ライフサイエンスコーパス: osteogenesis

1 , is identified as coupling angiogenesis and osteogenesis.

2 treatment inhibited expression of markers of osteogenesis.

3 letal involvement is likely due to decreased osteogenesis.

4 Wnt pathway activity during NELL-1 and BMP2 osteogenesis.

5 involved in accelerating the early steps of osteogenesis.

6 resorption and promoting osteoblast-mediated osteogenesis.

7 s the repressive function of TALE factors in osteogenesis.

8 including adipogenesis, chondrogenesis, and osteogenesis.

9 on of Cdo1 in BMSCs inversely suppressed the osteogenesis.

10 ctin domain protein, Clec11a, which promotes osteogenesis.

11 e genes, however, enhanced magnesium-induced osteogenesis.

12 nd 21 d reached a peak value at day 7 during osteogenesis.

13 enes involved in chondrocyte hypertrophy and osteogenesis.

14 direct receptor-mediated action to stimulate osteogenesis.

15 reside in a niche that exhibits features of osteogenesis.

16 omote the various stages of angiogenesis and osteogenesis.

17 pregulation of the imprinted gene H19 during osteogenesis.

18 of metabolic homoeostasis, haemopoiesis, and osteogenesis.

19 the importance of osteoactivin (OA/Gpnmb) in osteogenesis.

20 arding MSC participation in adipogenesis and osteogenesis.

21 sion and thereby stimulate BMP signaling and osteogenesis.

22 cytoskeleton up-regulates HDACs and prevents osteogenesis.

23 nt substrate to promote low-dose BMP-induced osteogenesis.

24 regulation by MAPK-activating signals during osteogenesis.

25 biology, screening compounds, and exploring osteogenesis.

26 (CD31(hi)Emcn(hi)), couples angiogenesis and osteogenesis.

27 ed adipocyte differentiation and antagonized osteogenesis.

28 have been previously shown to be involved in osteogenesis.

29 ression, and the timing of key events during osteogenesis.

30 vident bone-loss phenotype and show impaired osteogenesis.

31 ent with exogenous myocilin further enhanced osteogenesis.

32 about molecular mechanisms of Osx-controlled osteogenesis.

33 d canonical Smads to integrate BMP-2-induced osteogenesis.

34 Bone microbial contamination can impair osteogenesis.

35 elf remains intact and is induced to undergo osteogenesis.

36 Specific microbial contamination can impair osteogenesis.

37 (VEGF) is involved in both angiogenesis and osteogenesis.

38 he bone marrow, which leads to impairment of osteogenesis.

39 ile strain (1 Hz, 4 hours/day) enhances hASC osteogenesis.

40 xpansion by hypoosmotic pressure accelerates osteogenesis.

41 r (VEGF), which drives both angiogenesis and osteogenesis.

42 s nucleation point for mineralization during osteogenesis.

43 bility to ameliorate prostate cancer-induced osteogenesis.

44 volume expansion is associated with enhanced osteogenesis.

45 racture repair through stimulated endogenous osteogenesis.

46 ng of the Panx3 ER Ca(2+) channel to promote osteogenesis.

47 calization of RUNX2, but not YAP, to promote osteogenesis.

48 tin-associated protein-like 4 (Cntnap4), for osteogenesis.

49 scription factor 2 (Runx2) in Nell-1-induced osteogenesis.

50 Cx43(-/-) mice, Panx3 is upstream of Cx43 in osteogenesis.

51 mpound, T63, as an efficient up-regulator of osteogenesis.

52 Mkx prevents PDL degeneration by regulating osteogenesis.

53 tidomimetic-coated nanotopographies promoted osteogenesis.

54 d but separate processes: chondrogenesis and osteogenesis.

55 Deltaosx1)) displayed a severe inhibition of osteogenesis accompanied by p53 upregulation, effects th

56 ading and high (low) tractions, and favoured osteogenesis (adipogenesis).

57 0-fold changed tethering, but did not affect osteogenesis, adipogenesis, surface-protein unfolding or

58 and Bglap, which encode the major markers of osteogenesis alkaline phosphatase and osteocalcin.

59 This reflected local effects of LepR on osteogenesis and adipogenesis by bone marrow stromal cel

60 regulator of the age-related switch between osteogenesis and adipogenesis of BMSCs and may represent

61 We found that osteogenesis and adipogenesis were characterized by dist

62 as RUNX2 and PPARgamma are indispensable for osteogenesis and adipogenesis, respectively.

