ライフサイエンスコーパス: osteogenesis

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

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

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

4 arding MSC participation in adipogenesis and osteogenesis.

5 sion and thereby stimulate BMP signaling and osteogenesis.

6 Mkx prevents PDL degeneration by regulating osteogenesis.

7 tidomimetic-coated nanotopographies promoted osteogenesis.

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

9 regulation by MAPK-activating signals during osteogenesis.

10 biology, screening compounds, and exploring osteogenesis.

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

12 ed adipocyte differentiation and antagonized osteogenesis.

13 have been previously shown to be involved in osteogenesis.

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

15 ent with exogenous myocilin further enhanced osteogenesis.

16 about molecular mechanisms of Osx-controlled osteogenesis.

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

18 Bone microbial contamination can impair osteogenesis.

19 elf remains intact and is induced to undergo osteogenesis.

20 Specific microbial contamination can impair osteogenesis.

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

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

23 negative mutants of FGD1 or Cdc42 suppressed osteogenesis.

24 d but separate processes: chondrogenesis and osteogenesis.

25 le coculture model for the in vitro study of osteogenesis.

26 the biological functions of this protein in osteogenesis.

27 emporal regulation of gene expression during osteogenesis.

28 g of DMP1 is an activation step essential to osteogenesis.

29 l for fracture healing, bone remodeling, and osteogenesis.

30 induce genes associated with later stages of osteogenesis.

31 the effects of phenamil on BMP signaling and osteogenesis.

32 and RUNX2 are crucial in the programming of osteogenesis.

33 Akt2 as a critical mediator of IGF-regulated osteogenesis.

34 unx2, Osx, and Dspp during odontogenesis and osteogenesis.

35 hat elastin degradation products may promote osteogenesis.

36 ce that pRb has multiple regulatory roles in osteogenesis.

37 and dynamic profile during mouse ASC (mASC) osteogenesis.

38 , is identified as coupling angiogenesis and osteogenesis.

39 treatment inhibited expression of markers of osteogenesis.

40 letal involvement is likely due to decreased osteogenesis.

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

42 involved in accelerating the early steps of osteogenesis.

43 resorption and promoting osteoblast-mediated osteogenesis.

44 s the repressive function of TALE factors in osteogenesis.

45 including adipogenesis, chondrogenesis, and osteogenesis.

46 on of Cdo1 in BMSCs inversely suppressed the osteogenesis.

47 ctin domain protein, Clec11a, which promotes osteogenesis.

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

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

50 direct receptor-mediated action to stimulate osteogenesis.

51 reside in a niche that exhibits features of osteogenesis.

52 omote the various stages of angiogenesis and osteogenesis.

53 pregulation of the imprinted gene H19 during osteogenesis.

54 of metabolic homoeostasis, haemopoiesis, 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 the endoglin pathway suggested that enhanced osteogenesis among CD105(low) adipose-derived cells is l

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

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

62 We found that osteogenesis and adipogenesis were characterized by dist

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

64 Osteogenesis and angiogenesis are associated with each o

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

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

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

68 at increase actomyosin contractility promote osteogenesis and are consistent with in vivo characteris

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

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

71 iogenesis and migration of cells involved in osteogenesis and bone remodeling.

72 This was associated with increased osteogenesis and calcium accumulation.

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

74 It is a negative regulator of osteogenesis and considered a viable drug target for ost

75 specific cellular processes that may lead to osteogenesis and eventually for understanding the regene

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

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

78 BMPs can induce osteogenesis and inhibit myogenesis of mesenchymal stem

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

80 le in regulating genes that are essential in osteogenesis and intersects with the bone-specific trans

81 ranscription factor, Runx2, is essential for osteogenesis and is controlled by both distal (P1) and p

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

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

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

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

86 in differentiation assays of chondrogenesis, osteogenesis and myogenesis.

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

88 ts calcification independent of BMP-2-driven osteogenesis and only in the absence of pyrophosphate, c

89 Wnt inhibitors secreted by MM cells inhibit osteogenesis and promote osteoclastogenesis, therefore r

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

91 ortant role for FGD1/Cdc42 signaling in hMSC osteogenesis and suggest that the defects in bone remode

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

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

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

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

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

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

98 It resembles skeletal osteogenesis, and many bone cells as well as bone-relate

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

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

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

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

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

104 subjected to flow cytometry and quantitative osteogenesis assay.

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

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

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

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

109 es further demonstrate that miR-29b promotes osteogenesis by directly down-regulating known inhibitor

110 udies suggest that contractile cells promote osteogenesis by enhancing c-Jun N-terminal kinase (JNK)

111 beta) inhibitors and PPARgamma inhibitors on osteogenesis by hMSCs.

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

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

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

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

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

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

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

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

120 vel of new bone formation, but the extent of osteogenesis depended on the type of implant.

121 Osteogenesis depends on a coordinated network of signals

122 Osteogenesis during bone modeling and remodeling is coup

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

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

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

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

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

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

129 st1 and Twist2 in the context of myogenesis, osteogenesis, immune system development and cancer.

