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

1 wed that Hdac7 suppresses Runx2 activity and osteoblast differentiation.

2 cerbated osteoclast activation and defective osteoblast differentiation.

3 ession of Runx2, the earliest determinant of osteoblast differentiation.

4 involved in wound healing, angiogenesis, and osteoblast differentiation.

5 identify pathways responsible for decreased osteoblast differentiation.

6 roles in skeletal development by regulating osteoblast differentiation.

7 -bp sequence that mediates responsiveness to osteoblast differentiation.

8 d to uncover osteogenic miRs of interest for osteoblast differentiation.

9 organization of the Runx2-P1 promoter during osteoblast differentiation.

10 nd Schnurri-2, which have been implicated in osteoblast differentiation.

11 /beta-catenin interactions are necessary for osteoblast differentiation.

12 osphatase and osterix that are necessary for osteoblast differentiation.

13 rs in a large number of processes, including osteoblast differentiation.

14 PI 3-kinase)/Akt signaling by BMP-2 leads to osteoblast differentiation.

15 MP-2-down-regulated miRNA, as a regulator of osteoblast differentiation.

16 contributor to the cell-cell contact-induced osteoblast differentiation.

17 ependent osteocalcin (Ocn) transcription and osteoblast differentiation.

18 h expression and for its paracrine effect on osteoblast differentiation.

19 ix protein that is a critical determinant of osteoblast differentiation.

20 -34) is significantly induced by BMP2 during osteoblast differentiation.

21 , B3 receptors on the osteoblast to suppress osteoblast differentiation.

22 ic pathway by which these microRNAs regulate osteoblast differentiation.

23 ion of Sost, Wnt-beta-catenin signaling, and osteoblast differentiation.

24 PS patients, was associated with an abnormal osteoblast differentiation.

25 s been extensively studied in the context of osteoblast differentiation.

26 pression and show that BRD4 is essential for osteoblast differentiation.

27 ption factor required for bone formation and osteoblast differentiation.

28 sion of ATF4-dependent Ocn transcription and osteoblast differentiation.

29 ion as well as Wnt-induced proliferation and osteoblast differentiation.

30 of Runx2, a transcription factor integral to osteoblast differentiation.

31 hannel and gap junction activities inhibited osteoblast differentiation.

32 luding the MEKK2 signaling pathway, inducing osteoblast differentiation.

33 of Dkk2 mRNA, which plays a role in terminal osteoblast differentiation.

34 Tcf reporter activity, and promotes terminal osteoblast differentiation.

35 n Fgf2(-/-) bone marrow stromal cells during osteoblast differentiation.

36 bone destruction in mice, but also inhibits osteoblast differentiation.

37 s, plays an essential role in the control of osteoblast differentiation.

38 vation of stress-induced p38 MAPK leading to osteoblast differentiation.

39 ctin isoforms and the mediating receptors in osteoblast differentiation.

40 ed in a regulatory circuit that can modulate osteoblast differentiation.

41 lls to and in the bone matrix, and inhibited osteoblast differentiation.

42 is a negative regulator of BMP signaling and osteoblast differentiation.

43 B2 by the cluster miRs during progression of osteoblast differentiation.

44 y and number as well as a cofactor promoting osteoblast differentiation.

45 ling cascade to regulate gene expression and osteoblast differentiation.

46 dly reduced bone mass secondary to defective osteoblast differentiation.

47 d us to investigate the effects of LOX-PP on osteoblast differentiation.

48 get genes such as Runx 2, a key modulator of osteoblast differentiation.

49 g to a gene expression program important for osteoblast differentiation.

50 expressed in osteoblasts and is required for osteoblast differentiation.

51 ce revealed that BDNF knockdown can suppress osteoblast differentiation.

52 miRs that are up-regulated through stages of osteoblast differentiation.

53 the well characterized multistage process of osteoblast differentiation.

54 activates alpha4beta1 integrin and augments osteoblast differentiation.

55 on of a large number of genes while inducing osteoblast differentiation.

56 lding and cross-linking; mineralisation; and osteoblast differentiation.

57 differentiation may occur at the expense of osteoblast differentiation.

58 smic acetyl-CoA levels impairs Wnt3a-induced osteoblast differentiation.

59 eloma, and TSP1-TGF-beta activation inhibits osteoblast differentiation.

60 d Gsalpha and Gq/11 act downstream of PTH on osteoblast differentiation.