63 Osteogenesis and angiogenesis are associated with each o

64 o a bone defect, the phage nanofibers induce osteogenesis and angiogenesis by activating endotheliali

65 echanisms of how metal ions can enhance both osteogenesis and angiogenesis.

66 ting a potential role of Osx in coordinating osteogenesis and angiogenesis.

67 f NELL-1 to direct BMP2-treated cells toward osteogenesis and away from adipogenesis requires intact

68 ted that small molecular phenamil synergized osteogenesis and bone formation with BMP2 in a rat criti

69 adation pathway could help enhance efficient osteogenesis and bone matrix regeneration.

70 gic activity and can trigger events, such as osteogenesis and bone regeneration.

71 This was associated with increased osteogenesis and calcium accumulation.

72 lishes Foxp1/2/4 proteins as coordinators of osteogenesis and chondrocyte hypertrophy in developing l

73 ether calreticulin controls a switch between osteogenesis and chondrogenesis in mouse ESCs through NF

74 nd differentiation potentials (adipogenesis, osteogenesis and fibrogenesis).

75 Further investigation indicated increased osteogenesis and higher new bone formation rates in both

76 e mass by shifting lineage allocation toward osteogenesis and inducing lipolysis of mature marrow adi

77 BMPs can induce osteogenesis and inhibit myogenesis of mesenchymal stem

78 confirmed that NELL-1 enhances BMP2-induced osteogenesis and inhibits BMP2-induced adipogenesis.

79 a universal feature of human ageing, impairs osteogenesis and is associated with accelerated bone los

80 dysplasia (OFD) is a congenital disorder of osteogenesis and is typically sporadic and characterized

81 rmine the function of Cx43 at early steps of osteogenesis and its role in the ODDD skeletal phenotype

82 This calcification shares features with osteogenesis and may involve osteogenic factors.

83 tely 195 regulates angiogenesis coupled with osteogenesis and may represent a potential therapeutic t

84 mal stem cells, is used to locally stimulate osteogenesis and mineralization in order to produce inte

85 in differentiation assays of chondrogenesis, osteogenesis and myogenesis.

86 strontium, etc., have been shown to increase osteogenesis and neovascularization.

87 OST levels that resulted in dysregulation of osteogenesis and osteoclastogenesis and bone loss.

88 (LIV), increases mesenchymal stem cell (MSC) osteogenesis and proliferation.

89 By day 28, de novo osteogenesis and scaffold-tissue integration were eviden

90 during development for the control of early osteogenesis and skeletal growth.

91 ts but importantly, also promoted endogenous osteogenesis and the maturation of resident osteoblasts.

92 l mesenchyme by the concomitant induction of osteogenesis and the suppression of chondrogenesis.

93 aging negatively affects MSC replication and osteogenesis and whether these features could be altered

94 single high dose of VEGF on angiogenesis and osteogenesis and, illustrates the potential of XCT in de

95 has key roles in regulating chondrogenesis, osteogenesis, and bone and mineral homeostasis.

96 ndifferentiated, or undergoing adipogenesis, osteogenesis, and chondrogenesis).

97 n chemically defined medium specifically for osteogenesis, and concurrently attenuated Runx2 and Osx

98 ood flow leads to defective angiogenesis and osteogenesis, and downregulation of Notch signalling in

99 BM-MSCs exhibited comparable proliferation, osteogenesis, and immunosuppression.

100 n of master genes involved in the control of osteogenesis, and markedly prevents osteoblast generatio

101 i into Zn can improve the cytocompatibility, osteogenesis, and osseointegration.

102 mSSC niche factors can be potent inducers of osteogenesis, and several specific combinations of recom

103 e signatures in mobile MPCs correlating with osteogenesis, and signatures from immobile MPCs with adi

104 ase of fracture healing in old animals slows osteogenesis, and suggests a pharmacologic approach that

105 itical role for mesenchymal stromal cells in osteogenesis, and temporal changes in cellular compositi

106 The second probe aims to monitor osteogenesis, and was generated by conjugating the drug

107 Although chondrogenesis and osteogenesis are considered as two separate processes du

108 We conclude that chondrogenesis and osteogenesis are one continuous developmental and lineag

109 enescence, depleted MSPCs pool, and impaired osteogenesis as well as osteoporosis in later life.

