ライフサイエンスコーパス: osteoclast formation

1 hat PAM compounds showed great inhibition of osteoclast formation.

2 their enhanced support of MM-cell growth and osteoclast formation.

3 optosis in myeloma cell lines, and increases osteoclast formation.

4 tivator for NF-kappaB ligand (RANKL)-induced osteoclast formation.

5 lear which of them are essential sources for osteoclast formation.

6 ligand, and osteoprotegerin; and up-regulate osteoclast formation.

7 sfunction, also showed higher propensity for osteoclast formation.

8 , caused osteoclast apoptosis, and inhibited osteoclast formation.

9 ment and thereby decrease MM cell growth and osteoclast formation.

10 by RNA interference abrogates tumor-induced osteoclast formation.

11 RANKL expression, accounting for a delay in osteoclast formation.

12 survival, while its overexpression decreases osteoclast formation.

13 ulating cell-fusion events involved in human osteoclast formation.

14 ment and may directly or indirectly modulate osteoclast formation.

15 a transcription factor required in OCPs for osteoclast formation.

16 Here we show an unexpected role of Btk in osteoclast formation.

17 ed medium stimulated in vitro multinucleated osteoclast formation.

18 alveolar bone loss through directly blocking osteoclast formation.

19 ner and consequently stimulate TRAP-positive osteoclast formation.

20 ow-derived PSV10 stromal cell line to induce osteoclast formation.

21 lunts the effects of TNFalpha in stimulating osteoclast formation.

22 tion in response to RANKL, thereby enhancing osteoclast formation.

23 increased osteoclast survival, not increased osteoclast formation.

24 r-kappaB (RANK) ligand (RANKL) and inhibited osteoclast formation.

25 ceptor mediates the effects of annexin II on osteoclast formation.

26 a direct target of NFATc1 in RANKL-dependent osteoclast formation.

27 at is produced by osteoclasts and stimulates osteoclast formation.

28 th healthy controls and that IL-3 stimulates osteoclast formation.

29 ucing ligand-induced apoptosis and decreased osteoclast formation.

30 timulating the production of an inhibitor of osteoclast formation.

31 EGFR signaling regulated osteoclast formation.

32 erin (OPG) and anti-TNF antibodies inhibited osteoclast formation.

33 appaB ligand (RANKL), a cytokine that drives osteoclast formation.

34 s, such as MIP-1alpha and/or IL-6, to induce osteoclast formation.

35 of cancellous bone volume and inhibition of osteoclast formation.

36 on of osteoprotegerin (OPG), an inhibitor of osteoclast formation.

37 the osteoblast lineage is a prerequisite for osteoclast formation.

38 that stellate reticulum-derived PTHrP drives osteoclast formation.

39 r activator of NF-kappaB) required to induce osteoclast formation.

40 activation of pathways that are involved in osteoclast formation.

41 teoblastic cell line (UAMS-32) that supports osteoclast formation.

42 toward alveolar bone and is associated with osteoclast formation.

43 RANK is essential in osteoclast formation.

44 in (OPG) is a secreted protein that inhibits osteoclast formation.

45 surface CSF-1 alone is sufficient to support osteoclast formation.

46 mechanistically linked to the inhibition of osteoclast formation.

47 ect bone resorption but moderately inhibited osteoclast formation.

48 ndrocytes also express RANKL/OPG and support osteoclast formation.

49 t differentiation and the ability to support osteoclast formation.

50 ), takes a role in modulating osteoblast and osteoclast formation.

51 sis of tibiae through negative regulation of osteoclast formation.

52 s, but it was linked to reduced RANKL-driven osteoclast formation.

53 to inflammatory bone loss, owing to enhanced osteoclast formation.

54 oumermycin A1 and novobiocin) did not affect osteoclast formation.

55 ression of Hsf1 enhanced 17-AAG effects upon osteoclast formation.

56 eated with RANKL or with TNFalpha to promote osteoclast formation.

57 which attenuated the effect of IL-1alpha on osteoclast formation.

58 using a unique gene footprint and to inhibit osteoclast formation.

59 nation of TRAF6, thus limiting RANKL-induced osteoclast formation.

60 ling is critical for stromal cell support of osteoclast formation.

61 to be necessary and sufficient for enhanced osteoclast formation.

62 , cytokines that exhibit opposing effects on osteoclast formation.

63 marrow macrophages attenuates RANKL-induced osteoclast formation.

