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1 hase (eNOS), and bone morphogenic protein 4 (BMP-4).
2 ion to express bone morphogenetic protein 4 (BMP-4).
3 ted endothelial mRNA expression of BMP-2 and BMP-4.
4 ge determination in the absence of exogenous BMP-4.
5 ased endothelial expression of BMP-2 but not BMP-4.
6 ly and selectively to radiolabeled BMP-2 and BMP-4.
7 sponsive to the growth suppressive effect of BMP-4.
8 resistant to the growth-inhibitory effect of BMP-4.
9 decreased by high concentrations of BMP-2 or BMP-4.
10 thelial growth factor (VEGF) synergizes with BMP-4.
11 to stimulate BMP-2 and, to a lesser degree, BMP-4.
12 G may mediate apoptotic signals generated by BMP-4.
13 that is activated by the ventralizing signal BMP-4.
14 ttern of expression of Smad8 mirrors that of BMP-4.
15 b morphogenesis might be mediated in part by BMP-4.
16 ve cells are not affected by the presence of BMP-4.
17 ion of bone morphogenetic protein (BMP)-2 or BMP-4.
18 and blocked the interaction between MGP and BMP-4.
19 cells led to loss of ability of MGP to bind BMP-4.
20 ues, indicating tissue-specific targeting of BMP-4.
21 r the physical interaction between TSP-1 and BMP-4.
22 enhances utilization of ActRIIA by BMP-2 and BMP-4.
26 ow that the BMP-10 prodomain, in contrast to BMP-4, -5, and -7 prodomains, can inhibit the bioactivit
33 ro64 and the Gla residues, and the effect on BMP-4 activity, and binding of BMP-4 and calcium was tes
34 s the activity and signaling range of mature BMP-4 after it has been released from the prodomain.
38 nd heparin unless prebound to Chordin and/or BMP-4, although Drosophila TSG has been reported to bind
39 at an increase in ALK1 expression induced by BMP-4, an angiogenic stimulus, preceded induction of ALK
40 hemistry identified strong mRNA labeling for BMP-4 and -7 in the theca cells and BMP receptor types I
41 stem, we examined the effects of recombinant BMP-4 and -7 on FSH (follicle-stimulating hormone)-induc
43 knockdown of DKK-1, a Wnt inhibitor, induced BMP-4 and 6 expression and promoter activation in PCa ce
44 little effect on the affinity of chordin for BMP-4 and BMP-7 but C-terminal cleavage increases the ef
45 Furthermore, through a cell-autonomous loop BMP-4 and BMP-7 intensified Smad1/5 signaling though a f
47 the effect on BMP-4 activity, and binding of BMP-4 and calcium was tested using luciferase reporter g
49 Elevated miR-143 expression correlated with BMP-4 and CK8 expression, and elevated miR-205 expressio
50 well with the GFP signal after upregulating BMP-4 and co-expressing GFP using adenovirus, and the kn
51 ion, we subsequently examined sensitivity to BMP-4 and expression of BMP-RII, BMP-RIA, and BMP-RIB in
55 naling pathway and whether ONH cells secrete BMP-4 and respond to exogenous BMP-4 through this pathwa
58 phogenetic genes, including up-regulation of BMP-4 and Sp-c expression as well as an increase in Flk-
61 were induced when ectoderm was treated with BMP-4 and the mesoderm inducers, activin, or fibroblast
62 ted to cardiomyocytes by using activin A and BMP-4 and then placed into suspension on a rotating orbi
63 to undergo chondrogenic differentiation with BMP-4 and transforming growth factor beta3 (TGFbeta3).
68 eptide (PDGFRb), bone morphogenic protein 4 (BMP-4), and stem cell factor (SCF) constituted a common
69 tor 2 (Flk-1), bone morphogenetic protein 4 (Bmp-4), and the transcription factors of the Brachyury T
71 In the present study, we show that BMP-2, BMP-4, and BMP-6 are endogenous ligands for HJV in hepat
72 hat the bone morphogenetic proteins (BMP)-2, BMP-4, and BMP-7 can promote the development of tyrosine
73 upts complex formation involving ALK2, ALK1, BMP-4, and BMP-9 required for the induction of both BMP
74 a, NMDA1, GAP-43, ChAT, BDNF, nestin, BMP-2, BMP-4, and EGR1, was increased, approximately 10- to 100
75 is differentially regulated by activin, Vg1, BMP-4, and fibroblast growth factor, supporting a model
76 ine aortic endothelial cells, as mediated by BMP-4, and osteogenesis in calcifying vascular cells, as
78 id cells began to be detected with 0.5 ng/mL BMP-4, and their levels plateaued at approximately 2 ng/
80 d expression of Gremlin by TM cells inhibits BMP-4 antagonism of TGF-beta2 and leads to increased ECM
88 nd found that the absence of bgn caused less BMP-4 binding, which reduced the sensitivity of osteobla
89 f A33 cells to noggin, a naturally occurring BMP-4-binding antagonist, during this critical time wind
92 ), we characterized the expression of BMP-2, BMP-4, BMP-5, and BMP-7; BMP type II receptor (BMPRII);
96 s to evaluate receptor utilization by BMP-2, BMP-4, BMP-6, and BMP-7 in primary human mesenchymal ste
98 mbers of the BMP subfamily, including BMP-2, BMP-4, BMP-7, and GDF-5, with similar kinetics and ligan
103 of the PC family have the ability to cleave BMP-4, but of these, only furin and PC6B are sensitive t
104 s the activity and signaling range of mature BMP-4, but the mechanism by which this occurs is unknown
107 on in whole embryos, we see no activation of BMP-4 by VoxG4A, demonstrating that this activation is i
113 Wnt pathway genes, beta-catenin, Zfp432, and Bmp-4 Consistent with increased beta-catenin levels in s
117 Thus, VEGF is a synergistic enhancer for the BMP-4-dependent differentiation processes, and it seems
118 20 ng/mL VEGF synergistically augmented the BMP-4-dependent generation of erythro-myeloid CFCs and l
119 ation of dendritic cells or splenocytes with BMP-4 did not affect lipopolysaccharide-stimulated produ
122 kably, this cell line expresses and secretes BMP-4 during proliferation in the same time window that
131 before primitive streak formation, and that BMP-4 expression is downregulated as the streak starts t
137 ease pellets, releasing 500 nanograms/day of BMP-4 for a maximum of 3 months, were implanted beneath
139 31-50% by 3 months, and at 6 months, after 3 BMP-4-free months, force was still decreased by 20-31%.
