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1 exed with conventional plasmid DNA (encoding BMP-2).
2 expression of bone morphogenetic protein 2 (BMP-2).
3 tration-approved bone morphogenic protein 2 (BMP-2).
4 al in treated animals that was equivalent to BMP-2.
5 pendent transcription of CSF-1, osterix, and BMP-2.
6 ls display directed migration in response to BMP-2.
7 of multinucleated osteoclasts in response to BMP-2.
8 lates phosphorylation of Smad in response to BMP-2.
9 of GATA-6, and this is reversed by exogenous BMP-2.
10 9 in the manner that Alk3 is positioned onto BMP-2.
11 in calcifying vascular cells, as mediated by BMP-2.
12 a phenomenon that could be fully rescued by BMP-2.
13 and mimicked by stimulation with recombinant BMP-2.
14 y for motility in response to S100A4/Mts1 or BMP-2.
15 interaction and the interaction of HJV with BMP-2.
16 ity of the clinically licensed growth factor BMP-2.
17 action only between the collagen IIa vWC and BMP-2.
18 e 1 (ALK1) and ALK5 downstream TGF-beta1 and BMP-2.
19 ation marker of odontoblasts is regulated by BMP-2.
20 ralisation beyond the current gold-standard, BMP-2.
21 and BMP-7, but not the frog Cerberus ligand BMP-2.
22 tro by periosteal cells treated with Ihh and BMP-2.
23 METHODS AND Both S100A4/Mts1 (500 ng/mL) and BMP-2 (10 ng/mL) induce migration of hPASMCs in a novel
24 ked in saline, bone morphogenetic protein-2 (BMP-2; 200 ng), 1 muM CGS21680 (A2AR agonist, EC50 = 160
25 a-binding proteins and between prodomains of BMP-2, -4, -7, and -10 and GDF-5 and fibrillins, raising
26 affinity docking site for the propeptides of BMP-2, -4, -7, and -10 and GDF-5, but not GDF-8, and loc
27 e I receptor Alk1, but not other Alks, while BMP-2, -4, and -7 bind and signal through Alk3, and the
33 A greater reliance on BMPR2 was observed for BMP-2/4 relative to BMP-6/7, whereas ACVR2A was more cri
34 MPR1A and ACVR1A expression, suggesting that BMP-2/4 signal in part through ACVR1A/BMPR1A heterodimer
37 ese results suggest different mechanisms for BMP-2/4- and BMP-6/7-induced osteoblastic differentiatio
38 main of TSP-1 is likely responsible for this BMP-2/4-binding activity, an assertion based on sequence
40 we identified for the first time TSP-1 as a BMP-2/-4 antagonist and presented a structural basis for
42 rkedly enhanced bone regeneration as well as BMP-2 8 wk after surgery (60 +/- 2%, 79 +/- 2%, and 75 +
43 ECFCs produced bone morphogenetic protein-2 (BMP-2), a potent osteoinductive molecule, and increases
44 ffold alone and as much bone regeneration as BMP-2, a growth factor currently used to promote bone re
45 cocultures that were stimulated with EMD and BMP-2 achieved significantly higher levels of these fact
46 rats, it was shown that PEI-cmRNA (encoding BMP-2)-activated matrices promoted significantly enhance
48 we found a novel signaling pathway in which BMP-2 activates Dspp gene transcription via Dlx3/Osx pat
50 s containing lyophilized adenovirus encoding BMP-2 (AdBMP-2) or freely suspended AdBMP-2 were transpl
52 vested from C57/BL6 mice, transfected with a BMP-2 adenovirus, seeded on collagen scaffolds (ossicles
53 However, in vitro studies demonstrate that BMP-2 alone does not influence blastema cell migration,
54 BMPR1A and ligation of the BMP receptor with BMP-2 also activated GTP-Rho A of these SMCs, while DN B
55 3-kinase/Akt signaling acting downstream of BMP-2 also drives NFATc1 expression and transcriptional
56 firmed that recombinant human TSP-1 can bind BMP-2 and -4 and antagonize their effects on C3H10T1/2 c
64 urvival by regulating endoderm expression of BMP-2 and BM during embryonic epithelial morphogenesis.
