ライフサイエンスコーパス: osteoblast

1 rectly and negatively regulates bone mass in osteoblasts.

2 ingle p53 mutation (p53R172H) or p53 loss in osteoblasts.

3 wed no effect on OPG expression in calvarial osteoblasts.

4 n activation and reduced Fgf18 expression in osteoblasts.

5 ed bone damage by accelerating DNA repair in osteoblasts.

6 nternalized into cells without harming human osteoblasts.

7 lated versus protein anabolism signatures of osteoblasts.

8 tain homeostasis of bone tissue by providing osteoblasts.

9 ion; and 3) residual biocompatibility toward osteoblasts.

10 gen alpha, resulting in generation of mature osteoblasts.

11 and bone as well as in in vitro cultures of osteoblasts.

12 osed of both Dspp(+) odontoblasts and Bsp(+) osteoblasts.

13 2 mediated the inhibitory actions of Saa3 on osteoblasts.

14 ed the hematopoietic-supportive functions of osteoblasts.

15 tor activator of NF-kappaB ligand (RANKL) in osteoblasts.

16 steoprotegerin ratio in Runx2-overexpressing osteoblasts.

17 y in either osteoblast progenitors or mature osteoblasts.

18 ptors in the regulation of bone formation by osteoblasts.

19 in BMP-2-stimulated regulation of NFATc1 in osteoblasts.

20 good biocompatibility of surfaces to Saos-2 osteoblasts.

21 sed mineralization by and differentiation of osteoblasts.

22 C function with the bone-forming function of osteoblasts.

23 and drives their differentiation into mature osteoblasts.

24 more circular surface when co-cultured with osteoblasts.

25 defective intramembranous bone formation by osteoblasts.

26 lated the deposition of a new bone matrix by osteoblasts.

27 tivator TAZ form a mechanosensing complex in osteoblasts.

28 ve stress-mediated dysfunction in human bone osteoblasts.

29 ) T cell depletion had no apparent impact on osteoblast ablation in association with PVM infection.

30 Osteoblast ablation was associated with elevated levels

31 The impairment in osteoblast activity correlated with reduced mTORC1 signa

32 s and are major regulators of osteoclast and osteoblast activity, but their contribution to multiple

33 the molecular level to reciprocally regulate osteoblast and adipocyte differentiation, indicating tha

34 n, and thrombocytopenia as well as recovered osteoblast and HSPC abundance and improved the hematopoi

35 chestrators of bone remodeling; they control osteoblast and osteoclast activities both directly via c

36 y seen in Runx2 transgenic mice affects both osteoblast and osteoclast differentiation and activity.

37 Ticagrelor regulates osteoblast and osteoclast function and promotes bone for

38 ctivator of NF-kB ligand), two regulators of osteoblast and osteoclast function.

39 nds can ultimately regulate Wnt signaling in osteoblast and osteoclast precursors, known to regulate

40 PLZF is also essential in osteoblast and spermatogonial development.

41 at Bzb significantly increased the number of osteoblasts and activity in the irradiated area and supp

42 Since osteoblasts and adipocytes are derived from the same pre

43 was secondary to a decrease in the number of osteoblasts and bone formation rate while the osteoclast

44 f several cell types, including bone forming osteoblasts and bone resorbing osteoclasts.

45 argement due to mutant collagen retention in osteoblasts and fibroblasts of mutant fish was shown by

46 ondrocytes impaired their differentiation to osteoblasts and impaired endochondral ossification.

47 ator of Wnt/beta-catenin pathway activity in osteoblasts and indicate that the abnormal Wnt/beta-cate

48 d depletion of EMILIN-1 in primary calvarial osteoblasts and MC3T3-E1 cells only fibulin-4 matrix dep

49 Murine primary osteoblasts and MC3T3-E1 cells were exposed to compressi

50 l and other osteogenic marker genes in mouse osteoblasts and mesenchymal stem cell-like cells.

