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1 abolic factor, bone morphogenetic protein-7 (BMP-7).
2  on pSMAD1/5/9 were observed when induced by BMP-7.
3  1 week later by an intraventricular dose of BMP-7.
4 f two other known GC mitogens, activin-A and BMP-7.
5 ived both the enalapril and the high dose of BMP-7.
6  I TGF-beta family receptor for activins and BMP-7.
7 ct with tissues expressing BMP-2, BMP-4, and BMP-7.
8  endogenous epidermis inducers are BMP-4 and BMP-7.
9 BMP genes leading to expression of BMP-4 and BMP-7.
10 F-1 suppresses noggin, a potent inhibitor of BMP-7.
11  CM with BMP-7, or CM with both TGFbeta1 and BMP-7.
12 iabetic kidney disease by AGE inhibitors and BMP-7.
13 (12.5 mg/kg body wt per d), group 3 received BMP-7 (50 or 300 microg/kg), and group 4 received both t
14      Interestingly, we found that miR-22 and BMP-7/6 are in a regulatory feedback circuit, whereby no
15  mice demonstrated a significant increase in BMP-7/6 expression and their downstream targets.
16 y analyzing the potential miRNAs that target BMP-7/6 in silica, we identified miR-22 as a potent miRN
17 we examined the regulatory role of miRNAs on BMP-7/6 signaling.
18           We found that expression levels of BMP-7/6 were significantly elevated in the kidneys of th
19 ck circuit, whereby not only miR-22 inhibits BMP-7/6, but miR-22 by itself is induced by BMP-7/6.
20 dentified miR-22 as a potent miRNA targeting BMP-7/6.
21  BMP-7/6, but miR-22 by itself is induced by BMP-7/6.
22                Bone morphogenetic protein 7 (BMP-7), a member of the TGFbeta superfamily, is also inv
23                                              BMP-7, a member of the transforming growth factor-beta (
24  by the Smad-binding sites was responsive to BMP-7, a protein with known protective effects against i
25 tion treatment, IGF-1 activated Smad2, while BMP-7 activated Smad1/5/8 and Smad3, thus inducing all S
26                                 Furthermore, BMP-7 activated the VEGF promoter.
27        Here, we describe a new MMP-dependent BMP-7 activation mechanism from ECM-targeted pools via s
28  binary complexes such as BMP-2/BMPR Ia-ECD, BMP-7/ActRII-ECD, and activin/ActRIIb-ECD, respectively,
29 uorescent protein (Ad-GFP or control virus), BMP-7 (Ad-BMP-7), or an antagonist of BMP bioactivity, n
30 h affinity ActRIIB ligand, whereas BMP-2 and BMP-7 affinities for ActRIIB are at least 100-fold lower
31  at the corresponding positions of BMP-2 and BMP-7 allowed for molecular engineering of recombinant B
32                               Maintenance of BMP-7 also reduces glomerular fibrosis and interstitial
33                                              BMP-7 also reverses vascular calcification in CKD, and r
34 the effects of bone morphogenetic protein-7 (BMP-7), also named osteogenic protein-1 (OP-1), on the p
35 phorylation or nuclear accumulation, nor did BMP-7 alter phosphorylated Smad3 dephosphorylation or de
36 ameliorated by bone morphogenetic protein-7 (BMP-7), an efficacious agent in treating animal models o
37 oblastoma x glioma hybrid cells treated with BMP-7, an inducer of L1 and neural cell adhesion molecul
38 -mesenchymal transition and survival factors BMP-7 and Bcl-2 and preserved capillary density in rat c
39 R and functional activity assays with BMP-2, BMP-7 and GDF-5 as ligands.
40 ssay, complex formation was demonstrated for BMP-7 and growth and differentiation factor-8 (GDF-8), w
41      Combination growth factor therapy using BMP-7 and IGF-1 may have considerable promise in the tre
42 ucleus pulposus (NP) cells were treated with BMP-7 and IGF-1.