140 ent cleavage at the S2 site liberates mature BMP-4 from the prodomain, thereby stabilizing the protei
141 ese results with complex formation by BMP-2, BMP-4 (full-length and shortened propeptides), BMP-10, a
142 promoter deletions for both human BMP-2 and BMP-4 fused to the luciferase reporter gene were analyze
145 ne morphogenetic protein-2 and -4 (BMP-2 and BMP-4) genes, we examined the effects of noggin, an endo
147 , TGF-beta1, and bone morphogenic protein 4 (BMP-4) have various effects on hematopoiesis, including
149 mice, a model for atherosclerosis, levels of BMP-4, HSP70, MGP, and interleukin-6 were elevated in th
154 metabolism, signaling, and transcription by BMP-4 in keratinocytes and fibroblasts is likely to be a
155 the cardiogenic-inducing capacities of BMP-2/BMP-4 in mesoderm, however, we find that BMP-2 or BMP-4
158 ant-negative Smad1 converted the response to BMP-4 in proximal PASMCs from inhibitory to proliferativ
159 unoblot analysis was used to detect secreted BMP-4 in serum-free conditioned media of ONH cells and i
160 We have altered the activity of BMP-2 or BMP-4 in the ectoderm of the feather field by expressing
162 SCs expressing bone morphogenetic protein 4 (BMP-4) in combination with MDSCs expressing VEGF or sFlt
164 cytokines such as activin A, TGF-beta1, and BMP-4, including differentiation of a hematopoietic cell
165 s of neural crest cells, exogenous BMP-2 and BMP-4 increased the expression of BMPR-IA but decreased
167 immunopurified E12 ENS precursors, BMP-2 and BMP-4 induced nuclear translocation of phosphorylated Sm
170 r and the requirement of AP-1(JunD/c-Fos) in BMP-4-induced hematopoiesis during Xenopus hematopoiesis
172 secreted ASPN bound to BMP-4 and restricted BMP-4-induced MSC differentiation prior to lineage commi
179 that bone morphogenetic protein (BMP)-2 and BMP-4 inhibited TNF-mediated apoptosis by inhibition of
181 in mesoderm, however, we find that BMP-2 or BMP-4 inhibits cardiac myogenesis prior to stage 3, demo
189 tigation, an independent approach shows that BMP-4 is required for stable commitment of pluripotent s
195 of BMP signaling pathways because exogenous BMP-4 led to phosphorylation of Smad1, p38(MAPK), and ER
196 dies abolished the inhibitory effect of high BMP-4 levels on ALK1 expression and the induction of MGP
198 e domain, or vice versa, with or without the BMP-4 linker domain revealed that the linker domain is o
199 recursors containing the BMP-7 prodomain and BMP-4 mature domain, or vice versa, with or without the
203 , we propose that Vox acts in establishing a BMP-4 morphogen gradient by restricting the expression d
205 1 and MB8), the fluorescent intensities from BMP-4 mRNA correlated well with the GFP signal after upr
206 retinopathy there was a striking decrease in BMP-4 mRNA in the retina within 6 hours of the onset of
207 tensive study of the target accessibility of BMP-4 mRNA using 10 different designs of molecular beaco
208 g GFP using adenovirus, and the knockdown of BMP-4 mRNA using siRNA significantly reduced the beacon
210 ation in the same time window that exogenous BMP-4 must be added to naive 10T1/2 cells to induce maxi
212 milarly to that of BMP-2 and interacted with BMP-4 on a protein level as determined by co-immunopreci
213 noggin, an endogenous inhibitor of BMP-2 and BMP-4 on bone formation stimulated by these compounds an