51 EB1 are characteristic of both p53-deficient osteoblasts and OS.

52 We show that osteoblasts and osteoclasts can be differentiated from h

53 ss (LBM) phenotype is the result of both the osteoblasts and osteoclasts from BgnFmod KO mice having

54 Coordination between osteoblasts and osteoclasts is required for bone health

55 ains were significantly less internalized by osteoblasts and osteoclasts than CC18 and CC28 C. acnes

56 Human osteoblasts and osteoclasts were infected by live C. acn

57 e inflammatory cell infiltration, numbers of osteoblasts and osteoclasts, and receptor activator of n

58 ed bone formation and resorption mediated by osteoblasts and osteoclasts, respectively.

59 ect the microenvironment, which involves the osteoblasts and osteoclasts.

60 ll mice and the impacts of loss of Bmpr1b on osteoblasts and osteoclasts.

61 ulator of the critical communication between osteoblasts and osteoclasts.

62 henotypes of mice lacking these receptors in osteoblasts and osteocytes (osteocalcin-Cre).

63 on of chondrocyte-derived bone cells to form osteoblasts and osteocytes in metaphyses.

64 hape and size except for a sharp increase in osteoblasts and osteocytes, leading to a profound increa

65 istochemistry localized ACVR2A and ACVR2B to osteoblasts and osteocytes.

66 strate a causal role of Plexin-B1 for CIL in osteoblasts and reveals a previously unknown effect of S

67 pothesized that targeted deletion of Alpl in osteoblasts and selected dental cells ( Col1a1-cKO) or d

68 dings demonstrate that communication between osteoblasts and sensory nerves through NGF-TrkA signalin

69 ively regulating the expression of CXLC12 on osteoblasts and their differentiation.

70 atment accelerated DNA repair in bone-lining osteoblasts and thus promoted their survival.

71 ALP activity in osteoblasts and TRAP activity in RAW264.7 cells co-cultu

72 emodelling, osteoclasts induce chemotaxis of osteoblasts and yet maintain spatial segregation.

73 carried out by mesenchymal stem cell-derived osteoblasts, and bone resorption, carried out by monocyt

74 c-Kit was expressed in both osteoclasts and osteoblasts, and c-Kit expression was decreased in W(sh)

75 s ( Col1a1-cKO) or deletion in chondrocytes, osteoblasts, and craniofacial mesenchyme ( Prx1-cKO) wou

76 lves a dynamic interplay among chondrocytes, osteoblasts, and endothelial cells.

77 lineages including chondrocytes, adipocytes, osteoblasts, and multiple neuronal cell types.

78 paracrine interactions between tumor cells, osteoblasts, and osteoclasts.

79 st-specific gene expression in bone, loss of osteoblasts, and reduced serum markers of bone formation

80 lineage, hastens their differentiation into osteoblasts, and suppresses their differentiation into a

81 stimulating interleukin-6 (IL6) release from osteoblasts, and triggers skeletal colonization by activ

82 increases osteoblast numbers by suppressing osteoblast apoptosis and activating bone-lining cells.

83 IL-27 also inhibited osteoblast apoptosis through increased Egr-2 expression,

84 Osteoblasts are bone forming cells some of which become

85 te differentiation of osteocytes from mature osteoblasts are poorly understood.

86 eptidase responsible for pro-OCN cleavage in osteoblasts are still unknown.

87 These observations posit osteoblasts as remote regulators of lung cancer and iden

88 that SREBF1 is expressed in murine and human osteoblasts, as well as in human muscle tissue.

89 pendent manner alter cell morphology towards osteoblast-associated characteristics.

90 verlap between hypertrophic chondrocytes and osteoblasts at the chondro-osseous border in the fractur

91 o mature hypertrophic chondrocytes to become osteoblasts at the epiphysis.

92 tabolic defects of the mice lacking furin in osteoblasts became more apparent under pair-feeding cond

93 cient OPG mutant, we further show that in an osteoblast/bone marrow macrophage co-culture system, imm

94 Osteoblasts build bone, becoming embedded in bone matrix

95 have low bone mass associated with decreased osteoblast but increased osteocyte numbers.

96 miR-874 inhibits CCNE1 expression in primary osteoblasts, but in aggressive osteosarcomas, miR-874 is

97 clusion, introduction of the HCS mutation in osteoblasts, but not in osteoclasts, causes osteopenia.

