ライフサイエンスコーパス: osteoclast formation

1 , caused osteoclast apoptosis, and inhibited osteoclast formation.

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

3 by RNA interference abrogates tumor-induced osteoclast formation.

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

5 survival, while its overexpression decreases osteoclast formation.

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

7 ment and may directly or indirectly modulate osteoclast formation.

8 a transcription factor required in OCPs for osteoclast formation.

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

10 ed medium stimulated in vitro multinucleated osteoclast formation.

11 ner and consequently stimulate TRAP-positive osteoclast formation.

12 mechanistically linked to the inhibition of osteoclast formation.

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

14 lunts the effects of TNFalpha in stimulating osteoclast formation.

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

16 increased osteoclast survival, not increased osteoclast formation.

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

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

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

20 at is produced by osteoclasts and stimulates osteoclast formation.

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

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

23 ucing ligand-induced apoptosis and decreased osteoclast formation.

24 timulating the production of an inhibitor of osteoclast formation.

25 t differentiation and the ability to support osteoclast formation.

26 EGFR signaling regulated osteoclast formation.

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

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

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

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

31 of cancellous bone volume and inhibition of osteoclast formation.

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

33 the osteoblast lineage is a prerequisite for osteoclast formation.

34 that stellate reticulum-derived PTHrP drives osteoclast formation.

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

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

37 toward alveolar bone and is associated with osteoclast formation.

38 RANK is essential in osteoclast formation.

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

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

41 ns of ATP (20-200 microM) reduced or blocked osteoclast formation.

42 Sp-1 and increased M-CSF gene expression and osteoclast formation.

43 there is insufficient to induce substantial osteoclast formation.

44 sis of tibiae through negative regulation of osteoclast formation.

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

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

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

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

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

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

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

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

53 to be necessary and sufficient for enhanced osteoclast formation.

54 , cytokines that exhibit opposing effects on osteoclast formation.

55 marrow macrophages attenuates RANKL-induced osteoclast formation.

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

57 hat PAM compounds showed great inhibition of osteoclast formation.

58 activation of pathways that are involved in osteoclast formation.

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

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

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

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

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

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

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

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

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

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

69 Osteoclast formation and activation are controlled by ma

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

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

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

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

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

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

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

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

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

79 umber of known inhibitory factors that block osteoclast formation and bone resorption are limited.

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

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

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

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

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

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

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

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

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

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

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

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

92 that OIP-1 is a novel, specific inhibitor of osteoclast formation and bone resorption.

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

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

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

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

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

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

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

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

101 sphatase activity plays an important role in osteoclast formation and function and is a putative mole

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

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

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

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

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

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

108 ndicating that estrogen negatively regulates osteoclast formation and function, but how it does this

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 ating factor (M-CSF) is essential for murine osteoclast formation and its role in human hematopoiesis

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

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

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

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

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

133 Pathological stimulation of osteoclast formation and resorption occurs in postmenopa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 57 also showed potent inhibitory activity on osteoclast formation, and it was confirmed by a cell via

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

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

154 direct cell-to-cell contact is critical for osteoclast formation, and suggest that differential regu

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

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

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

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

159 Enoxacin inhibited osteoclast formation at concentrations where osteoblast

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

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

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

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

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

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

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

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

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

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

170 e ability of estrogen deficiency to increase osteoclast formation by enhancing stromal cell productio

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

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

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

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

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

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

177 -1(-/-) mice showed decreased multinucleated osteoclast formation compared with WT mice.

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

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

180 Osteoclast formation depends on the concerted action of

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

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

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

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

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

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

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

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

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

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

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

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

193 Human osteoclast formation from mononuclear phagocyte precurso

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

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

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

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

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

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

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

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

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

203 n occurred (0.2-2 microM), ATP also enhanced osteoclast formation in 10 day mouse marrow cultures, by

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

205 nd to induce substantial bone resorption and osteoclast formation in a dose-responsive and time-depen

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

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

208 , markedly impaired their ability to support osteoclast formation in a mouse coculture model of osteo

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

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

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

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

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

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

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

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

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

218 ent fails to block M-CSF mRNA expression and osteoclast formation in ovariectomized mice lacking Egr-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 Osteoclast formation induced by these cytokines requires

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

247 Inhibition of osteoclast formation is a potential strategy to prevent

248 Osteoclast formation is dependent on the ability of TGF-

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

250 Osteoclast formation is regulated by balancing between t

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

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

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

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

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

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

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

258 1beta (P < 0.01 ), TNF-alpha (P < 0.05), and osteoclast formation (P < 0.01) occurred in the presence

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

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

261 with the known role of IL-1alpha and IL-6 in osteoclast formation provide insight into the mechanism

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 Osteoclast formation was assayed by TRAP staining and bo

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

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

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

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

283 Comparable osteoclast formation was not detected in cultures of nor

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

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

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

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

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

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

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

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

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

293 Suppression of osteoclast formation with osteoprotegerin dose-dependent

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

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