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

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

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

133 Osteogenesis imperfecta (OI or brittle bone disease) is

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

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

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

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

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

139 Osteogenesis imperfecta (OI) is a genetic disorder in co

140 Osteogenesis imperfecta (OI) is a genetic disorder that

141 Osteogenesis imperfecta (OI) is a heritable bone disease

142 Osteogenesis imperfecta (OI) is a heritable connective t

143 Osteogenesis imperfecta (OI) is a heritable disorder of

144 Osteogenesis imperfecta (OI) is a heritable disorder tha

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

146 Osteogenesis imperfecta (OI) is a skeletal disorder prim

147 Osteogenesis imperfecta (OI) is an inherited brittle bon

148 Osteogenesis imperfecta (OI) is characterized by bone fr

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

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

151 , respectively, two novel recessive forms of osteogenesis imperfecta (OI) with severe to lethal bone

152 Osteogenesis imperfecta (OI), also known as brittle bone

153 The clinical severity of Osteogenesis Imperfecta (OI), also known as the brittle

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

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

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

157 in the perinatal period to severe deforming osteogenesis imperfecta (OI).

158 mechanism underlying pathophysiology of the osteogenesis imperfecta (OI).

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

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

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

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

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

164 Children with osteogenesis imperfecta are often treated with intraveno

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

166 rted here may play a role in the etiology of osteogenesis imperfecta by affecting collagen secretion

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

168 d partial answers to questions about 'other' osteogenesis imperfecta genes in patients with an osteog

169 s in severe/lethal and recessively inherited osteogenesis imperfecta has provided partial answers to

170 Osteogenesis imperfecta is a heritable disorder that cau

171 Osteogenesis imperfecta is a phenotypically and molecula

172 The hereditary bone disorder osteogenesis imperfecta is often caused by missense muta

173 The osteogenesis imperfecta mouse (OIM), lacking procollagen

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

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

176 Osteogenesis imperfecta or 'brittle bone disease' has ma

177 genesis imperfecta genes in patients with an osteogenesis imperfecta phenotype but no COL1A1 and COL1

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

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

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

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

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

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

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

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

186 in patients with recessive severe or lethal osteogenesis imperfecta types.

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

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

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

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

191 roxylase 1 [P3H1]) cause autosomal recessive osteogenesis imperfecta with rhizomelia (shortening of p

192 We identified two siblings who had recessive osteogenesis imperfecta without rhizomelia.

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

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

195 7 were reported in severe recessive forms of osteogenesis imperfecta, and homozygous knockout is leth

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

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

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

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

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

201 type I collagen result in autosomal dominant osteogenesis imperfecta, whereas mutations in either of

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

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

204 this paradigm shift in the understanding of osteogenesis imperfecta.

205 odded investigations into common pathways in osteogenesis imperfecta.

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

207 ls affected by osteoporosis or children with osteogenesis imperfecta.

208 pted as 'standard of care' for children with osteogenesis imperfecta.

209 hopedic approaches to care for children with osteogenesis imperfecta.

210 pe I collagen are common molecular causes of osteogenesis imperfecta.

211 cts inhibiting its formation cause recessive osteogenesis imperfecta.

212 the pathogenesis, diagnosis and treatment of osteogenesis imperfecta.

213 fective surgical management of children with osteogenesis imperfecta.

214 lts in the dominant hereditary bone disorder osteogenesis imperfecta.

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

216 rapeutic window and an approach for treating osteogenesis imperfecta.

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

218 1 combined with BMP2 significantly optimizes osteogenesis in a rodent femoral segmental defect model

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

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

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

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

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

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

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

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

227 sis in 3T3-L1 cells but negatively regulates osteogenesis in MC3T3-E1 cells.

228 auses accelerated Wnt signaling and enhanced osteogenesis in mesenchymal stem/progenitor cells, irres

229 icrobial contamination may have an impact on osteogenesis in osseous regeneration.

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

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

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

233 and function of APP were investigated during osteogenesis in vitro and in vivo.

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

235 -2 (BMP-2) work synergistically to encourage osteogenesis in vitro.

236 s of osteoblast differentiation and promotes osteogenesis in vitro.

237 To visualize catS activity and osteogenesis in vivo, we coadministered catS-activatable

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

239 ant role of a canonical Wnt gradient in hMSC osteogenesis in vivo.

240 Induced osteogenesis includes a program of microRNAs (miRs) to r

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

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

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

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

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

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

247 Associated with the heterotopic osteogenesis is an upregulation of Bmp signaling in this

248 Wnt inhibition of osteogenesis is associated with decreased expression of

249 However, whether osteogenesis is necessary for prostate tumor growth in b

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

251 luster gain of function (i.e., inhibition of osteogenesis) is rescued by the exogenous expression of

252 ic protein (BMP) pathway, a key regulator of osteogenesis, is profoundly altered.

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

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

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

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

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

258 of three-dimensional microenvironments, with osteogenesis occurring predominantly at 11-30 kPa.

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

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

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

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

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

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

265 The process of osteogenesis of repair in humans seems to be multifactor

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

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

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

269 same area-display different adipogenesis and osteogenesis profiles.

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

271 Thus, mASCs undergoing osteogenesis recapitulate the in vivo osteogenic differe

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

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

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

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

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

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

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

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

287 sensitivities of hMSCs to Wnt inhibition of osteogenesis versus adipogenesis, which favors osteoblas

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

289 Osteogenesis was also accelerated in Hmgb2(-/-) MSC.

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 Signs of osteogenesis were present in the cocultures in unstimula

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

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

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

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

298 or constitutively active Cdc42 promoted hMSC osteogenesis, while inhibiting Cdc42 signaling by either

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