiation.

73 esis Irf8 by DNA methylation is required for osteoclast differentiation.

74 c gene activation concomitant with defective osteoclast differentiation.

75 the IREalpha/XBP1-mediated arm of the UPR in osteoclast differentiation.

76 actor-kappaB ligand (RANKL) is essential for osteoclast differentiation, activation, and survival.

77 the effectiveness of C-PC as an inhibitor of osteoclast differentiation, activity, and survival in vi

78 ty while siRNA targeting MMP9 also inhibited osteoclast differentiation although had little effect on

79 RANK and RANKL, the key regulators of osteoclast differentiation and activation, also play an

80 paB ligand (RANKL), which is responsible for osteoclast differentiation and activation.

81 ence of Nlrp3 and Caspase-1 in Rankl-induced osteoclast differentiation and activity and on LPS-induc

82 defines a key regulatory node that controls osteoclast differentiation and activity downstream of RA

83 In vitro, IL-33 treatment inhibited osteoclast differentiation and activity even in the pres

84 Regulation of osteoclast differentiation and activity is important for

85 transgenic mice affects both osteoblast and osteoclast differentiation and activity.

86 xpression as well as the effects of IL-33 on osteoclast differentiation and activity.

87 y play a pivotal role in the control of both osteoclast differentiation and apoptosis in the systems

88 t facilitates bone colonization by fostering osteoclast differentiation and bone degradation and also

89 parib treatment or PARP1/2 deletion promotes osteoclast differentiation and bone loss.

90 These results indicate that RvE1 modulates osteoclast differentiation and bone remodeling by direct

91 requirement for costimulatory signaling for osteoclast differentiation and bone remodeling.

92 or osteoprotegerin are the key regulators of osteoclast differentiation and bone remodeling.

93 ce with arthritis, a significant increase in osteoclast differentiation and bone resorption was obser

94 t together with MCP-1, it could also promote osteoclast differentiation and bone resorption.

95 gest a novel role for this DLX-3 mutation in osteoclast differentiation and bone resorption.

96 a previously unrecognized role in promoting osteoclast differentiation and bone resorption.

97 togenesis model, PPI-2458 potently inhibited osteoclast differentiation and bone resorption.

98 ppa-B ligand (RANKL), a cytokine crucial for osteoclast differentiation and bone resorption.

99 ond RANKL receptor that negatively regulates osteoclast differentiation and bone resorption.

100 on leads to low bone mass owing to augmented osteoclast differentiation and bone resorption.

101 asts and osteoclasts to suppress PTH-induced osteoclast differentiation and bone resorption.

102 These defects are the result of impaired osteoclast differentiation and compromised receptor acti

103 rsors, we hypothesized that MDSC may undergo osteoclast differentiation and contribute to enhanced bo

104 th a genetic deficiency of CYLD had aberrant osteoclast differentiation and developed severe osteopor

105 elevated homocysteine, hypoxia, coagulation, Osteoclast differentiation and endochondral ossification

106 show that Wnt5a secreted by ATL cells favors osteoclast differentiation and expression of RANK.

107 In BMMs, spleen cells, and RAW264.7 cells, osteoclast differentiation and formation stimulated by M

108 from patients with DSS, we observed reduced osteoclast differentiation and function (demineralizatio

109 A(2A) receptor agonist, CGS21680, inhibited osteoclast differentiation and function (half maximal in

110 Forced expression of NUMBL inhibits osteoclast differentiation and function as evident by re

111 provide new molecular mechanisms controlling osteoclast differentiation and function by the miRNA sys

112 a highlight SLC4A2 as a critical mediator of osteoclast differentiation and function in vitro and in

113 species production, and markedly facilitated osteoclast differentiation and function in vitro.

114 ti-resorptive properties, directly impairing osteoclast differentiation and function through a seroto

115 ng in maintaining bone quality by regulating osteoclast differentiation and function through cAMP/PKA

116 es was evaluated by immunoassay, while human osteoclast differentiation and function were assessed vi

117 ly of transcription factors is regulation of osteoclast differentiation and function, which in turn c

118 uman T lymphocyte RANKL production and human osteoclast differentiation and function.

119 suggests a new mechanism for the control of osteoclast differentiation and function.

120 rapies calls for a holistic understanding of osteoclast differentiation and function.