65 pattern, we examined the functional roles of BMP-2 and BMP signaling in post-EMT valvulogenesis by us
68 Increased glucose augmented expression of BMP-2 and BMP-4; the BMP inhibitors matrix Gla protein (
69 K cells express type I and II BMP receptors, BMP-2 and BMP-6 ligands, and phosphorylated isoforms of
71 known high affinity ActRIIB ligand, whereas BMP-2 and BMP-7 affinities for ActRIIB are at least 100-
72 ne residue at the corresponding positions of BMP-2 and BMP-7 allowed for molecular engineering of rec
75 ity of these vWC domains to directly bind to BMP-2 and detected an interaction only between the colla
77 onstructs - (1) Lv-BMP/GFP, containing human BMP-2 and green fluorescent protein (GFP) gene (BMP grou
79 Thus, the proteolysis and activation of pro-BMP-2 and mature BMP-2 by FSAP can regulate cell differe
84 pids inhibit osteogenic signaling induced by BMP-2 and PTH, raising the possibility that hyperlipidem
85 els stimulates new bone formation as well as BMP-2 and represents a novel approach to stimulating bon
87 allowed us to conclude that all, except for BMP-2 and the short BMP-4 propeptides, formed complexes
89 conclusion, Nov binds BMP-2 and antagonizes BMP-2 and Wnt activity, and its overexpression inhibits
91 expression of bone morphogenetic protein 2 (BMP-2) and the transcription factor RUNX2, which normall
92 rowth factors, bone morphogenetic protein 2 (BMP-2) and vascular endothelial growth factor (VEGF).
93 1 (TGFbeta-1), bone morphogenetic protein-2 (BMP-2), and BMP-6 were measured by real-time RT-PCR, and
96 lume, expression of osteogenic genes (RUNX2, BMP-2, and ColI), bone formation rate (BFR), and mineral
97 of BMSCs of wild-type and Bag-1(+/-) mice to BMP-2, and promoted robust BMP-2-stimulated osteogenic d
100 ctor runx2, neither warfarin, BMP-2, nor the BMP-2 antagonist noggin altered runx2 mRNA content in ao
103 ical PC cleavage site, giving rise to mature BMP-2 (Arg(282) downward arrowGln(283)), as well as in t
105 P enhances the biological activity of mature BMP-2 as well as its pro-form, as shown by osteogenic di
106 ding proinflammatory TGFbeta1 and osteogenic BMP-2, as well as glycosaminoglycans such as heparan sul
107 , we identified the requirements of c-Abl in BMP-2 autoregulation and the expressions of alkaline pho
108 h in turn would influence the amount of free BMP-2 available for binding to its receptors and trigger
109 y activation and expression of TGF-beta1 and BMP-2 between healthy and diseased tendon tissues and ce
113 n of these results with complex formation by BMP-2, BMP-4 (full-length and shortened propeptides), BM
115 sis (MS), we characterized the expression of BMP-2, BMP-4, BMP-5, and BMP-7; BMP type II receptor (BM
116 microglia/macrophages, and neurons expressed BMP-2, BMP-4, BMP-5, and BMP-7; BMPRII; and pSMAD1/5/8.
118 tudy was to evaluate receptor utilization by BMP-2, BMP-4, BMP-6, and BMP-7 in primary human mesenchy
119 iple members of the BMP subfamily, including BMP-2, BMP-4, BMP-7, and GDF-5, with similar kinetics an
124 ctively, whereas only one of six mice of the BMP-2/BMSC combination showed evidence of metastatic spr
127 ariants with the corresponding residues from BMP-2 bound BG(ZP-C) more weakly than corresponding alan
128 n of the periostin promoter, were induced by BMP-2 but repressed by noggin in cushion mesenchymal cel
129 lysis and activation of pro-BMP-2 and mature BMP-2 by FSAP can regulate cell differentiation and calc
130 e explored the physiological presentation of BMP-2 by using a biomaterial that harbors tunable mechan
131 enesis, there is evidence that high doses of BMP-2 can lead to side effects, including inflammation a
132 ins of two proteins thought to interact with BMP-2: collagen IIA and matricellular protein CCN3.
133 crog (optimal) or 0.1 microg (suboptimal) of BMP-2 combined with 0, 2, 4, or 8 microg of GST-BGN.
135 modified ribonucleic acid (cmRNA) (encoding BMP-2) complexed with polyethylenimine (PEI) and made co
137 adigm in which bone morphogenetic protein 2 (BMP-2) consecutively and interdependently activates the
140 uronic acid (HA)-based hydrogel was used for BMP-2 delivery to evaluate the influence of hydrogel deg
142 P-2, while genes with roles in inhibition of BMP-2-directed osteoblastogenesis were significantly upr
143 nificant downregulation of E2/ER-facilitated BMP-2-directed osteogenic differentiation of BMSCs.