61 Our data suggest that ANO5 plays a role in osteoblast differentiation.

62 tenin must be precisely regulated for normal osteoblast differentiation.

63 ls to secrete an inhibitor of PTH-stimulated osteoblast differentiation.

64 suppression of which is sufficient to induce osteoblast differentiation.

65 cer cell viability, osteoclast formation and osteoblast differentiation.

66 n Wnt signaling and subsequent inhibition of osteoblast differentiation.

67 and KDM8 are the candidate KDMs required for osteoblast differentiation.

68 ppaB ligand (RANKL)-binding peptide promotes osteoblast differentiation.

69 Fbw7alpha restored Runx2 levels and promoted osteoblast differentiation.

70 otubules by pretreatment with Taxol inhibits osteoblast differentiation.

71 ates the mTORC2-Akt signaling cascade during osteoblast differentiation.

72 lso led to reduced Runx2 transactivation and osteoblast differentiation.

73 Here, an early marker of osteoblast differentiation, alkaline phosphatase, is ide

74 NAs interact with signaling molecules during osteoblast differentiation, allowing for fine-tuning of

75 production, which, in addition to enhancing osteoblast differentiation, also stimulates osteoprotege

76 nscription factor responsible for regulating osteoblast differentiation (ALSPAC: P = 5.8 x 10(-4); Au

77 factors crucial for skeletal development and osteoblast differentiation among those significantly upr

78 ological inhibition of PI3K activity reduced osteoblast differentiation and abolished Wnt regulatory

79 Lithium chloride also increased osteoblast differentiation and activity in vitro in agre

80 s and bone mineral density through increased osteoblast differentiation and activity.

81 sion corresponds with distinct events during osteoblast differentiation and affects bone development

82 ts demonstrated that PKD1 contributes to the osteoblast differentiation and bone development via elev

83 , we investigated whether miRs implicated in osteoblast differentiation and bone formation are involv

84 ription factor Osterix (Osx) is required for osteoblast differentiation and bone formation during emb

85 IL-3 also enhances osteoblast differentiation and bone formation from mesen

86 Alg2 suppressed osteoblast differentiation and bone formation in culture

87 ngly demonstrated that JMJD3 is required for osteoblast differentiation and bone formation in mice.

88 erentiation in vitro, its role as a whole in osteoblast differentiation and bone formation in vivo re

89 ctivity and cooperated with RUNX2 to promote osteoblast differentiation and bone formation in vivo.

90 ur findings suggest that FGF2 stimulation of osteoblast differentiation and bone formation is mediate

91 e show that p38 activity in myeloma inhibits osteoblast differentiation and bone formation, but also

92 ors Runx2 and Osx (Osterix) are required for osteoblast differentiation and bone formation.

93 -specific transcription factor essential for osteoblast differentiation and bone formation.

94 growth factor 2 (FGF2) positively modulates osteoblast differentiation and bone formation.

95 and calcium transport play a key role during osteoblast differentiation and bone formation.

96 e) develop osteopenia associated with normal osteoblast differentiation and bone formation.

97 of Gsalpha in osteoblasts, PTH can stimulate osteoblast differentiation and bone formation.

98 been identified as an essential regulator of osteoblast differentiation and bone formation.

99 nt regulatory roles for type XII collagen in osteoblast differentiation and bone matrix formation.

100 Osx) is a transcription factor essential for osteoblast differentiation and bone mineralization.

101 eletion of Jmjd3 resulted in severe delay of osteoblast differentiation and bone ossification in mice

102 g are compromised in their ability to induce osteoblast differentiation and consequently are ineffici

103 we determined that this loop is required for osteoblast differentiation and embryonic skeletal format

104 acetylase inhibitors (HDIs) promote terminal osteoblast differentiation and extracellular matrix prod

105 directs cells within the bone marrow toward osteoblast differentiation and favors the maintenance of

106 P. gingivalis lipids inhibited osteoblast differentiation and fluorescence expression o

107 how that the DeltaF508-CFTR mutation impairs osteoblast differentiation and function as a result of o

108 pha,25-dihydroxyvitamin D3 (1,25 (OH)2D3) on osteoblast differentiation and function differ significa

109 ued Wnt target gene expression and corrected osteoblast differentiation and function in bone marrow s

110 ta-catenin signaling can rescue the abnormal osteoblast differentiation and function induced by the p

111 Osteoblast differentiation and function were not affecte

112 5 proteins at levels appropriate for optimal osteoblast differentiation and function, at least in par

113 The latter is part of a broad defect in osteoblast differentiation and function, which also resu

114 /beta-catenin pathway, which is critical for osteoblast differentiation and function.