110 Application of rhVEGF(165) enhanced osteogenesis, as evidenced by increased human osteoblast

111 e synergistic effect of Nell-1 with BMP-2 on osteogenesis, as well as the advantages of Nell-1 as an

112 subjected to flow cytometry and quantitative osteogenesis assay.

113 th CA and TCN were effective in accelerating osteogenesis at the interface between bone grafts and re

114 steoblasts, thus abrogating angiogenesis and osteogenesis both in mouse bone and in vitro.

115 ated the ability to promote angiogenesis and osteogenesis both in vitro and in vivo, the specific ele

116 likely associated with the observed impaired osteogenesis both in vitro and in vivo.

117 Leptin increased adipogenesis and reduced osteogenesis by activating Jak2/Stat3 signaling in bone

118 -resistant calcium aluminosilicate cement on osteogenesis by differentiated hDPSCs is more likely to

119 etastatic prostate cancer provokes extensive osteogenesis by driving the recruitment and osteoblastic

120 Recombinant human Clec11a promoted osteogenesis by human bone marrow stromal cells in cultu

121 in/LepR signaling regulates adipogenesis and osteogenesis by mesenchymal stromal cells in the bone ma

122 ts reveal that NCM establishes the timing of osteogenesis by regulating cell cycle progression in a s

123 Recombinant Clec11a promoted osteogenesis by stromal cells in culture and increased b

124 onstrate that Fbw7alpha negatively regulates osteogenesis by targeting Runx2 for ubiquitin-mediated d

125 ted RUNX2, a transcription factor germane to osteogenesis/chondrogenesis, and increased migratory abi

126 depend on the activation and recruitment of osteogenesis-competent skeletal stem and progenitor cell

127 ations including tumor growth, angiogenesis, osteogenesis, coronary perfusion, and oxygen delivery.

128 rx1-Cre;Lepr(fl/fl) mice exhibited increased osteogenesis, decreased adipogenesis, and accelerated fr

129 Osteogenesis depends on a coordinated network of signals

130 Osteogenesis during bone modeling and remodeling is coup

131 rate that chondrocyte-derived Atf4 regulates osteogenesis during development and bone remodeling post

132 as a regulator of chondrocyte maturation and osteogenesis during the spheno-occipital synchondrosis d

133 inking, whereas upregulating tension induced osteogenesis even in the restrictive environment.

134 and evaluated their effects on adipogenesis, osteogenesis, gene expression, and nuclear receptor acti

135 tin, a protein involved in odontogenesis and osteogenesis, has been suggested as a biomarker of renal

136 owth plate, factors that regulate periosteal osteogenesis have not been studied as intensively.

137 that activate bone-specific programs during osteogenesis have remained underexplored.

138 ch as cranio-lenticulo-sutural dysplasia and osteogenesis imperfect, caused by mutations in the COPII

139 e model of the genetic brittle bone disease, osteogenesis imperfect, oim, is characterized by a repla

140 l myostatin deficiency to a mouse model with osteogenesis imperfecta (Col1a2(oim)), a heritable conne

141 Mutations in WNT1 cause osteogenesis imperfecta (OI) and early-onset osteoporosi

142 Osteogenesis imperfecta (OI) comprises a genetically het

143 Adults with osteogenesis imperfecta (OI) have a high risk of fractur

144 More than 90% of people who have osteogenesis imperfecta (OI) have heterozygous mutations

145 Classical osteogenesis imperfecta (OI) is a bone disease caused by

146 Osteogenesis imperfecta (OI) is a collagen-related bone

147 Osteogenesis imperfecta (OI) is a genetic disorder that

148 Osteogenesis imperfecta (OI) is a heritable bone disease

149 Osteogenesis imperfecta (OI) is a heritable connective t

150 Osteogenesis imperfecta (OI) is a heritable disorder of

151 Osteogenesis imperfecta (OI) is a heritable disorder tha

152 Osteogenesis imperfecta (OI) is a heritable disorder, in

153 Osteogenesis imperfecta (OI) is a skeletal disorder char

154 Osteogenesis imperfecta (OI) is an inherited brittle bon

155 Osteogenesis imperfecta (OI) is characterized primarily

156 oduct of the SERPINF1 gene, are the cause of osteogenesis imperfecta (OI) type VI.

157 or bone tissue, the metabolic syndrome, and osteogenesis imperfecta (OI) type VI.

158 Osteogenesis imperfecta (OI), or brittle bone disease, i

159 hich leads to a number of conditions such as osteogenesis imperfecta (OI).