144 present study, bone morphogenetic protein-2/BMP-2-directed osteogenic differentiation of bone marrow
145 pression profiling and identified miR-322, a BMP-2-down-regulated miRNA, as a regulator of osteoblast
146 t-transcriptional silencing of TFII-I during BMP-2-driven osteoblast differentiation in the C2C12 cel
147 MGP inhibits calcification independent of BMP-2-driven osteogenesis and only in the absence of pyr
154 The roles of TLR2 and TLR4 in oxLDL-induced BMP-2 expression were determined by pretreatment with ne
155 Inhibition of NF-kappaB and ERK1/2 reduced BMP-2 expression whereas inhibition of p38 MAPK had no e
156 influence cell proliferation, down-regulated BMP-2 expression, and showed no effect on BMP receptor t
157 e receptor (TLR) 2 and TLR4 in oxLDL-induced BMP-2 expression, and the signaling pathways involved.
161 irate concentrate (BMAC) and growth factors (BMP-2, FGF-2, and FGF-8) and 2) increase matrix strength
164 derived BGN on bone morphogenetic protein 2 (BMP-2) function, which is exerted likely via the BGN cor
165 inhibition of microtubule assembly enhances BMP-2 gene transcription and subsequent bone formation,
167 N-terminal heparin binding region of mature BMP-2, generating a truncated mature BMP-2 peptide (Arg(
169 d that upon treatment with recombinant human BMP 2 in high-density micromass culture, mutant disc cel
171 ry, and provascularized characteristics over BMP-2 in bone tissue engineering, is highlighted, which
173 ls containing significantly reduced doses of BMP-2 in combination with physiologically relevant doses
174 ese data show a role of NFATc1 downstream of BMP-2 in mouse bone development and provide novel eviden
175 known to be critical for AV EMT, the role of BMP-2 in post-EMT AV valvulogenesis remains to be elucid
178 rkC suppresses bone morphogenetic protein 2 (BMP-2)-induced Smad1 phosphorylation and transcriptional
180 her OP3-4, a RANKL-binding peptide, promotes BMP-2-induced bone formation in the murine maxilla using
181 of OP3-4 by subperiosteal injection promoted BMP-2-induced bone formation, which could lead to the de
183 ase inhibitor GW4869, significantly enhanced BMP-2-induced differentiation and maturation of chondroc
185 ure, GW4869 treatment significantly promoted BMP-2-induced hypertrophic maturation and calcification
186 sitol 3-kinase/Akt, and Ca(2+) signaling for BMP-2-induced NFATc1 expression through an autoregulator
191 alphavbeta3 integrin is required to mediate BMP-2-induced Smad signaling through a Cdc42-Src-FAK-ILK
195 he mutation of the heparin binding region of BMP-2 inhibited the processing by FSAP but not by PC.
200 lyzed in comparison to the carrier-injected, BMP-2-injected, and control-peptide-BMP-2-injected group
207 d NFATc1, we analyzed bones from OB-specific BMP-2 knock-out mice for NFATc1 expression by immunohist
209 fied arteries, bone morphogenetic protein 2 (BMP-2)levels were increased at the time of injury sugges
215 tic knockout of Akt2, did not interfere with BMP-2-mediated signaling but resulted in inhibition of o
216 in response to injury, factors that subvert BMP-2-mediated tandem activation of Wnt-betaC and Wnt-PC
217 thout activating RhoA-Rac1 not only prevents BMP-2-mediated vascular smooth muscle cell motility but
221 ranscription factor runx2, neither warfarin, BMP-2, nor the BMP-2 antagonist noggin altered runx2 mRN
222 ation, the synergistic effect of Nell-1 with BMP-2 on osteogenesis, as well as the advantages of Nell
224 calvarial defect model when transduced with BMP 2 or 4; however, the contribution of the donor cells
225 it tip regeneration, and that treatment with BMP-2 or -7 induces a regenerative response following am
226 ced pSMAD1/5/9 levels when induced either by BMP-2 or BMP-7, suggesting that ACVR1 is the major recep
229 zed two kinds of plasmid DNA encoding either BMP-2 or FGF-2 formulated into polyethylenimine (PEI) co
230 Our studies demonstrate how a single ligand (BMP-2 or S100A4/Mts1) can recruit multiple cell surface
231 is regulated by numerous factors, including BMP-2, parathyroid hormone, and 1alpha,25-dihydroxyvitam
236 e complex of crossveinless-2 (CV-2) vWC1 and BMP-2 previously revealed one mode of the vWC/BMP-bindin
238 e of MSCs with ECFCs transduced to knockdown BMP-2 production abrogated the osteogenic response to le
239 atical model, where mechanical regulation of BMP-2 production mediates rates of cellular proliferatio
242 oxidized low density lipoprotein (oxLDL) on BMP-2 protein expression in human coronary artery endoth
243 Stimulation with oxLDL increased cellular BMP-2 protein levels in a dose-dependent manner (40-160
244 very of active bone morphogenetic protein-2 (BMP-2) protein to responsive target cells, such as bone
245 gulates a multistep process to control first BMP-2 receptor activity and second the inhibitory role o
246 MMP-1 and -8), bone morphogenetic protein-2 (BMP-2), receptor activator of nuclear factor kappaB (RAN
250 tly, two hydrogel formulations with distinct BMP-2 release profiles were evaluated in a critical-size
251 lls from BMP group showed >1,000-fold higher BMP-2 release, and the majority of them stained intensel
252 such side effects by reducing the amount of BMP-2 required to obtain a sufficient amount of bone.