115 their overexpression in osteoblasts enhanced osteoblast differentiation and function.

116 that the DeltaF508-CFTR mutation alters both osteoblast differentiation and function.

117 d tissues and that the influence of ENPP1 on osteoblast differentiation and gene expression may inclu

118 Here, we show that miR-218 is induced during osteoblast differentiation and has potent osteogenic pro

119 aematopoietic cells stimulate proliferation, osteoblast differentiation and inhibit senescence of MSC

120 nase signaling in mesenchymal cells enhances osteoblast differentiation and inhibits chondrocyte diff

121 but EZH2 expression declines during terminal osteoblast differentiation and matrix production.

122 Thus, NHERF1 is required for normal osteoblast differentiation and matrix synthesis.

123 t essential for the subsequent inhibition of osteoblast differentiation and mineralization in long-te

124 Similarly, osteoblast differentiation and mineralization were delay

125 Therefore, an agomir of miR-874-3p induced osteoblast differentiation and mineralization.

126 opment of the bone lineage itself, including osteoblast differentiation and morphogenetic outgrowth,

127 Osteoblast differentiation and morphology was assessed b

128 tional regulators that control self-renewal, osteoblast differentiation and negative Bmp autoregulati

129 tnatally revealed that Osx was essential for osteoblast differentiation and new bone formation in gro

130 uired for mesoderm- and neural crest-derived osteoblast differentiation and normal skeletal developme

131 In bone, it is known to regulate osteoblast differentiation and osteoclast activity.

132 and bone loss, but only ASC feeding restores osteoblast differentiation and prevents their dysplastic

133 hondrocytes co-express genes associated with osteoblast differentiation and produce extensive mineral

134 aN is only detectable in the later stages of osteoblast differentiation and promotes osteogenesis in

135 hat PEDF counters Wnt signaling to allow for osteoblast differentiation and provides a mechanistic in

136 mma alters the balance between adipocyte and osteoblast differentiation and provides checkpoint regul

137 defective canonical Wnt signaling, impaired osteoblast differentiation and reduced bone mineralizati

138 rest both in marrow and spleen and increased osteoblast differentiation and reduced ubiquitin-mediate

139 insulin signaling in the osteoblast ensures osteoblast differentiation and stimulates osteocalcin pr

140 for ARID2-containing complexes in promoting osteoblast differentiation and supports a view that the

141 tion, a reverse signal by ephrinB1 inhibited osteoblast differentiation and suppressed BSP gene expre

142 Blocking EZH2 activity promotes osteoblast differentiation and suppresses adipogenic dif

143 ysis, we inferred that Bicc1 was involved in osteoblast differentiation and that polycystic kidney di

144 agents enhanced parathyroid hormone-induced osteoblast differentiation and the ability to support os

145 iguanide group, has been shown to facilitate osteoblast differentiation and thus may exhibit a favora

146 steoblast progenitors reversed the increased osteoblast differentiation and, by boosting accumulation

147 tion with and inhibition of ERK activity and osteoblast differentiation, and knockin of a mutation in

148 we find that miR-29a is necessary for human osteoblast differentiation, and miR-29a is increased dur

149 n control convergent or divergent effects on osteoblast differentiation, and osteoclastogenesis may a

150 miRNAs (except miR-218) significantly impede osteoblast differentiation, and their effects can be rev

151 rs indicates that Vegfa-dependent effects on osteoblast differentiation are mediated by Vegf receptor

152 lying PKD1-mediated the bone development and osteoblast differentiation are not fully understood.

153 (NCEs) that have shown BMP-2 stimulation and osteoblast differentiation are reported.