121 t these three factors have critical roles in osteoclast differentiation and function.

122 ression of the M-CSFR, which is critical for osteoclast differentiation and function.

123 at MYC drives metabolic reprogramming during osteoclast differentiation and functions as a metabolic

124 We conclude that Cx37 is required for osteoclast differentiation and fusion, and its absence l

125 2ME(2) also suppresses osteoclast differentiation and induces apoptosis of matu

126 a critical mechanism that limits TNF-induced osteoclast differentiation and inflammatory bone resorpt

127 mily, Limd1, is uniquely up-regulated during osteoclast differentiation and interacts with Traf6, a c

128 ption factor (MITF) is required for terminal osteoclast differentiation and is a signaling effector e

129 ption factor (MITF) is required for terminal osteoclast differentiation and is a target for signaling

130 6-deficient monocytes rescues RANKL-mediated osteoclast differentiation and LPS-stimulated interleuki

131 oclast progenitor survival, but its roles in osteoclast differentiation and mature osteoclast functio

132 tor activator of NF-kappaB ligand-stimulated osteoclast differentiation and may regulate bone turnove

133 or of nuclear factor kappaB ligand-dependent osteoclast differentiation and MMP-9 secretion.

134 Conversely, NUMBL-null BMMs, show increased osteoclast differentiation and mRNA expression of osteoc

135 receptor activator of NF-kappaB-independent osteoclast differentiation and nuclear accumulation of t

136 In mouse and human, XN inhibited osteoclast differentiation and osteoclast formation at t

137 logical or pathological functions, including osteoclast differentiation and osteoporosis.

138 steoblast differentiation sets the stage for osteoclast differentiation and overall promotes osteolys

139 We previously reported that IL-3 inhibits osteoclast differentiation and pathological bone loss.

140 ands secreted by breast cancer cells promote osteoclast differentiation and potentiate the activity o

141 , an alternative P2Y12 antagonist, inhibited osteoclast differentiation and promoted osteoblast diffe

142 on, which increases PI(4,5)P(2), also delays osteoclast differentiation and reduces cell number but i

143 Osteoclast differentiation and resorption activity was e

144 irisin including upregulation of markers for osteoclast differentiation and resorption, as well as os

145 in bone marrow-derived precursors disrupted osteoclast differentiation and selectively repressed tra

146 odontal pathogen Porphyromonas gingivalis on osteoclast differentiation and show that P. gingivalis d

147 NF-kappaB signaling is essential for osteoclast differentiation and skeletal homeostasis.

148 eby OA/Gpnmb acts as a negative regulator of osteoclast differentiation and survival but not function

149 IKKalpha or IKKbeta resulted with defective osteoclast differentiation and survival.

150 rrow and spleen, which resulted in increased osteoclast differentiation and systemic bone loss.

151 at CCR3 deficiency influences osteoblast and osteoclast differentiation and that it is associated wit

152 the DCSTAMP gene has an established role in osteoclast differentiation and the associations seen bet

153 ty, IL-6 must signal in osteoblasts to favor osteoclast differentiation and the release of bioactive

154 The pre-osteoclast cell pool, osteoclast differentiation, and bone resorption in respo

155 F target gene promoters Acp5 and Ctsk during osteoclast differentiation, and FUS knockdown abolished

156 r lymphoid organogenesis, B cell maturation, osteoclast differentiation, and inflammation in mammals(

157 Iron is essential for osteoclast differentiation, and iron overload in a varie

158 e in cellular proliferation, monocyte cells, osteoclast differentiation, and matrix degradation.

159 ed with inflammation, affects osteoblast and osteoclast differentiation, and may play a role in IRR.

160 he mechanisms that regulate all the steps of osteoclast differentiation are not entirely known.

161 We examined osteoclast differentiation as the number of primary muri

162 JQ1 is a potent inhibitor of osteoblast and osteoclast differentiation as well as bone tumour develo

163 icantly reduces CIA monocyte recruitment and osteoclast differentiation as well as potent joint monoc

164 d T cells c1 (NFATc1), a master regulator of osteoclast differentiation, as well as reduced expressio

165 nized role for Dim1 as a master modulator of osteoclast differentiation, as well as the molecular mec

166 the LTB4 pathway in bone loss, we performed osteoclast differentiation assays by stimulating with M-

167 , and NFATc1, suggesting that Tak1 regulates osteoclast differentiation at multiple stages via multip

168 not immediate, peaking 2 days after inducing osteoclast differentiation both in vivo and in vitro.