98 ptin receptor (LepR)-positive cells, whereas osteoblasts can be classified as positive for Runx2, a m

99 both TNFalpha and RANKL, BgnFmod KO derived osteoblasts cannot retain these cytokines in the vicinit

100 and A287P proteins were also examined in an osteoblast cell line by treatment with cycloheximide, a

101 e system, immobilization of OPG by HS at the osteoblast cell surface substantially lowers the inhibit

102 /SCID) with endothelial-specific deletion of osteoblast cell-fate determinant OSX compared with bigen

103 show that cardiac fibroblasts (CFs) adopt an osteoblast cell-like fate and contribute directly to hea

104 in skeletal tissues through its secretion by osteoblasts, chondrocytes, and mesenchymal cells.

105 ridging collagens, primarily associated with osteoblast communication, and other non-collagenous prot

106 fere with the proliferation and viability of osteoblasts, confirming their high biocompatibility.

107 were profiled in murine primary osteoblasts, osteoblast cultures and primary OS cell cultures (from p

108 t show significant changes in vitro However, osteoblasts deficient in ACVR2A exhibited enhanced diffe

109 When isolated from the calvaria, Ppia(-/-) osteoblasts demonstrate decreased osteogenic differentia

110 cient mice, indicating that SMURF2 regulates osteoblast-dependent osteoclast activity rather than dir

111 Bone marrow stromal cells and osteoblasts derived from these mice showed impaired oste

112 ext-generation sequencing we show that human osteoblast-derived EVs contain highly abundant miRNAs sp

113 Osteocalcin (OCN) is an osteoblast-derived hormone that increases energy expendi

114 rm the bone metastasis-promoting function of osteoblast-derived Jagged1 using osteoblast-specific Jag

115 In addition, osteoblast-derived LCN2 inhibits food intake.

116 unction experiments in mice demonstrate that osteoblast-derived LCN2 maintains glucose homeostasis by

117 Finally, osteoblast-derived VEGF stimulated osteoclast formation

118 Salubrinal also protected osteoblast development by upregulating the levels of ATF

119 duced trabecular development and activity of osteoblast development, confirmed by Micro-CT and histol

120 mited the investigation of BAG-1 function in osteoblast development.

121 modulation of E2-facilitated BMP-2-directed osteoblast development.

122 combined WWOX and p53 inactivation in mature osteoblasts did not accelerate osteosarcomagenesis compa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Upon induction of osteoblast differentiation, T63 inhibited adipogenic dif

147 roles in skeletal development by regulating osteoblast differentiation.

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

149 ctin isoforms and the mediating receptors in osteoblast differentiation.

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

151 ce revealed that BDNF knockdown can suppress osteoblast differentiation.

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

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

154 activates alpha4beta1 integrin and augments osteoblast differentiation.

155 differentiation may occur at the expense of osteoblast differentiation.

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

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

158 Smurf2-deficient osteoblasts display increased expression of RANKL, the c

159 neutrophils as myeloid cell effectors of the osteoblast-driven protumoral response.

160 +) cells contribute to both chondrocytes and osteoblasts during bone fracture healing.

161 ts in prostate cancer through endothelial-to-osteoblast (EC-to-OSB) conversion.

162 ial cells that have undergone endothelial-to-osteoblast (EC-to-OSB) conversion.

163 st that fibronectin isoforms produced by the osteoblasts enhance their differentiation.

164 t a model in which Dlx recruitment of Sp7 to osteoblast enhancers underlies Sp7-directed osteoblast s

165 Accordingly, Notch2 activation in osteoblast-enriched cultures from Notch2(COIN) mice indu

166 c analyses in mice, lipocalin 2 (LCN2) as an osteoblast-enriched, secreted protein.

167 he role of magnitude in adaptive response of osteoblasts exposed to compressive stress.

168 Primary osteoblasts expressed activin signaling components, incl

169 nd hypetrophic chondrocytes and finally into osteoblasts expressing Col1 and BSP during postnatal day

170 ion of HSCs resulted in part from decreasing osteoblast expression of HSC retention factors.