43                                Pax-2, Sox-3, BMP-7 and Notch are all expressed in placodal ectoderm f
44         Oligodendrocytes expressed BMP-2 and BMP-7 and pSMAD1/5/8.
45 or inhibitor-1 promoter in PTCs treated with BMP-7 and TGF-beta compared with TGF-beta alone.
46 sults provide evidence of cross talk between BMP-7 and TGF-beta1 in the regulation of EMT in health a
47 ysomes during oocyte maturation, whereas the BMP-7 and XSTK9 mRNAs were recruited during the early st
48 utic efficacy of bone morphogenic protein-7 (BMP-7) and inhibitors of advanced glycation end products
49                Bone morphogenetic protein-7 (BMP-7) and its related BMP-6 have recently emerged as ke
50 c potential of bone morphogenetic protein 7 (BMP-7) and transforming growth factor beta1 (TGFbeta1)-i
51 signaling by the low affinity ligands BMP-2, BMP-7, and BMP-9.
52 f the BMP subfamily, including BMP-2, BMP-4, BMP-7, and GDF-5, with similar kinetics and ligand bindi
53 , noggin, attenuated the anabolic effects of BMP-7, and noggin was substantially increased by BMP-7,
54 e also measured the effects of BMP-2, BMP-4, BMP-7, and the BMP inhibitor LDN-193189 on the expressio
55  of IGFBP-3 with bone morphogenic protein-7 (BMP-7), another member of the TGF-beta superfamily, resu
56 s absent in the liver, but the receptors for BMP-7 are present on adult hepatocytes.
57 ibrillin-1 and bone morphogenetic protein-7 (BMP-7) are mediated by the prodomain of growth factor co
58 lectively, our results argue for the role of BMP-7 as a kidney- and bone-produced endogenous regulato
59 o establish a role for endogenous glomerular BMP-7 as an autocrine regulator of podocyte integrity in
60  successfully reversed with a bone anabolic, BMP-7, associated with a reduction in plasma phosphorus.
61                                          The BMP-7-binding affinity of site-specific variants of Nogg
62 BMPR1A, another BMP type 1 receptor, whereas BMP-7 binds to ACVR1 to activate SMAD1/5/9 signaling.
63 onstrated that bone morphogenetic protein-7 (BMP-7) blunted the development of fibrosis in a rat mode
64 d the expression of BMP-2, BMP-4, BMP-5, and BMP-7; BMP type II receptor (BMPRII); and phosphorylated
65 d as being in contact with the ligand in the BMP-7-BMPR-II complex but are found mutated in genetic d
66       The expression of BMP-2, BMP-4, BMP-5, BMP-7, BMPRII, and pSMAD1/5/8 was quantified by immunost
67 d neurons expressed BMP-2, BMP-4, BMP-5, and BMP-7; BMPRII; and pSMAD1/5/8.
68 ic growth was induced by exposure to NGF and BMP-7 (bone morphogenetic protein-7).
69 ect on the affinity of chordin for BMP-4 and BMP-7 but C-terminal cleavage increases the efficacy of
70 cal role as a negative feedback regulator of BMP-7 but not BMP-6-induced biological responses.
71 GF-beta family ligands Activin B, BMP-6, and BMP-7, but not the frog Cerberus ligand BMP-2.
72       Epithelial expression is also seen for Bmp-7, but transcripts are less dramatically upregulated
73 t maintenance of renal (especially podocyte) BMP-7 by transgenic expression reduces diabetic renal in
74 e morphogenetic proteins (BMP)-2, BMP-4, and BMP-7 can promote the development of tyrosine hydroxylas
75 actions with other signaling pathways, chick BMP-7 (cBMP-7) was cloned.
76 thods elucidated the interaction between the BMP-7 complex and the extracellular domains of its type
77 hadowing electron microscopy of molecules of BMP-7 complex bound to fibrillin-1 confirmed these findi
78 pabilities between the growth factor and the BMP-7 complex in multiple in vitro bioactivity assays.