64 it does not participate in RANKL-stimulated osteoclast formation.

65 TNFalpha treatment enhanced osteoclast formation 2.5-fold in HLA-B27-expressing cell

66 oclasts, a biochemical function critical for osteoclast formation, actin organization and motility.

67 an autocrine modulator of cytokine-mediated osteoclast formation/activation.

68 of normal mice evoked a striking increase in osteoclast formation, an effect dependent on RANK/RANKL

69 at TNF-alpha dysregulation leads to enhanced osteoclast formation and accelerated loss of cartilage.

70 Osteoclast formation and activation are controlled by ma

71 To analyze molecular regulation of osteoclast formation and activation, we examined the exp

72 Furthermore, rabbit osteoclast formation and activity also are inhibited by

73 Parathyroid hormone (PTH) induces osteoclast formation and activity by increasing the rati

74 ave anti-osteoclastogenic effects and reduce osteoclast formation and activity by inducing their apop

75 ondingly, MIP-1 delta significantly enhanced osteoclast formation and activity in response to RANKL i

76 Tumor necrosis factor-alpha (TNF) enhances osteoclast formation and activity leading to bone loss i

77 olysis with 2-deoxy-D-glucose (2-DG) reduced osteoclast formation and activity under both basal and h

78 factor receptor family member that inhibits osteoclast formation and activity was examined for its a

79 -deficient mice to study the role of CCR3 in osteoclast formation and activity.

80 have been implicated as factors that enhance osteoclast formation and bone destruction in patients wi

81 of marrow cells from iNOS-/- mice) increased osteoclast formation and bone pit resorption, indicating

82 osteoclastogenesis, but the role of CCR3 in osteoclast formation and bone remodeling in adult mice i

83 lts demonstrated that CFZ blocks PTH-induced osteoclast formation and bone resorption by its addition

84 that LPS P. gingivalis stimulates periosteal osteoclast formation and bone resorption by stimulating

85 RBP-J deficiency enables TNF-alpha to induce osteoclast formation and bone resorption in DAP12-defici

86 , we have prepared compounds able to inhibit osteoclast formation and bone resorption in vitro at con

87 parent compound, flurbiprofen, at inhibiting osteoclast formation and bone resorption in vitro, and t

88 ATPase) and microfilaments, and also between osteoclast formation and bone resorption in vitro.

89 toid joint destruction result from increased osteoclast formation and bone resorption induced by rece

90 In contrast, osteoclast formation and bone resorption were both reduc

91 Intriguingly, inhibiting osteoclast formation and bone resorption, and altering t

92 cessive RANKL signaling leads to superfluous osteoclast formation and bone resorption, is widespread

93 e interleukin 8 (IL-8) stimulates both human osteoclast formation and bone resorption.

94 ndings establish a critical role for CD38 in osteoclast formation and bone resorption.

95 1 alpha (HIF-1alpha) transcription factor on osteoclast formation and bone resorption.

96 to promoting bone formation, Wnt4 inhibited osteoclast formation and bone resorption.

97 ective function might cause a more excessive osteoclast formation and contribute to greater osteolysi

98 n delays RANK ligand-induced (RANKL-induced) osteoclast formation and cytoskeletal organization.

99 tivirus-mediated short hairpin RNAs inhibits osteoclast formation and decreases cellular ferrous iron

100 asts exhibit a stronger potential to support osteoclast formation and differentiation.

101 gand (RANKL) of osteoblasts is essential for osteoclast formation and differentiation.

102 We therefore establish that Lyn regulates osteoclast formation and does it in a manner antithetica

103 ppaB ligand (RANKL), cytokines essential for osteoclast formation and expressed by a variety of cell

104 d RAW264.7 cells were evaluated by analyzing osteoclast formation and expression of genes important i

105 These data suggest that Cdc42 regulates osteoclast formation and function and may represent a pr

106 Thus, SHIP negatively regulates osteoclast formation and function and the absence of thi

107 ctural determinants of the RANK that mediate osteoclast formation and function have not been definiti

108 hus, the impact of inflammatory cytokines on osteoclast formation and function was among the most imp

109 NFI-A overexpression decreased osteoclast formation and function with down-regulation o

110 The RANKL/RANK pathway is critical for both osteoclast formation and function, and these effects are

111 Motif 1, in contrast to its minimal role in osteoclast formation and function, plays a predominant r

112 eas Motif 2 and Motif 3 are highly potent in osteoclast formation and function, they exert a moderate

113 ppaB ligand (RANKL) is the key regulator for osteoclast formation and function.