171 tic, functional genomic annotation and human osteoblast expression studies; (2) gene-function predict

172 Pre-osteoblasts fail to differentiate leading to severe intr

173 erse lineages into adipocytes, chondrocytes, osteoblasts, fibroblasts, and myofibroblasts.

174 Primary osteoblasts from mutant mice are defective in supporting

175 anical loading is related to the creation of osteoblasts from skeletal stem cells.

176 M) resulted in rapid and substantial loss of osteoblasts from the bone surface.

177 d hormone (PTH) is an important regulator of osteoblast function and is the only anabolic therapy cur

178 caused in part by decreased mTORC1-dependent osteoblast function resulting from loss of WNT1 signalin

179 hypertrophic chondrocytes into bone-forming osteoblasts has been reported, yet the underlying molecu

180 tic and osteoclastic differentiation through osteoblasts in a magnitude-dependent manner.

181 ver that Gli1(+) cells progressively produce osteoblasts in all skeletal sites.

182 target transgene of ECM1 in chondrocytes or osteoblasts in mice leads to striking defects in cartila

183 ng bone resorption, inactivation of furin in osteoblasts in mice resulted in decreased circulating le

184 The tumor-associated osteoblasts in PCa bone metastasis specimens and patient

185 ssociated endothelial cells can give rise to osteoblasts in prostate cancer through endothelial-to-os

186 mmary, our data demonstrate dramatic loss of osteoblasts in response to virus infection and associate

187 cells to hijack R-spondins produced by (pre)osteoblasts in the BM niche, resulting in Wnt (co)recept

188 rate that chondrocytes transdifferentiate to osteoblasts in the growth plate and during regeneration,

189 To investigate activin signaling in osteoblasts in vivo, we analyzed the skeletal phenotypes

190 eralizes normally, supporting the idea of an osteoblast-independent mechanism for teleost vertebral c

191 PCa cells with differentiated primary human osteoblasts induced CRIPTO and GRP78 expression in cance

192 We show that Cxcl9 produced by osteoblasts interacts with vascular endothelial growth f

193 of the canonical Wnt/beta-catenin pathway in osteoblast is modulated by Runx2.

194 Ca cells, however this suppressive effect of osteoblasts is significantly reduced by the reduction of

195 otegerin (OPG), a decoy receptor secreted by osteoblasts, is a major negative regulator of bone resor

196 moresistance of bone metastases, mediated by osteoblast Jagged1-induced tumor Notch signaling.

197 Osteoblasts lacking ACVR2B did not show significant chan

198 vitro In contrast, Notch2(COIN) inversion in osteoblasts led to generalized osteopenia associated wit

199 tion, RANKL upregulation in human mandibular osteoblast-like cells (HMOBs) were stimulated with PGE2.

200 ate that Gli1(+) cells are a major source of osteoblast-like cells during calcification in the media

201 tiation of vascular smooth muscle cells into osteoblast-like cells, we investigated whether miRs impl

202 he mesenchymal maturation program toward the osteoblast lineage and is mechanistically distinct from

203 senchymal stem cell (hMSC) commitment to the osteoblast lineage and modulates Wnt/beta-catenin signal

204 By deleting the receptor Bmpr1a in osteoblast lineage cells with Dmp1-Cre, we observed a dr

205 coordinate beta-catenin signaling within the osteoblast lineage during embryonic and postnatal bone d

206 oreover, mice with loss of RNF146 within the osteoblast lineage had increased fat stores and were glu

207 teriparatide's actions on early cells of the osteoblast lineage has been demonstrated.

208 omoter-driven cre to mark early cells of the osteoblast lineage in adult mice.

209 tivation of Wnt/betacatenin signaling in the osteoblast lineage leads to an increase in bone mass thr

210 Selective deletion of Smurf2 in the osteoblast lineage recapitulates the phenotype of germli

211 poietic (e.g. T and B-cell) and mesenchymal (osteoblast lineage, chondrocyte) cell types.

212 increases the numbers of early cells of the osteoblast lineage, hastens their differentiation into o

213 dependent upon expression of Gsalpha in the osteoblast lineage.