154 Satb2 is critical for osteoblast differentiation as a special AT-rich binding

155 Parbendazole stimulates osteoblast differentiation as indicated by increased alk

156 et2 silencing prevents Sp7 expression during osteoblast differentiation as it impairs DNA demethylati

157 combinant Saa3 protein functionally inhibits osteoblast differentiation as reflected by reductions in

158 hypertrophic chondrocyte differentiation and osteoblast differentiation as well as the initiation of

159 knockdown significantly impaired AA-induced osteoblast differentiation, as detected by reduced expre

160 eoblast proliferation, but strongly promoted osteoblast differentiation, as reflected by stimulation

161 activation in MSCs contributes to decreased osteoblast differentiation associated with RA and sugges

162 ated signaling but resulted in inhibition of osteoblast differentiation at an early step that precede

163 a regulator of perichondrial vascularity and osteoblast differentiation at early stages of bone devel

164 or two periods of bone formation, to promote osteoblast differentiation before birth, and control bon

165 y identified the A2BAR as a new regulator of osteoblast differentiation, bone formation, and fracture

166 m cells from NHERF1-null mice showed limited osteoblast differentiation but enhanced adipocyte differ

167 y produced ephrin B1 mediates its effects on osteoblast differentiation by a novel molecular mechanis

168 naturally occurring isothiocyanate, promotes osteoblast differentiation by epigenetic mechanisms.

169 appears to be a new regulator that promotes osteoblast differentiation by functioning as an ER Ca(2+

170 hancer-binding protein 3 (Hivep3) suppresses osteoblast differentiation by inducing proteasomal degra

171 n factor Runx2 controls bone development and osteoblast differentiation by regulating expression of a

172 Glucose uptake favors osteoblast differentiation by suppressing the AMPK-depen

173 ADAR1 regulates osteoblast differentiation by, at least in part, modulat

174 ing factors, RANKL and PTHrP, even after the osteoblast differentiation ceases and apoptosis sets in.

175 velengths were more effective in stimulating osteoblast differentiation compared to 660 nm and 810 nm

176 Despite enhanced osteoblast differentiation, coupled osteoclastogenesis i

177 of CD47 strongly impairs SIRPalpha-dependent osteoblast differentiation, deteriorate bone formation,

178 s compared with WT MSCs, suggesting impaired osteoblast differentiation due to p85alpha deficiency in

179 ween RUNX2 and Glut1 determines the onset of osteoblast differentiation during development and the ex

180 Indian hedgehog (Ihh) is indispensable for osteoblast differentiation during embryonic development

181 edgehog (Ihh) signaling is indispensable for osteoblast differentiation during endochondral bone deve

182 al required for coordinating chondrocyte and osteoblast differentiation during endochondral bone deve

183 ation of palatal mesenchyme condensation and osteoblast differentiation during palatal bone formation

184 est that p85alpha plays an essential role in osteoblast differentiation from MSCs by repressing the a

185 logical stimulation of Hh signaling enhanced osteoblast differentiation from Osx-expressing cells iso

186 npo1 abrogated Oxt-induced expression of the osteoblast differentiation genes osterix (Sp7), Atf4, bo

187 fracture physiology with lower expression of osteoblast differentiation genes.

188 r beta-catenin binding and the expression of osteoblast differentiation genes.

189 ession of the osterix gene and perhaps other osteoblast differentiation genes.

190 Although the transcriptional regulation of osteoblast differentiation has been well characterized,

191 echanism through which Wnt signaling induces osteoblast differentiation in an osteoblast-adipocyte bi

192 o keep in mind the role of the Hh pathway in osteoblast differentiation in an otherwise predominant o

193 nc-finger transcription factor that controls osteoblast differentiation in mammals.

194 eoclastic bone resorption but did not impair osteoblast differentiation in MC3T3-E1.

195 in signaling to induce senescence and reduce osteoblast differentiation in MSCs.

196 Finally, MLL4 is required for efficient osteoblast differentiation in part by countering LSD1 H3

197 Thus, Wnt signaling induces osteoblast differentiation in part through histone deace

198 in osteosarcoma cells and upon induction of osteoblast differentiation in primary mouse bone marrow

199 showed decreased proliferation and impaired osteoblast differentiation in response to BMP2 or BMP6 s

200 n tumor cells and osteoblasts and influences osteoblast differentiation in response to tumor cells.

201 s study, we found defects in chondrocyte and osteoblast differentiation in Spop-null mutant mice.

202 Only Hivep3 siRNA promoted osteoblast differentiation in ST-2 cells, whereas all th

203 onal silencing of TFII-I during BMP-2-driven osteoblast differentiation in the C2C12 cell line.

204 Hedgehog (Hh) signaling is essential for osteoblast differentiation in the endochondral skeleton

205 f either Lrp5 or Lrp6 did not overtly affect osteoblast differentiation in the mouse embryo.