169 tivation sustains proliferation but prevents osteoclast differentiation, both causing osteopetrosis.

170 Knockdown of HIF-1alpha did not affect osteoclast differentiation but prevented the increase in

171 one destruction not only relies on increased osteoclast differentiation, but also on the presence of

172 promote Rankl expression in osteoblasts and osteoclast differentiation by enhancing cyclic adenosine

173 osteoclastogenesis and show that MTX induces osteoclast differentiation by generating a pro-osteoclas

174 Moreover, JQ1 also inhibits osteoclast differentiation by interfering with BRD4-depe

175 c expression of Dim1 decreases RANKL-induced osteoclast differentiation by silencing NFATc1 and its t

176 gulated during osteoclastogenesis suppresses osteoclast differentiation by targeting important osteoc

177 showed that Hh signaling indirectly induced osteoclast differentiation by upregulating osteoblast ex

178 ntrast, beta-catenin heterozygosity enhances osteoclast differentiation, causing osteoporosis.

179 arrow cells rendered a 5-fold lower level of osteoclast differentiation compared with Cx37(+/+) cell

180 synovial fluid-driven monocyte migration and osteoclast differentiation compared with each factor alo

181 56) in congenital hypothyroid mice activates osteoclast differentiation, confirming once again our pr

182 lear accumulation of NFATc1 and consequently osteoclast differentiation consistent with the ability o

183 s, miR-16 and miR-378, which are elevated in osteoclast differentiation, correlate with bone metastas

184 more potent in osteoblast proliferation and osteoclast differentiation culture systems, as well as i

185 Remarkably, osteoclast differentiation did not occur in MDSC isolate

186 Pharmacological activation of RXRs inhibited osteoclast differentiation due to the formation of RXR/l

187 strate that Gsalpha signaling also regulates osteoclast differentiation during bone modeling and remo

188 by mRNA expression of genes associated with osteoclast differentiation, enhanced osteoclast number,

189 minal binding protein) and Sin3A, but during osteoclast differentiation, Eos association with Ctsk an

190 gene deletion experiments in mice, that the osteoclast differentiation factor RANKL promotes lysosom

191 g serum IL-6 was found on chromosome 14 near osteoclast differentiation factor Tnfsf11.

192 h receptor activator of NF-kappaB ligand, an osteoclast differentiation factor, they did not complete

193 factor (m-CSF), critical osteoblast-derived osteoclast differentiation factors.

194 inant LRRc17 protein inhibited RANKL-induced osteoclast differentiation from bone marrow precursors,

195 ; ectopic NFATc1 expression rescues impaired osteoclast differentiation from deletion of RGS10; phosp

196 re, we investigated the effects of S100A9 on osteoclast differentiation from human CD14(+) circulatin

197 The alarmin S100A9 hampers osteoclast differentiation from human circulating precur

198 Histamine and Th17 cytokines induced the osteoclast differentiation from monocytes and JNJ7777120

199 Osteoclast differentiation from monocytes was unaffected

200 We conclude that NF-kappaB controls early osteoclast differentiation from precursors induced direc

201 currently unknown whether, besides increased osteoclast differentiation from undifferentiated precurs

202 appaB ligand (RANKL) plays a crucial role in osteoclast differentiation, function, and survival.

203 Bisphosphonates inhibit osteoclast differentiation/function via inhibition of Ra

204 MiRNA profiling of monocyte-to-osteoclast differentiation identified miR-142-3p as a mi

205 and Jag1 in a direct manner, and influences osteoclast differentiation in a non-cell-autonomous fash

206 tor(s) shed by tumor-derived MT1-MMP enhance osteoclast differentiation in a RANKL-dependent manner.

207 n of PPAR-gamma by rosiglitazone exacerbates osteoclast differentiation in a receptor-dependent manne

208 a dominant negative TCF4 not only increases osteoclast differentiation in a tumor-bone co-culture sy

209 osteoblast differentiation without affecting osteoclast differentiation in bone.