216 However, the proproliferative effect of BMP-4 on peripheral PASMCs was found to be p38MAPK/ERK-d
219 These compounds increased BMP-2 but not BMP-4 or BMP-6 mRNA expression in osteoblastic cells, su
222 Spatial distributions of morphogens, such as BMP-4, play important roles in the pattern formation.
225 oplasmic reticulum, and thus cleavage of the BMP-4 precursor when overexpressed in Xenopus oocytes an
226 s with preserved ability to bind and inhibit BMP-4 prevented osteogenic differentiation and calcifica
227 ain is only functional in the context of the BMP-4 prodomain, and that differential cleavage around t
228 stem cells to bone morphogenetic protein-4 (BMP-4) produced cells that convert into adipocytes at hi
229 gulatory information for the human BMP-2 and BMP-4 promoters and clarify the human BMP-2 gene transcr
230 olated and characterized the human BMP-2 and BMP-4 promoters and report substantially more upstream s
232 ude that all, except for BMP-2 and the short BMP-4 propeptides, formed complexes with their growth fa
233 ive BMP-4 receptor, or ectoderm treated with BMP-4 protein in the presence or absence of cycloheximid
235 ectoderm expressing a constitutively active BMP-4 receptor, or ectoderm treated with BMP-4 protein i
236 ked by coexpression with a dominant negative BMP-4 receptor, showing that GATA-1 requires the BMP sig
239 we show that the pro- and mature domains of BMP-4 remain noncovalently associated after S1 cleavage,
240 that MDSC-based therapy involving sFlt-1 and BMP-4 repairs articular cartilage in OA mainly by having
241 f BMP-RII in TSU-Pr1 cells not only restored BMP-4 responsiveness but also significantly decreased tu
244 ctivity of Smad7 may be due to inhibition of BMP-4 signaling because Smad7 can also block BMP-4-media
246 is induced in response to components of the BMP-4 signaling pathway in injected animal cap explants.
247 changes in the expression of members of the BMP-4 signaling pathway, that distinguish A33 preadipocy
250 s embryos phenocopies the effect of blocking BMP-4 signaling, leading to induction of a secondary axi
253 n granulosa cells and cultured in vitro with BMP-4 stimulation for three different durations In addit
255 uclear factor-kappaB in CAECs, and BMP-2 and BMP-4 substantially increased adhesion of monocytic THP-
256 fter exposure to Bone Morphogenic Protein-4 (BMP-4), suggesting that cyclin G may mediate apoptotic s
257 mimicked by TGF-beta2 and -beta3 but not by BMP-4, suggesting a TGF-beta signal-specific effect.
258 es and the surrounding keratinocytes express BMP-4, suggesting both autocrine and paracrine effects o
259 d muscle size caused by sustained release of BMP-4 suggests that myogenic signaling factors may provi
262 xTsg is expressed ventrally as part of the BMP-4 synexpression group and encodes a secreted BMP-bin
265 ganized vasculature, which is reminiscent of BMP-4, TGF-beta1 and TGF-beta type II receptor knockout
266 plemented with bone morphogenetic protein 4 (BMP-4), the numbers of primary hematopoietic clusters in
267 ed glucose augmented expression of BMP-2 and BMP-4; the BMP inhibitors matrix Gla protein (MGP) and N
271 xpressing cells by the addition of exogenous BMP-4, thus establishing a functional role for BMP-4 dur
272 ation of control ES cells, while addition of BMP-4 to noggin expressants strikingly inhibited neurona
273 results indicate that Siah2 acts upstream of BMP-4 to regulate factors that control the commitment of
275 ced to express bone morphogenetic protein 4 (BMP-4) to differentiate into chondrocytes in vitro and i
278 apoptosis were also observed in sFlt-1- and BMP-4-transduced MDSCs compared with a combination of VE
280 SCs compared with a combination of VEGF- and BMP-4-transduced MDSCs or with BMP-4-transduced MDSCs al
281 e of MDSCs and OA chondrocytes revealed that BMP-4-transduced MDSCs produced the largest pellets, whi
282 er cartilage repair in animals that received BMP-4-transduced MDSCs than in those that received MDSCs
283 ro chondrogenic differentiation of LacZ- and BMP-4-transduced MDSCs with or without transforming grow
285 tested whether bone morphogenetic protein-4 (BMP-4)-treated or HOXB4-transduced ES-derived hematopoie
286 iptase-polymerase chain reaction analysis of BMP-4-treated rhesus monkey ES cells demonstrated an up-
288 Global microarray analysis revealed that BMP-4 treatment induces distinct and cell type-specific
292 the response of bgn-deficient osteoblasts to BMP-4 was completely rescued by reintroduction of biglyc
295 ring the 7 days of in vitro differentiation, BMP-4 was required within the first 4 days, whereas VEGF
297 tor to express bone morphogenetic protein 4 (BMP-4) were coimplanted with MDSCs transduced to express
298 Furthermore, bone morphogenetic protein 4 (BMP-4), which also induces AKT activation, increased TGF
299 17 simultaneously inhibits the expression of BMP-4 while augmenting the BMP antagonist, Gremlin-1.
300 oth FGF-4 and SHH induce local expression of Bmp-4, while BMP-4 suppresses local expression of both.