114 odulators have been shown to have effects on osteoclast formation and function.

115 ber of cytokines have been shown to regulate osteoclast formation and function.

116 rk, NF-kappaB, and Akt to result in enhanced osteoclast formation and function.

117 EET564; and Motif 3, 604PVQEQG609) mediating osteoclast formation and function.

118 common HIV PIs, ritonavir and indinavir, on osteoclast formation and function.

119 and Akt signaling pathways, both critical to osteoclast formation and function.

120 QEET(559-564); and PTM6, PVQEQG(604-609)) in osteoclast formation and function.

121 ), and PVQEQG(604-609)) capable of mediating osteoclast formation and function.

122 protegerin (OPG), a protein known to inhibit osteoclast formation and function.

123 n-induced bone loss is mediated by increased osteoclast formation and function.

124 ctivator of NF-kappaB ligand (RANKL)-induced osteoclast formation and functional activity in a STAT6-

125 nding of the molecular mechanisms regulating osteoclast formation and functions and their interaction

126 All aspects of osteoclast formation and functions are regulated by macr

127 ompared to wild-type controls due to reduced osteoclast formation and increased osteoblast numbers, r

128 -kappaB activation, IKKalpha and IKKbeta, in osteoclast formation and inflammation-induced bone loss.

129 Furthermore, in vitro NAC prevented osteoclast formation and NF-kappaB activation.

130 nt impact on prostate cancer cell viability, osteoclast formation and osteoblast differentiation.

131 vivo function of chondrocyte-produced OPG in osteoclast formation and postnatal bone growth has not b

132 These results suggest that Phlpp1 suppresses osteoclast formation and production of paracrine factors

133 eoclast precursors but indirectly stimulates osteoclast formation and promotes bone resorption by sti

134 cells also offers a system for the study of osteoclast formation and regulation.

135 ydroxamate-based MMP9 inhibitor reduced both osteoclast formation and resorption activity while siRNA

136 Pathological stimulation of osteoclast formation and resorption occurs in postmenopa

137 The effects of HCT1026 on osteoclast formation and resorption were determined in v

138 differentiated into osteoclasts showed that osteoclast formation and resorptive activity were attenu

139 he medium [Na(+)] dose-dependently increased osteoclast formation and resorptive activity.

140 ense knockdown of SOCS-3 strongly suppressed osteoclast formation and significantly blunted the respo

141 TSH inhibits osteoclast formation and survival by attenuating JNK/c-j

142 echanism underlying its complex functions in osteoclast formation and survival, thus laying a foundat

143 Thus, miR-29 is a positive regulator of osteoclast formation and targets RNAs important for cyto

144 h that STAT3 is essential for gp130-mediated osteoclast formation and that the target of STAT3 during

145 rthermore, AAV-sh-Ac45 significantly reduced osteoclast formation and the expression of proinflammato

146 nderlying BMSC support of MM cell growth and osteoclast formation and therefore represents a therapeu

147 actor-kappaB ligand (RANKL) is essential for osteoclast formation and thought to be supplied by osteo

148 mpounds, 1d and 5d, suppressed RANKL-induced osteoclast formation and TRAP activity dose-dependently.

149 ss, may benefit from treatments that inhibit osteoclast formation and/or function.

150 the PRF/BCP displayed an inhibitory role in osteoclasts formation and its molecular mechanism of act

151 X-308 induced potent (60%-80%) inhibition of osteoclast formation, and a 10- to 100-fold lower concen

152 arthritis, and clinical signs of arthritis, osteoclast formation, and bone erosion were assessed.

153 four other TLR2 ligands on bone resorption, osteoclast formation, and gene expression in wild type a

154 tics of synovial inflammation, bone erosion, osteoclast formation, and growth of bony spurs was perfo

155 n on RA and mouse myeloid cell chemotaxis or osteoclast formation, and in addition, to uncover the si

156 57 also showed potent inhibitory activity on osteoclast formation, and it was confirmed by a cell via

157 issue, loss of connective tissue attachment, osteoclast formation, and loss of alveolar bone.