214 ociated athanogene-1 (BAG-1) is expressed by osteoblast-lineage cells; early embryonic lethality in B

215 nd elevated expression of osteocalcin in the osteoblasts localized in necrotic regions.

216 ic depletion of CD8(+) T lymphocytes limited osteoblast loss associated with LCMV infection.

217 loss of PKD1 mediated the downregulation of osteoblast markers and impaired osteoblast differentiati

218 iation and bone development via elevation of osteoblast markers through activation of STAT3 and p38 M

219 n not modulated by OCN, thus suggesting that osteoblasts may secrete additional hormones that regulat

220 d additive decrements in bone mass, impaired osteoblast-mediated bone formation, and enhanced bone ma

221 esistin increased Wnt signalling activation, osteoblast metabolic activity, and bone nodule formation

222 nal transduction, bone nodule formation, and osteoblast metabolic activity.

223 Notably, PTHrP1-17 promotes osteoblast migration and mineralization in vitro, and sy

224 t senescent-cell conditioned medium impaired osteoblast mineralization and enhanced osteoclast-progen

225 Besides osteoblasts, MMPs also give rise to bone marrow adipocyt

226 he capacity of EVs derived from mineralising osteoblasts (MO-EVs) to induce mineralisation in mesench

227 EVs derived from non-mineralising osteoblasts (NMO-EVs) were not found to enhance minerali

228 To activate Notch2 in osteoclasts or osteoblasts, Notch2(COIN) mice were bred with mice expre

229 ytes stimulated bone formation by increasing osteoblast number and activity, which was due in part to

230 last numbers, with no significant effects on osteoblast number and function.

231 ed greater bone volume by twofold and higher osteoblast number by threefold, compared with the contro

232 mice, which was due to a marked increase in osteoblast number that was likely to be driven by hyperp

233 ment with anti-sclerostin antibody increased osteoblast numbers and bone formation rate but did not i

234 , PTH administration significantly increased osteoblast numbers and bone formation rate in both contr

235 Teriparatide increases osteoblast numbers by suppressing osteoblast apoptosis a

236 Osteoblast numbers in SR625 group were significantly hig

237 steoclast (OC) numbers, but had no change in osteoblast numbers or bone formation rate.

238 R625, and SR900 groups, significantly higher osteoblast numbers were detected than in control group (

239 o reduced osteoclast formation and increased osteoblast numbers, respectively.

240 ostasis depends on the functional balance of osteoblasts (OBs) and osteoclasts (OCs).

241 led by dual actions of osteoclasts (OCs) and osteoblasts (OBs).

242 sfunction in the terminal differentiation of osteoblasts obtained from the developing calvaria of DSP

243 proliferation, and differentiation of Saos-2 osteoblasts on new and treated disks were assayed by pro

244 ion patterns were profiled in murine primary osteoblasts, osteoblast cultures and primary OS cell cul

245 However, the role of IL-3 in regulation of osteoblast-osteoclast interactions and underlying mechan

246 Primary human osteoblast/osteoclast co-cultures were seeded onto Ti su

247 dy mitochondrial abnormalities in individual osteoblasts, osteoclasts and osteocytes are limited and

248 Here, we show that mature osteoblast/osteocyte-specific ablation of PPARgamma in m

249 and (4) analysis of gene expression in mouse osteoblasts, osteocytes and osteoclasts.

250 chanotransduction of mesenchymal stem cells, osteoblasts, osteocytes, and chondrocytes.

251 23, and its expression was recently found in osteoblasts/osteocytes.

252 d by the suppression of the endosteum-lining osteoblast population.

253 w that teriparatide increases the numbers of osteoblast precursors and drives their differentiation i

254 Ano5 gene knock-down with shRNA in MC3T3-E1 osteoblast precursors we saw elevated expression of oste

255 for teriparatide-mediated increases in early osteoblast precursors.

256 HS-dependent fashion, syndecan-1 also binds osteoblast-produced R-spondin, which represses Fzd degra

257 ion by activating osteoclastogenesis through osteoblast production of RANKL and IL6.