254 tant role for TLR2 and TLR4 in mediating the BMP-2 response to oxLDL in human CAECs and indicate that
256 rate that overexpression of miR-322 enhances BMP-2 response, increasing the expression of Osx and oth
257 observed in the complex between CV-2 vWC and BMP-2, revealing an alternative mode of interaction betw
259 e coupled with bone morphogenetic protein-2 (BMP-2), seeded with bone marrow stromal cells (BMSC), an
260 showed that inhibitory effects of ox-PAPC on BMP-2 signaling were associated with inhibition of SMAD
261 1, a well established downstream molecule of BMP-2 signaling, as a putative target of miR-199a(*).
264 der calcifying conditions , stimulation with BMP-2 significantly increased cell proliferation, howeve
267 for TbetaRIII function, we demonstrate that BMP-2 specifically stimulates TbetaRIII-mediated epithel
268 f-2, Fgf-18, and bone morphogenic protein 2 (Bmp-2)] still were present in Fgf-9(+/-) mice, they coul
269 In the present investigation, we found that BMP-2 stimulated expression and nuclear translocation of
271 peptide, an inhibitor of NFATc1, suppressed BMP-2-stimulated NFATc1 transcription, confirming its au
273 ag-1(+/-) mice to BMP-2, and promoted robust BMP-2-stimulated osteogenic differentiation of BMSCs.
274 inhibition of c-Abl significantly suppressed BMP-2-stimulated PI 3-kinase activity and its downstream
276 pertrophic chondrocytes led to inhibition of Bmp-2-stimulated, BMP-responsive element-dependent Col X
277 new chemical entities (NCEs) that have shown BMP-2 stimulation and osteoblast differentiation are rep
279 l and MC3T3 osteoblastic cells increased the BMP-2 stimulatory effect on alkaline phosphatase activit
281 way, since this pathway is known to regulate BMP-2 transcription in osteoblasts and microtubules have
284 in four of four mice bearing scaffolds with BMP-2 treatment and with BMSC treatment, respectively, w
285 n of common cardiogenic factors, Nkx-2.5 and Bmp-2, until HH Stage 10, when a tubular heart has forme
290 N-terminal sequencing indicated that pro-BMP-2 was cleaved by FSAP at the canonical PC cleavage s
293 ded with simvastatin (pro or active drug) or BMP-2, we have demonstrated osteogenic differentiation w
294 dues, BG bound bone morphogenetic protein 2 (BMP-2) weakly or not at all, and TGF-beta2 variants with
296 MAD1/5/9 (pSMAD1/5/9) levels when induced by BMP-2, whereas no impacts on pSMAD1/5/9 were observed wh
297 ltures of Bag-1(+/-) BMSCs supplemented with BMP-2, while genes with roles in inhibition of BMP-2-dir
298 ll interference RNA (siRNA) or antagonism of BMP-2 with noggin prevented matrix mineralization in vit
299 surface not only provided immobilization of BMP-2 with prolonged bioavailability, but also enhanced
300 -2 (FGF-2) and bone morphogenetic protein-2 (BMP-2) work synergistically to encourage osteogenesis in