206 erlapping domains of PDGF-PI3K signaling and osteoblast differentiation in the palate and increased o

207 nitors or chondrocytes resulted in premature osteoblast differentiation in the perichondrium, coupled

208 We conclude that TSH enhances osteoblast differentiation in U2OS cells that is, in par

209 related suppression of Ocn transcription and osteoblast differentiation in vitro and in vivo.

210 ggin inhibition and more potent in promoting osteoblast differentiation in vitro and inducing bone re

211 K4 and H3K36 (H3K36me), negatively regulates osteoblast differentiation in vitro by inhibiting the ac

212 Compound 11 induced osteoblast differentiation in vitro, and this effect was

213 , even though Hh signaling directly promotes osteoblast differentiation in vitro, constitutive activa

214 idence indicated the involvement of JMJD3 in osteoblast differentiation in vitro, its role as a whole

215 beta-catenin did induce a slight increase of osteoblast differentiation in vitro, these cells display

216 nmb, as an osteogenic factor that stimulates osteoblast differentiation in vitro.

217 signaling axis, whereas it promotes terminal osteoblast differentiation in vitro.

218 one formation in vivo, nor did it compromise osteoblast differentiation in vitro.

219 ited osteoclast differentiation and promoted osteoblast differentiation in vitro.

220 a Mek/MAPK inhibitor, significantly enhanced osteoblast differentiation in WT and p85alpha(-/-) MSCs.

221 ol cultures indicating that Tgfbr2 regulates osteoblast differentiation independent of regulating pro

222 grates Wnt/beta-catenin signaling to promote osteoblast differentiation independently of cell adhesio

223 one marrow cells, alendronate did not affect osteoblast differentiation, indicating the need for pre-

224 Osteoblast differentiation is an attractive model for ti

225 Furthermore, the effect of dipyridamole on osteoblast differentiation is diminished in both A2BR- a

226 The impact of VDR, RUNX2, and C/EBPbeta on osteoblast differentiation is exemplified by their actio

227 a-catenin signalling, a pathway important in osteoblast differentiation, is modulated in the early re

228 Runx2, a master regulator of osteoblast differentiation, is tightly regulated at both

229 Despite evidence of a role for pRB in osteoblast differentiation, it is unknown whether it fun

230 the role of OC as an essential modulator of osteoblast differentiation, knockdown of miR-138 or addi

231 imic, and OC small interfering RNA inhibited osteoblast differentiation marker alkaline phosphatase a

232 There was increased expression of osteoblast differentiation marker genes and reduced expr

233 iation, as detected by reduced expression of osteoblast differentiation marker genes.

234 Osteoblast differentiation markers and Wnt target gene e

235 ntifying cell densities, cell proliferation, osteoblast differentiation markers, and capillaries in h

236 ere were significantly higher mRNA levels of osteoblast differentiation markers, including COL1A1, AL

237 genes that are expressed in association with osteoblast differentiation, matrix deposition, and miner

238 s defined developmental profiles and affects osteoblast differentiation, mineralization, and calvaria

239 Chromatin immunoprecipitation analysis in an osteoblast differentiation model shows that Alpl and Bgl

240 a nucleoside transport inhibitor, stimulate osteoblast differentiation of cells from patients with M

241 ng on the recruitment, proliferation, and/or osteoblast differentiation of endosteal mesenchymal prog

242 velengths were more effective in stimulating osteoblast differentiation of human adipose-derived stem

243 on of Hh signaling impairs proliferation and osteoblast differentiation of MMPs.

244 odified MSCs and EPCs dramatically increased osteoblast differentiation of MSCs and endothelial diffe

245 PEDF inhibited adipogenesis and promoted osteoblast differentiation of murine MSCs, osteoblast pr

246 APK pathway in vitro abrogates the increased osteoblast differentiation of Nbr1(tr/tr) cells.

247 al lipids demonstrated inhibitory effects on osteoblast differentiation only after the proliferation

248 ions in SMAD6, an inhibitor of BMP - induced osteoblast differentiation (p<10(-20)).

249 oducing visual markers of distinct stages of osteoblast differentiation, pOBCol3.6GFP (3.6GFP; preost

250 During osteoblast differentiation, pRB directly targets Alpl an

251 ng osteoblasts, and show that TSH stimulates osteoblast differentiation primarily through the activat

252 scription factor network for fine-tuning the osteoblast differentiation program.