210 In vitro, irisin (2-10 ng/mL) increased osteoclast differentiation in C57BL/6J mouse bone marrow

211 n the present study, effects of retinoids on osteoclast differentiation in cultured mouse bone marrow

212 TRAP-staining revealed no osteoclast differentiation in EPAC1/2-KO cells.

213 skolin treatment increased pCREB and rescued osteoclast differentiation in Gnas(+/p-) by reducing Nfa

214 a modulator of Ca(2+)-induced NFAT-dependent osteoclast differentiation in inflammatory bone loss.

215 nd examined the effects on bone modeling and osteoclast differentiation in mice.

216 eloid progenitors prior to the initiation of osteoclast differentiation in response to the appropriat

217 n IKKbeta-null osteoclast OCPs and to rescue osteoclast differentiation in the absence of IKKbeta thr

218 promising OXPHOS, but nonetheless diminishes osteoclast differentiation in vitro.

219 in explants and in vivo but did not decrease osteoclast differentiation in vitro.

220 t osteoblasts lacking Cnb1 failed to support osteoclast differentiation in vitro.

221 of inflammatory cytokines and could increase osteoclast differentiation in vitro.

222 llular domain (ECD) binds RANKL and inhibits osteoclast differentiation in vivo.

223 t all miR-29 family members increased during osteoclast differentiation, in concert with mRNAs for th

224 c1 induces Nur77 expression at late stage of osteoclast differentiation; in turn, Nur77 transcription

225 at Fzd8 and beta-catenin negatively regulate osteoclast differentiation independent of osteoblasts an

226 ovel function of PDGF-D in the regulation of osteoclast differentiation, independent of the RANKL/RAN

227 H4R mediates RANKL expression and osteoclast differentiation induced by histamine and Th17

228 It inhibits the osteoclast differentiation induced by ovariectomy in the

229 te target that is highly up-regulated during osteoclast differentiation induced by the cytokine recep

230 Among the diverse cytokines involved in osteoclast differentiation, interleukin (IL)-3 inhibits

231 The reduction of osteoclast differentiation is associated with activation

232 During bone homeostasis, osteoblast and osteoclast differentiation is coupled and regulated by m

233 the mechanism by which tumor cells influence osteoclast differentiation is crucial for improving trea

234 anism underlying IL-3-mediated inhibition of osteoclast differentiation is not fully understood.

235 Osteoclast differentiation is regulated by transcription

236 Furthermore, IL-3 inhibited RANKL-induced osteoclast differentiation less effectively in the STAT5

237 is increased relative to the wild type, and osteoclast differentiation markers are expressed at earl

238 ession correlates with impaired induction of osteoclast differentiation markers in response to RANKL

239 strogen agonist reduced RANKL stimulation of osteoclast differentiation markers or its down-regulatio

240 Talin1-deficient precursors normally express osteoclast differentiation markers when exposed to M-CSF

241 sts and their expression of mRNA for several osteoclast differentiation markers, whereas ES significa

242 steoblast activity and concurrently impaired osteoclast differentiation, maturation and functionality

243 ine- and chemokine-related pathways but also osteoclast differentiation may be involved in the effect

244 45L) mutant protein into the RAW 264.7 mouse osteoclast differentiation model.

245 Using mouse bone marrow and RAW264.7 osteoclast differentiation models we found that HSP90 in

246 that Fbn1(mgR/mgR) osteoblasts stimulate pre-osteoclast differentiation more than wild-type cells.

247 ctivator of NF-kappaB ligand (RANKL)-induced osteoclast differentiation occurred via the inhibition o

248 (A1R, A2AR, A2BR, and A3R) on osteoblast and osteoclast differentiation of cells derived from patient

249 ofylline and A2BR agonist BAY60-6583 inhibit osteoclast differentiation of cells from patients with M

250 e bone microenvironment as a requirement for osteoclast differentiation of MDSC.

251 r of NF-kappaB ligand (RANKL) and can induce osteoclast differentiation of myeloid cells expressing R

252 ls from both humans and mice promoted robust osteoclast differentiation of myeloid cells.