160 helix, lead to the hereditary bone disorder osteogenesis imperfecta (OI).

161 otease tolloid like 1 (TLL1) in mice lead to osteogenesis imperfecta (OI).

162 striking clinical benefits in children with osteogenesis imperfecta (OI); however, the underlying me

163 trolled trial, children aged 4-15 years with osteogenesis imperfecta and increased fracture risk were

164 osts, and to increase bone mass in models of osteogenesis imperfecta and muscular dystrophy.

165 d treatment, we describe the defects causing osteogenesis imperfecta and their mechanism and interrel

166 Children with osteogenesis imperfecta are often treated with intraveno

167 c discoveries has created a new paradigm for osteogenesis imperfecta as a collagen-related disorder,

168 rphogenetic protein 1 (BMP1) causes type XII osteogenesis imperfecta due to altered collagen maturati

169 Osteogenesis imperfecta is a phenotypically and molecula

170 The osteogenesis imperfecta mouse (OIM), lacking procollagen

171 onic lethality, and the scarcity of reported osteogenesis imperfecta mutations in this region.

172 n site may relate to the observed pattern of osteogenesis imperfecta mutations near the integrin bind

173 Osteogenesis imperfecta or 'brittle bone disease' has ma

174 essive mutations in both genes cause similar osteogenesis imperfecta phenotypes.

175 A 42-year-old premenopausal woman with osteogenesis imperfecta presents to the metabolic bone c

176 ail) referred for diagnosis or ruling out of osteogenesis imperfecta type I, a rare variant (rs140121

177 e bone fragility and a clinical diagnosis of osteogenesis imperfecta type IV, we identified two homoz

178 urrent mutation in the 5'-UTR of BRIL causes osteogenesis imperfecta type V.

179 pecific membrane protein that is involved in osteogenesis imperfecta type V.

180 s and improves bone plasticity in a model of osteogenesis imperfecta type VI via Wnt3a blockade.

181 d a recently proposed functional grouping of osteogenesis imperfecta types by shared mechanism to sim

182 ein-65 (FKBP65) defects cause types X and XI osteogenesis imperfecta via aberrant collagen crosslinki

183 d factor (PEDF) defects cause types V and VI osteogenesis imperfecta via defective bone mineralizatio

184 and cyclophilin B (CYPB) cause types VII-IX osteogenesis imperfecta via defective collagen post-tran

185 She has a daughter with osteogenesis imperfecta who is seen regularly in a speci

186 dysplasia), extracellular matrix production (osteogenesis imperfecta), mineralization (familial tumor

187 of extracellular matrix stiffness (e.g., in osteogenesis imperfecta).

188 7 were reported in severe recessive forms of osteogenesis imperfecta, and homozygous knockout is leth

189 Seal mice represent a model of human osteogenesis imperfecta, and reveal a previously unknown

190 ecurrent clinical fractures in children with osteogenesis imperfecta, and the drug was generally well

191 d role of Smpd3 as a candidate gene of human osteogenesis imperfecta, but suggests SMPD3 deficiency a

192 ophilin-B, impair opsin biogenesis and cause osteogenesis imperfecta, respectively.

193 n genes account for <10% of individuals with osteogenesis imperfecta, the characterization of these g

194 family with 2 siblings affected by recessive osteogenesis imperfecta, we identified a homozygous nons

195 Our findings may explain why osteogenesis imperfecta-causing mutations in both genes

196 ate the proteostasis defects associated with osteogenesis imperfecta-causing mutations within the col

197 lts in the dominant hereditary bone disorder osteogenesis imperfecta.

198 erones, have been described in patients with osteogenesis imperfecta.

199 rapeutic window and an approach for treating osteogenesis imperfecta.

200 initially suspected to have a severe type of osteogenesis imperfecta.

201 lin B or FKBP65 leads to a recessive form of osteogenesis imperfecta.

202 this paradigm shift in the understanding of osteogenesis imperfecta.

203 odded investigations into common pathways in osteogenesis imperfecta.

204 rded as a treatment option for children with osteogenesis imperfecta.

205 ls affected by osteoporosis or children with osteogenesis imperfecta.

206 x lead to pathologies including fibrosis and osteogenesis imperfecta.

207 of long bones, which are hallmarks of human osteogenesis imperfecta.

208 ate mechanotransduction pathways stimulating osteogenesis in 2D and 3D culture.