79    However, upon binding to fibrillin-1, the BMP-7 complex is rendered into a closed ring shape, whic
80 two prodomain propeptide chains and that the BMP-7 complex is structurally similar to the small trans
81              This interaction may target the BMP-7 complex to fibrillin microfibrils in the extracell
82 t upon prodomain binding to fibrillin-1, the BMP-7 complex undergoes a conformational change, which d
83                      The BMP-7 prodomain and BMP-7 complex, but not the separated growth factor dimer
84 evidence that PD cleavage by MMP-13 leads to BMP-7 CPLX disintegration and bioactive GF release.
85  demonstrated that PD-dependent targeting of BMP-7 CPLXs to the extracellular fibrillin microfibril (
86 of oral phosphate binders or intraperitoneal BMP-7 decreased expression of osterix and aortic mineral
87                                              BMP-7 did not inhibit Smad3 phosphorylation or nuclear a
88    It is concluded that maintenance of renal BMP-7 during the evolution of diabetic nephropathy reduc
89                    Compared to vehicle-rats, BMP-7 enhanced glucose utilization in the basal ganglia
90 cific expression profile of genes, including Bmp-7, EphA5/Cek-7, EphA4/Cek-8, and several chick homol
91                                              BMP-7 expression is absent in the liver, but the recepto
92                                              BMP-7 expression is highest in the kidney, and its genet
93                                              Bmp-7 expression patterns demonstrate dissociation in th
94 ncreased bone sialoprotein, osteocalcin, and BMP-7 expression.
95  a loss of renal bone morphogenic protein-7 (BMP-7) expression.
96            The osseous lesions treated by Ad-BMP-7 gene delivery demonstrated rapid chrondrogenesis,
97                  This study utilized ex vivo BMP-7 gene transfer to stimulate tissue engineering of a
98 ulation of bovine NP cells by both IGF-1 and BMP-7 greatly potentiated anabolism through complementar
99 l group and the CKD low-phosphate/calcitriol/BMP-7 groups had reduced phosphate levels compared with
100       We found that BMP-2, BMP-4, BMP-6, and BMP-7 had no direct effect on prostate cancer cell growt
101                                 Furthermore, BMP-7 had no effect on Smad3 signaling after siRNA-media
102                Bone morphogenetic protein-7 (BMP-7) has been shown to enhance dendritic growth and im
103                                     However, BMP-7 immunolocalization in other tissues known to be ac
104                Bone morphogenetic protein-7 (BMP-7) improves outcome in animal models of fibrotic ren
105 arent, suggesting that immunolocalization of BMP-7 in certain tissues represents specific extracellul
106                     Transgenic expression of BMP-7 in glomerular podocytes and proximal tubules preve
107 ptor utilization by BMP-2, BMP-4, BMP-6, and BMP-7 in primary human mesenchymal stem cells (hMSC), a
108 pendent reversal of TGF-beta1-induced EMT by BMP-7 in renal tubular epithelial cells and mammary duct
109 few studies have addressed the expression of BMP-7 in reproductive tissues, and the role of BMP-7 rem
110 ed nuclear accumulation of Smad-1 induced by BMP-7 in sympathetic neurons, suggesting a direct enhanc
111 his report demonstrates that the function of BMP-7 in the oviduct involves the induction of apoptosis
112                        Immunolocalization of BMP-7 in tissues like the kidney capsule and skin reveal
113 er exposure to bone morphogenetic protein-7 (BMP-7) in vitro.
114 s ameliorated by the skeletal anabolic agent BMP-7, in part through deposition of phosphate and incre
115                        PACAP and VIP reduced BMP-7-induced dendritic growth by approximately 70-90%,
116      In vitro lineage tracing confirmed that BMP-7-induced insulin-expressing cells arise mainly from
117 cyte apoptosis by modulation of TGF-beta and BMP-7-induced pro- and antiapoptotic signals.