253 a2 but not PLCgamma1 restores RANKL-mediated osteoclast differentiation of PLCgamma2-deficient bone m

254 es on these and other molecules that mediate osteoclast differentiation or function and thus serve as

255 Tofacitinib did not impact human osteoclast differentiation or function, but did decrease

256 the action of transcriptional regulators of osteoclast differentiation or is under the control of a

257 ical inhibition of glycolysis did not affect osteoclast differentiation or viability, it efficiently

258 increased phagocytic activity, and a greater osteoclast differentiation potential at suboptimal RANK-

259 ur data show that S100A9 impedes monocyte-to-osteoclast differentiation, probably via a reduction in

260 Thus, NEMO governs survival and osteoclast differentiation programs through serial regul

261 osteoclastogenesis in D2J mice and increased osteoclast differentiation rates ex vivo, marked by incr

262 Here we show that the osteoclast differentiation receptor RANK(4,5) couples fe

263 ation abilities of patDp/+ osteoblasts while osteoclast differentiation remained unchanged compared t

264 d with increased macrophage infiltration and osteoclast differentiation, respectively.

265 n (OPG), positive and negative regulators of osteoclast differentiation, respectively.

266 tion in the bone microenvironment stimulates osteoclast differentiation, resulting in uncoupling of r

267 oss significantly due to APR's inhibition on osteoclast differentiation shown in our in vitro studies

268 pid progress has been made in characterizing osteoclast differentiation signaling pathways, how recep

269 However, in the absence of RANKL and osteoclast differentiation, STAT6 binds the TRAP promote

270 t amino acid 536 (p65*(536)) plays a role in osteoclast differentiation stimulated by receptor activa

271 d that exposure to S100A9 during monocyte-to-osteoclast differentiation strongly decreased the number

272 We conclude that SR-A plays a role in normal osteoclast differentiation, suggesting a novel role for

273 hich preferentially binds to ACVR1, promotes osteoclast differentiation, suggesting ACVR1 is involved

274 binding of Cbl to PI3K negatively regulates osteoclast differentiation, survival, and signaling even

275 PAC2 are critical signaling intermediates in osteoclast differentiation that permit RANKL-stimulated

276 ulated a concentration-dependent increase in osteoclast differentiation that was receptor activator o

277 The c-Kit W(sh) mutation increased osteoclast differentiation, the number of committed oste

278 To characterize the OBs' ability to support osteoclast differentiation, the OBs from TIEG(+/+) and T

279 acting in concert to promote RANKL-dependent osteoclast differentiation, thereby creating an imbalanc

280 myeloid differentiation, which orchestrates osteoclast differentiation through activation of DNAX ac

281 cellular pathway that integrates the UPR and osteoclast differentiation through activation of the IRE

282 ncy causes trabecular bone loss by enhancing osteoclast differentiation through enhanced TNFalpha sig

283 thought to be the major player in regulating osteoclast differentiation through expressing RANKL/OPG

284 trichostatin A and sodium butyrate, suppress osteoclast differentiation through multiple mechanisms.

285 lasts, demonstrating that osteocytes control osteoclasts differentiation through Nrp-1 and Grn which

286 ity of differentiated osteoblasts to inhibit osteoclast differentiation; thus, they broaden our knowl

287 rs that integrate CSF-1/RANKL signals during osteoclast differentiation to initiate expression of tar

288 10 dramatically increased the sensitivity of osteoclast differentiation to RANKL signaling; the defic

289 est that Pax6 interferes with RANKL-mediated osteoclast differentiation together with Grg6.

290 eripheral blood B and T cells did not induce osteoclast differentiation, unless they were activated i

291 tion-calcineurin-NFATc1 signaling pathway in osteoclast differentiation using an in vivo model.

292 e, indicate that cellular stress can enhance osteoclast differentiation via Hsf1-dependent mechanisms

293 (ChIPac-seq) to an established cell model of osteoclast differentiation, we discovered that H3NT prot

294 Joint destruction and osteoclast differentiation were lower in MKK6(-/-), as w

295 EPAC1/2 stimulation significantly increased osteoclast differentiation, whereas EPAC1/2 inhibition d

296 ored the ability of TIEG(-/-) OBs to support osteoclast differentiation, whereas M-CSF alone or combi

297 pression similar to HDAC inhibitors inhibits osteoclast differentiation, whereas osteoclasts suppress

298 IL-4 is known to inhibit the RANKL-induced osteoclast differentiation while at the same time promot

299 to osteoblastic lesion formation by blocking osteoclast differentiation, while also contributing to o

300 ANs in osteoclast precursor cells attenuated osteoclast differentiation, while their overexpression i

301 acrophages from Dicer-deficient mice rescued osteoclast differentiation with up-regulation of PU.1 le