209 d periodontal tissue integrity, and enhanced osteogenesis in a periodontal inflammation model in vivo

210 1 combined with BMP2 significantly optimizes osteogenesis in a rodent femoral segmental defect model

211 thus highlight a potential avenue to promote osteogenesis in adipose-derived mesenchymal cells for sk

212 re required for coupling of angiogenesis and osteogenesis in areas where repair occurs by intramembra

213 steoblast-produced Cxcl9 in angiogenesis and osteogenesis in bone, and Cxcl9 can be targeted to eleva

214 sonic hedgehog (Shh)-mediated signaling and osteogenesis in C3H10T1/2 cells.

215 endothelial cells, as mediated by BMP-4, and osteogenesis in calcifying vascular cells, as mediated b

216 WNT3a also promoted osteogenesis in dental pulp cultures.

217 differentiation in the palate and increased osteogenesis in FGF mutants, indicating this differentia

218 -fat diet increased adipogenesis and reduced osteogenesis in limb bones from wild-type mice, but not

219 d reducing fibrosis, neovascularization, and osteogenesis in marrow.

220 integrin alpha5beta1, a factor that promotes osteogenesis in MSCs and therefore functioned as an oste

221 uma was clinically associated with increased osteogenesis in the appendicular skeleton.

222 defect in the coupling of chondrogenesis and osteogenesis in the cKO mice.

223 hese studies support a role of BMP4-mediated osteogenesis in the progression of prostate cancer in bo

224 t osteoprogenitor proliferation and elevated osteogenesis in the suture.

225 ked by an increase in cell proliferation and osteogenesis in utero, while other organ defects were no

226 sphate graphene (CaPG) intrinsically induces osteogenesis in vitro and in the presence of bone marrow

227 ty, we show that mesenchymal stem cell (MSC) osteogenesis in vitro, and cell deployment in vitro and

228 es maintained under conditions supportive of osteogenesis in vitro.

229 -2 (BMP-2) work synergistically to encourage osteogenesis in vitro.

230 erentiation into osteoblasts in vitro and in osteogenesis in vivo.

231 led as necessary for prostate cancer-induced osteogenesis in vivo.

232 Human MSCs exhibit similar damage, but osteogenesis increases-which is relevant to bone and to

233 ion or increased osmotic pressure diminishes osteogenesis, independent of cell morphology.

234 ars to be relatively permissive and supports osteogenesis independently by providing circulating mine

235 mokines and other angiogenic inducers during osteogenesis indicates the potential role of the secreto

236 c functions of the mature hormone to promote osteogenesis, indicating important roles for this circui

237 rdinated from the start and that adopting an osteogenesis-inducing and chondrogenesis-suppressing cel

238 ription of more than 1,000 genes involved in osteogenesis, inflammation, and oxidative stress.

239 les were used to investigate myeloma growth, osteogenesis inhibition, and myeloma-induced abnormaliti

240 ged cartilage callus formation and a delayed osteogenesis initiation and progression into mineralizat

241 tem cells with a FBN1 mutation is inhibited; osteogenesis is rescued by inhibition of TGF-beta signal

242 showed dramatically increased expression of osteogenesis marker genes only in the BMP group.

243 n by inducing proteasomal degradation of the osteogenesis master regulator Runx2.

244 tic osteolysis, and cell cycle arrest during osteogenesis may also contribute to bone loss in space.

245 examining the contributions of true ectopic osteogenesis, nonosseous calcification, and ectopic oste

246 Our results showed that osteogenesis not only increased both elastic and viscous

247 ation and mineralization were inhibited when osteogenesis of affected osteoblasts was driven in the p

248 expression of angiogenic markers during the osteogenesis of ASCs.

249 kers and enhanced the proliferation rate and osteogenesis of BlCs compared with mBMSCs and BCs via ac

250 of ET1 on enhancing adipogenesis of ASCs and osteogenesis of BMSCs was attenuated by blocking endothe

251 uretic peptide) inhibits myofibrogenesis and osteogenesis of cultured valve interstitial cells and is

252 that adipogenesis of ET1-pretreated ASCs and osteogenesis of ET1-pretreated BMSCs were increased comp

253 rs of electrical field stimulation to induce osteogenesis of human adipose-derived stem cells.