158 ibial and femoral metaphyses, an increase in osteoclast formation, and radiologic evidence of osteoly

159 Darc regulates BMD negatively by increasing osteoclast formation, and that the genetic association b

160 wo distinct signaling pathways; one promotes osteoclast formation, and the other, in collaboration wi

161 ption may be mediated by its effects on both osteoclast formation at an early stage and osteoclast ge

162 MIP-1alpha induced osteoclast formation at an optimal concentration of 0.05

163 Enoxacin inhibited osteoclast formation at concentrations where osteoblast

164 -culture systems by Northern blot as well as osteoclast formation at different stages of differentiat

165 XN inhibited osteoclast differentiation and osteoclast formation at the early stage.

166 cluding monocyte and macrophage recruitment, osteoclast formation, bone resorption, and cortical and

167 Our results suggest that estrogen modulates osteoclast formation both by down-regulating the express

168 ycin (17-AAG) causes bone loss by increasing osteoclast formation, but the mechanism underlying this

169 stages of osteoclast maturation to decrease osteoclast formation by 32.8%.

170 ed osteoclastogenesis and that it can induce osteoclast formation by a mechanism independent of RANKL

171 loid hematopoietic precursor cells decreases osteoclast formation by altering expression of the trans

172 Parathyroid hormone (PTH) stimulates osteoclast formation by binding to its receptor on strom

173 P. gingivalis modulates RANKL-induced osteoclast formation by differential induction of NFATc1

174 lays an important role in the suppression of osteoclast formation by IL-4 and may explain the benefic

175 mechanism whereby TRAF6 negatively regulates osteoclast formation by intracytoplasmic sequestration o

176 Inhibition of osteoclast formation by knockout Rankl in the osteocytes

177 Most resorption stimuli induce osteoclast formation by modulating RANKL gene expression

178 s of NF-kappaB and inhibits cytokine-induced osteoclast formation by osteoclast precursors.

179 activation of p55r, exogenous TNF stimulates osteoclast formation by p55r(+/+)p75r(-/-), but not p55r

180 and these fluids induced significantly less osteoclast formation compared with that of the wild-type

181 -1(-/-) mice showed decreased multinucleated osteoclast formation compared with WT mice.

182 valis differentially modulates RANKL-induced osteoclast formation contingent on the state of differen

183 e stimulatory effects of annexin II on human osteoclast formation, demonstrating that the receptor me

184 Osteoclast formation depends on the concerted action of

185 y parathyroid hormone (PTH) to undergo rapid osteoclast formation/differentiation with bone resorptio

186 IL-1 induced osteoclast formation directly from c-Fos-expressing OCPs

187 We report that RANKL and TNF can induce osteoclast formation directly from NF-kappaB p50/p52 dou

188 s (OCPs), but unlike TNF, it does not induce osteoclast formation directly from OCPs in vitro.

189 Here, we examined whether IL-1 can induce osteoclast formation directly from OCPs overexpressing c

190 uggested that RANKL-induced NO inhibition of osteoclast formation does not occur via NO activation of

191 uclear factor-kappa B ligand interaction for osteoclast formation during joint inflammation.

192 RSV notably inhibited the TNF-alpha-induced osteoclast formation, endothelial cell phenotypic change

193 endent, constitutively active TSHR abrogates osteoclast formation even under basal conditions and in

194 tant to RANK downregulation and committed to osteoclast formation, even though they retain phagocytic

195 They also support osteoclast formation from bone marrow precursors in resp

196 presence and absence of RANKL, LIGHT induced osteoclast formation from both human peripheral blood mo

197 OCPs on bone secreted IL-1, which induced osteoclast formation from c-Fos-expressing OCPs in the l

198 Human osteoclast formation from mononuclear phagocyte precurso

199 Plasma from treated rats induced osteoclast formation from normal bone marrow cells, whic

200 solated osteoclast precursors but stimulated osteoclast formation from those pretreated with RANKL in

201 L), a TNF-related molecule, is essential for osteoclast formation, function and survival through inte

202 RANKL stimulates osteoclast formation, function and survival, and each of

203 NK) and its ligand (RANKL) are essential for osteoclast formation, function, and survival.

204 B ligand (RANKL) is an essential mediator of osteoclast formation, function, and survival.

205 rast to PTHrP1-36, PTHrP1-17 does not affect osteoclast formation/function in vitro or in vivo.

206 ice, and the A(1)R antagonist DPCPX inhibits osteoclast formation (IC(50)=1 nM), with altered morphol

207 ability of osteoclast-derived EVs to inhibit osteoclast formation in 1,25-dihydroxyvitamin D3-stimula

208 alpha knockdown; HIF-2alpha siRNA increasing osteoclast formation in 3D.