253 itro, menin modulates osteoblastogenesis and osteoblast differentiation promoted and sustained by bon

254 nificant reductions in the expression of key osteoblast differentiation regulators.

255 ermined by the loss of expression of another osteoblast differentiation reporter, pOBCol3.6GFPcyan, a

256 hus, the mechanism through which Ihh induces osteoblast differentiation requires other effectors in a

257 thylation, represses the master regulator of osteoblast differentiation RUNX2 to promote myogenesis i

258 orylate and activate the master regulator of osteoblast differentiation, Runx2.

259 line or genetic knockout of Akt1 stimulated osteoblast differentiation secondary to increased expres

260 The stimulation of osteoblast differentiation sets the stage for osteoclast

261 fp521 and Runx2 contribute to the control of osteoblast differentiation, skeletal development, and bo

262 r Abl by lenti-shRNA in osteoblasts enhances osteoblast differentiation, suggesting that dasatinib en

263 the FGFR2 mutations in BBDS rescues delayed osteoblast differentiation, suggesting that p53 activati

264 Upon induction of osteoblast differentiation, T63 inhibited adipogenic dif

265 olated from these mice exhibited more robust osteoblast differentiation than normal in vitro.

266 e indicates an active requirement for pRB in osteoblast differentiation that correlates more directly

267 nt signaling, is indispensable for embryonic osteoblast differentiation, the roles of the key Wnt co-

268 ionally drives Wnt-related transcription and osteoblast differentiation, thereby creating a positive

269 Thus, Bmp signaling induces osteoblast differentiation through both Smad4- and mTORC

270 ntiation, suggesting that dasatinib enhances osteoblast differentiation through inhibition of both Sr

271 dentify Galphas as a key regulator of proper osteoblast differentiation through its maintenance of a

272 We find that miR-29b supports osteoblast differentiation through several mechanisms.

273 egulation of osteoblast markers and impaired osteoblast differentiation through STAT3 and p38 MAPK si

274 unction led to impaired bone development and osteoblast differentiation through STAT3 and p38 MAPK si

275 illin-2 control bone formation by regulating osteoblast differentiation through the differential modu

276 ian Hedgehog (Ihh) regulates chondrocyte and osteoblast differentiation through the Glioma-associated

277 2BAR KO mice resulted in lower expression of osteoblast differentiation transcription factors and the

278 in silenced cells inhibits estrogen-induced osteoblast differentiation, transcription factor up-regu

279 outline a new approach to the stimulation of osteoblast differentiation using small molecules that st

280 the known and candidate KDMs in myoblast and osteoblast differentiation using the C2C12 cell differen

281 , inhibits PTH-stimulated cAMP signaling and osteoblast differentiation via Galphai/o signaling.

282 Activin A, in turn, inhibited osteoblast differentiation via SMAD2-dependent distal-le

283 ts demonstrate that low-dose PDT can promote osteoblast differentiation via the activation of activat

284 Panx3 regulates both chondrocyte and osteoblast differentiation via the activation of intrace

285 The impaired p85alpha(-/-) osteoblast differentiation was associated with increased

286 e bone surrounding the tooth was reduced and osteoblast differentiation was disrupted likely contribu

287 yses of the molecular markers indicated that osteoblast differentiation was impaired in the mutant mo

288 The Hivep3 siRNA-mediated promotion of osteoblast differentiation was negated by forced Alg2 ex

289 Osteoblast differentiation was reduced when VEGF recepto

290 Complete biochemical and morphological osteoblast differentiation was restored in cells lacking

291 lthough it is well known that DKK-1 inhibits osteoblast differentiation, we found that together with

292 Adipocyte and osteoblast differentiation were assessed in bone marrow

293 2.7-11.3), which regulates lipid levels and osteoblast differentiation, were associated with risk of

294 ontin, a known factor of bone remodeling and osteoblast differentiation, were reduced dramatically in

295 While RUNX2 cannot induce osteoblast differentiation when glucose uptake is compro

296 icagrelor and dipyridamole on osteoclast and osteoblast differentiation whereas A2BR blockade abrogat

297 us expression of each of the miRs suppressed osteoblast differentiation, whereas antagomirs increased

298 from MDA-PCa-118b induced a higher level of osteoblast differentiation, which was significantly redu

299 sion levels confirmed a defect of Postn(-/-) osteoblast differentiation with and without PTH, as well

300 n of the Adar1 gene significantly suppressed osteoblast differentiation without affecting osteoclast