254 ed collagen synergizes with retinoids in the osteogenesis of human marrow mesenchymal stem cells (MSC

255 mechanism through which CaP minerals induce osteogenesis of human mesenchymal stem cells with an emp

256 sed expression of RanBP3L blocks BMP-induced osteogenesis of mouse bone marrow-derived mesenchymal st

257 mechanism linking matrix remodeling in 3D to osteogenesis of MSCs remains unclear.

258 , we found that EpEX treatment also enhances osteogenesis of MSCs under differentiation conditions, a

259 Characterization of regenerated bone reveals osteogenesis of organized, vascularized bone with histol

260 first time to confirm that Ade mediates the osteogenesis of rat BMSCs through the STAT3 signaling pa

261 The replication and osteogenesis of young or old MSCs maintained on young-EC

262 antagonist strongly drives lamin-A-dependent osteogenesis on rigid substrates, with pretreated xenogr

263 A precise imaging technique to evaluate osteogenesis, osteodifferentiation, and osseointegration

264 te that during the process of Osx-controlled osteogenesis, Osx has the ability to coordinately modula

265 increased valve thickening, myofibrogenesis, osteogenesis, proteoglycan synthesis, collagen accumulat

266 to impaired BMP-mediated chondrogenesis and osteogenesis, recapitulating the human disorder.

267 activated during regeneration and facilitate osteogenesis remains largely unknown.

268 However, the role of Cdo1 in osteogenesis remains unclear.

269 Pjkappa), key modulators of adipogenesis and osteogenesis, respectively.

270 key mediators of male sex determination and osteogenesis, respectively.

271 omic architecture favoring adipogenesis over osteogenesis, resulting in decreased formation of HO.

272 s and skeletal fragility, and over-exuberant osteogenesis results in heterotopic ossification (HO) of

273 Profiling of transcriptional genes for osteogenesis revealed a profound decrease in the homeodo

274 t signaling inhibitors during the process of osteogenesis: Sclerostin (SOST), Dickkopf2 (DKK2), and s

275 in 11 positional candidate genes related to osteogenesis, skeletal muscle development, growth, energ

276 matrix remodeling (CD44, Col1a1, integrins), osteogenesis (Sp7, Runx2, Bmp2), inflammation (Cxcl5, 10

277 min-A,C protein stoichiometry in MSCs versus osteogenesis (stiff).

278 nstrate that Tob2 is a negative regulator of osteogenesis that binds and mediates degradation of Osx

279 BMSCs) exhibit an age-dependent reduction in osteogenesis that is accompanied by an increased propens

280 substantially reversed the magnesium-induced osteogenesis that we observed in this model.

281 gulates the balance between adipogenesis and osteogenesis, the roles of additional regulators of this

282 etic protein 2 (BMP-2) is known to stimulate osteogenesis, there is evidence that high doses of BMP-2

283 d ERK1/2 pathways suggests the regulation of osteogenesis through interplay between these pathways.

284 strate a new molecular mechanism controlling osteogenesis through the specific miR-322/Tob2 regulatio

285 teoblasts, redirects SSC fate decisions from osteogenesis to adipo- and chondrogenesis.

286 uppressed traction, and caused a switch from osteogenesis to adipogenesis in the absence of changes t

287 by itself may affect key events of in vitro osteogenesis, ultimately resulting in enhanced matrix mi

288 ultipotency under maintenance conditions and osteogenesis under differentiation conditions.

289 induces aberrant proliferation and deficient osteogenesis via Notch and BMP signaling pathways, respe

290 Osteogenesis was not seen at the interface after 7 days.

291 To elucidate the importance of OA in osteogenesis, we characterized the skeletal phenotype of

292 identify unique gene functions essential for osteogenesis, we performed a forward genetic screen in z

293 ear localization of beta-catenin critical to osteogenesis were abrogated by calreticulin deficiency o

294 cellular matrix, macrophage polarization and osteogenesis were the major pathways affected by Notch1

295 ice did not show changes in proliferation or osteogenesis when compared to WT mice.

296 a downstream mediator of Hivep3, suppresses osteogenesis, whereas it promotes chondrogenesis.

297 tractility (seeded on 1 mum wells) underwent osteogenesis, whereas those with lower contractility (se

298 educed leading to decreased angiogenesis and osteogenesis, which is reverted by genetic reactivation

299 ts core MET receptor functions that regulate osteogenesis within cortical diaphyseal bone.

300 cultured hMSCs can undergo adipogenesis and osteogenesis without requiring cell transfer onto other