209 d that the GNPs, ALD and GNPs-ALD suppressed osteoclast formation in a dose-dependent manner.

210 tion of an activity that directly stimulates osteoclast formation in a manner independent of the key

211 and impacts chondrocyte differentiation and osteoclast formation in a manner that likely requires lo

212 This locally produced TSH suppresses osteoclast formation in a negative feedback loop.

213 nd RANKL-stimulated NF-kappaB activation and osteoclast formation in an osteoclast cellular model, RA

214 BaP and TCDD enhanced osteoclast formation in bone marrow cell cultures and ga

215 NKL) produced by osteocytes is essential for osteoclast formation in cancellous bone under physiologi

216 o administration of TNF-alpha prompts robust osteoclast formation in chimeric animals in which ss-gal

217 We report that murine osteoclast formation in culture is inhibited by both lov

218 oclasts stimulate angiogenesis, we modulated osteoclast formation in fetal mouse metatarsal explants

219 Impaired osteoclast formation in fXIIIA(-/-) mice was not due to

220 dysfunction enhances phagocytic function and osteoclast formation in macrophages.

221 TSH also suppresses osteoclast formation in murine macrophages and RAW-C3 ce

222 LPS P. gingivalis and Pam2 robustly enhanced osteoclast formation in periosteal/endosteal cell cultur

223 dramatic approximately fourfold increase in osteoclast formation in response to incubation for 6 day

224 osteoblastic IL-6 production and functional osteoclast formation in the absence of osteoblasts or RA

225 Finally, osteoblast-derived VEGF stimulated osteoclast formation in the final remodeling phase of th

226 the mimetics, OP3-4, significantly inhibited osteoclast formation in vitro (IC(50) = 10 microm) and e

227 IL-37 exhibit a dose-dependent inhibition of osteoclast formation in vitro (~78.9% and 97.7% inhibiti

228 show that TNF limits RANKL- and TNF-induced osteoclast formation in vitro and in vivo by increasing

229 enhancing BMSC support of MM cell growth and osteoclast formation in vitro and in vivo.

230 molecule mimic of osteoprotegerin to inhibit osteoclast formation in vitro and limit bone loss in an

231 ghly potent in promoting osteoblast-mediated osteoclast formation in vitro, a process essential to bo

232 MM cell interactions strongly contributed to osteoclast formation in vitro, because osteoclastogenesi

233 IKKalpha is required for RANK ligand-induced osteoclast formation in vitro, it is not needed in vivo.

234 ds FSH specifically and blocks its action on osteoclast formation in vitro.

235 eased osteoclast number in vivo and impaired osteoclast formation in vitro.

236 ly in osteoclast precursors (OCPs) to induce osteoclast formation in vitro.

237 ith sense PYK2 and caused: 1) a reduction in osteoclast formation in vitro; 2) inhibition of cell spr

238 r factor kappaB (NF-kappaB), is required for osteoclast formation in vivo and mice lacking both of th

239 In contrast, TNF induced robust osteoclast formation in vivo in mice lacking RANKL or RA

240 NF-kappaB p52, nor does it appear to induce osteoclast formation in vivo in the absence of RANKL.

241 cells in varying states of TNF-alpha-driven osteoclast formation in vivo, we generated chimeric mice

242 teo-chondroprogenitor cells but also support osteoclast formation in vivo.

243 promoted 1,25-dihydroxyvitamin D3-dependent osteoclast formation in whole mouse marrow cultures, and

244 ind, in contrast to the significant level of osteoclast formation in wild type marrow, osteoclastogen

245 PGHS inhibitors caused a similar drop in osteoclast formation in wild-type cultures.

246 umor cells, and (c) tumor cells that support osteoclast formation independent of RANKL secrete other

247 This sesquiterpene also inhibited the osteoclast formation induced by human breast tumor cells

248 These data indicate that (a) osteoclast formation induced by MDA-MET breast cancer ce

249 Osteoclast formation induced by these cytokines requires

250 f these events is not sufficient to restrain osteoclast formation, inhibit resorption, or stop bone l

251 Inhibition of osteoclast formation is a potential strategy to prevent

252 Osteoclast formation is dependent on the ability of TGF-

253 ts formed in the cocultures, suggesting that osteoclast formation is mediated by osteoclast different

254 Osteoclast formation is regulated by balancing between t

255 crophage infiltration, synovial hyperplasia, osteoclast formation, joint destruction, cathepsin activ

256 migration, and tube formation and inhibited osteoclast formation, migration, and adhesion.