258 For example, cell signaling networks direct osteoblast progenitors (pObs) to rebuild thin cylindrica

259 tumor suppressor Wwox selectively in either osteoblast progenitors or mature osteoblasts.

260 otif (TAZ) expression, which is required for osteoblast proliferation and differentiation through tra

261 that endogenous glucocorticoid signaling in osteoblasts promotes inflammation in murine immune arthr

262 n factors by RT-PCR: RUNX2, osterix, and the osteoblast protein, osteocalcin.

263 ifically toxic to tumor cells but not normal osteoblasts, raising the possibility that these may be t

264 activation at the leading edge of migrating osteoblasts readily induces local retraction and, unexpe

265 Furthermore, we show that Furin deletion in osteoblasts reduced appetite, a function not modulated b

266 ntiation further but significantly inhibited osteoblast-regualted osteoclastic differentiation.

267 Both osteoblastic and osteoblast-regulated osteoclastic differentiation were e

268 ast precursors we saw elevated expression of osteoblast-related genes such as Col1a1, osteocalcin, os

269 tilizes to specify cell fate of bone-forming osteoblasts remain poorly understood.

270 gulating the differentiation and activity of osteoblasts residing at the bone surface through the sec

271 The molecular mechanisms that transduce the osteoblast response to physical forces in the bone micro

272 To address this mechanism, we generated late-osteoblast-specific and osteocyte-specific WNT1 loss- an

273 rs C/EBPb, TEAD1, FOSL2 and JUND at putative osteoblast-specific enhancers.

274 LCMV and PVM infections resulted in reduced osteoblast-specific gene expression in bone, loss of ost

275 function of osteoblast-derived Jagged1 using osteoblast-specific Jagged1 transgenic mouse model.

276 Osteoblast-specific miR-23a cluster gain-of-function mic

277 igated the role of IL-3 on the regulation of osteoblast-specific molecules, receptor activator of NF-

278 osteoblast enhancers underlies Sp7-directed osteoblast specification.

279 decreased in W(sh)/W(sh)osteoclasts, but not osteoblasts, suggesting an indirect effect of c-Kit on b

280 suggest that Sp7 acts differently, engaging osteoblast targets in Dlx-containing regulatory complexe

281 the ability of S. aureus to replicate within osteoblasts, the bone-forming cells, greatly reducing da

282 ce contact inhibition of locomotion (CIL) in osteoblasts through its receptor Plexin-B1.

283 in mammals requires continuous production of osteoblasts throughout life.

284 h factor and prevents its binding to ECs and osteoblasts, thus abrogating angiogenesis and osteogenes

285 is the pivot of differentiation potency from osteoblast to adipocyte coupled with a decrease in self-

286 individual contributions of osteoclasts and osteoblasts to HCS osteopenia, we created a conditional-

287 therapy, which induces Jagged1 expression in osteoblasts to provide a survival niche for cancer cells

288 receptor (ACVR) type 2A, ACVR2B, or both, in osteoblasts, to determine the contribution of activin re

289 thus providing evidence that chondrocyte to osteoblast transdifferentiation is TH-dependent.

290 llagen, which play a critical role in MSC to osteoblast transition and servers as a downstream target

291 Osteoblast viability and differentiation were not negati

292 The effect of resistin on primary OA osteoblasts was determined by analysis of Wnt pathway si

293 Bacteria internalized into osteoblasts were reduced by the AMP.

294 balanced activities between osteoclasts and osteoblasts, which is regulated by various factors, incl

295 tion and mineralization abilities of patDp/+ osteoblasts while osteoclast differentiation remained un

296 tant p53 allele is expressed specifically in osteoblasts, while the tumor microenvironment remains wi

297 In contrast, deleting Bmpr1a in early osteoblasts with 3.6 Col 1-Cre had little impact on skel

298 4 as well as Runx2 was also present in mouse osteoblasts with no apparent change in expression level

299 Stimulation of primary OA osteoblasts with recombinant resistin increased Wnt sign

300 induce the profound up-regulation of NGF in osteoblasts within 1 h of loading.