257 NOTCH1 and NOTCH3 collaborate in regulating osteoclast formation, NOTCH1 is the dominant paralog.

258 We examined the effect on osteoclast formation of disrupting the prostaglandin G/H

259 Also, recipients of ABB exhibited increased osteoclast formation on the alveolar bone surface and si

260 our results indicate that IFN-gamma inhibits osteoclast formation only early in osteoclast differenti

261 ion, we evaluated the effects of TGF-beta on osteoclast formation, OPG protein secretion, mRNA expres

262 pecific genes (p < 0.05) alongside decreased osteoclast formation (p < 0.0001) in inflammatory (RANKL

263 1beta (P < 0.01 ), TNF-alpha (P < 0.05), and osteoclast formation (P < 0.01) occurred in the presence

264 eoclasts within the metaphyseal bone and the osteoclast formation potential of marrow cells on day 9.

265 n, and methotrexate, also directly increased osteoclast formation, potentially in an Hsf1-dependent m

266 activity of the conditioned medium; however, osteoclast formation stimulated by conditioned medium wa

267 dition of exogenous OPG completely inhibited osteoclast formation stimulated by EGF-like ligands, whi

268 f either dominant negative protein abolished osteoclast formation stimulated by IL-6 + soluble IL-6 r

269 vated by cytokines that induce resistance to osteoclast formation, such as IFN-gamma and M-CSF, and t

270 various pathological conditions by promoting osteoclast formation, survival, and function.

271 sis, immune cell function and bone-resorbing osteoclast formation, the expression of TRAIL in human m

272 stration, indicating that osteocytes control osteoclast formation through a PPR-mediated mechanism.

273 Here we show that IFN-gamma blunts osteoclast formation through direct targeting of osteocl

274 produced by breast cancer cells that induces osteoclast formation through upregulation of RANK ligand

275 and (RANKL) and supported MM cell growth and osteoclast formation to a much lower extent than normal

276 er LIGHT can regulate RANKL/cytokine-induced osteoclast formation, to identify the mechanism by which

277 vial fibroblasts and macrophages in abnormal osteoclast formation, using the recently described BXD2

278 dicate that C-PC has the potential to reduce osteoclast formation via blocking the degradation of cyt

279 on of eNOS/Akt pathway and markedly inhibits osteoclast formation via down-regulation of ERK/c-fos an

280 Thus, PTHrP seems to regulate osteoclast formation via mediation of the DF, in a manne

281 en cells with exogenous RANKL and found that osteoclast formation was 50% lower in PGHS-2(-/-) than i

282 The decreased osteoclast formation was accompanied by down-regulated e

283 Osteoclast formation was assayed by TRAP staining and bo

284 The effect of LIGHT on human and murine osteoclast formation was assessed in the presence and ab

285 ability of recombinant MIP-1alpha to induce osteoclast formation was determined by tartrate resistan

286 rrow cells demonstrated that 17-AAG-enhanced osteoclast formation was Hsf1-dependent.

287 Human osteoclast formation was increased by MDA-MET or A549 ce

288 IL-6 than those from C57BL/6 mice, abnormal osteoclast formation was not due to enhanced sensitivity

289 In addition, increased osteoclast formation was observed when osteoclast progen

290 , observed by micro-computed tomography, and osteoclast formation were decreased in Mk2(-/-) mice com

291 ffects of endogenously produced cytokines on osteoclast formation were determined with neutralizing a

292 The effects of IL-27 on osteoclast formation were evaluated by counting the numb

293 els of prostaglandin E(2), and periarticular osteoclast formation were inhibited by turmeric extract

294 interactions between DEX and D3 on RANKL and osteoclast formation were present in BMC from mice with

295 induced a heat shock response also enhanced osteoclast formation, whereas HSP90 inhibitors that did

296 Osteoclast formation, whether stimulated by 1,25-dihydro

297 mmatory response and was a potent inducer of osteoclast formation, while P. endodontalis was not.

298 Suppression of osteoclast formation with osteoprotegerin dose-dependent

299 rom CAST binds chemokines, known to regulate osteoclast formation, with reduced affinity compared wit

300 ur data show that enoxacin directly inhibits osteoclast formation without affecting cell viability by