118            Furthermore, addition of purified BMP-7 induces apoptosis in primary oviduct cells.
119                          Here we report that BMP-7 induces formation of epithelial cell aggregates in
120                                  Exposure to BMP-7 induces nuclear translocation of Smad1 (Sma- and M
121                            BMP-4, BMP-2, and BMP-7 inhibited basal and tumor necrosis factor alpha-st
122                             In this setting, BMP-7 inhibits epithelial-mesenchymal transition involvi
123 re, through a cell-autonomous loop BMP-4 and BMP-7 intensified Smad1/5 signaling though a feedforward
124               Furthermore, neither BMP-4 nor BMP-7 interfere with neural induction when misexpressed
125                   These results suggest that BMP-7 is able to act as a dopaminotrophic agent without
126                                              BMP-7 is an important regulator of skeletal remodeling a
127 e physiological circulating concentration of BMP-7 is between 100 and 300 pg/ml.
128                           In postnatal life, BMP-7 is expressed primarily in the kidney, and expressi
129 -7 significantly inhibit glomerular lesions, BMP-7 is most effective in the inhibition of tubular inf
130                                              BMP-7 is secreted as a stable complex consisting of a gr
131 nd biophysical methods are used to show that BMP-7 is secreted as a stable complex consisting of the
132                  Bone morphogenic protein-7 (BMP-7) is a key protein involved in liver organogenesis
133 systemic administration of recombinant human BMP-7 leads to repair of severely damaged renal tubular
134                                A second BMP, BMP-7, less studied than BMP-2 may have opposing actions
135 he ability of THR-123, a cyclic peptide with BMP-7-like activity, to regenerate beta-cell mass in dia
136 ovel pathway through which administration of BMP-7 may attenuate renal damage.
137        In addition, we provide evidence that BMP-7-mediated repair of renal injury is associated with
138 lular hyaluronan-cell interactions inhibited BMP-7-mediated Smad1 phosphorylation, nuclear translocat
139              Therefore, we hypothesized that BMP-7 might function as an endogenous regulator of adult
140 we hypothesized that systemic treatment with BMP-7 might induce MET involving adult renal fibroblasts
141 tanol also antagonized ethanol inhibition of BMP-7 morphogenesis in NG108-15 cells.
142                    We further focused on the BMP-7 mRNA and demonstrated that sequence elements withi
143                           Interestingly, the BMP-7 mRNA lacks the previously defined eCPE sequences p
144  3'UTR were necessary for recruitment of the BMP-7 mRNA to polysomes and sufficient to direct the add
145 ies (BMP-7, n=7; vehicle, n=8); LCBF series (BMP-7, n=6; vehicle, n=8).
146 animals groups were studied: LCMRglu series (BMP-7, n=7; vehicle, n=8); LCBF series (BMP-7, n=6; vehi
147  decreased motility, mimicking the effect of BMP-7 on embryonic metanephric mesenchyme to generate ep
148     In this study, we examined the effect of BMP-7 on functional recovery, local cerebral blood flow
149               Here, we studied the effect of BMP-7 on response to TGF-beta in the proximal tubular ce
150 or MG132 reproduced the inhibitory action of BMP-7 on Smad3 signaling.
151  1 (IGF-1) and bone morphogenetic protein 7 (BMP-7) on bovine spine discs and by elucidating the rele
152                                              BMP-7 or vehicle (volume, 25 microl) was administered in
153 protein (Ad-GFP or control virus), BMP-7 (Ad-BMP-7), or an antagonist of BMP bioactivity, noggin (Ad-
154 genic medium (CM), CM with TGFbeta1, CM with BMP-7, or CM with both TGFbeta1 and BMP-7.
155 ssion of bone morphogenetic protein (BMP)-2, BMP-7, osteopontin, and bone sialoprotein were evaluated
156  vivo when compared with its closely related BMP-7 paralog.
157 nd conserved MMP-13 cleavage site within the BMP-7 PD.
158 o EndMT, whereas bone morphogenic protein 7 (BMP-7) preserved the endothelial phenotype.
159 lost in PTCs after TGF-beta stimulation, but BMP-7 prevented this.
160                             We conclude that BMP-7 prevents TGF-beta-mediated loss of the transcripti
161 tivity of chimeric precursors containing the BMP-7 prodomain and BMP-4 mature domain, or vice versa,
162                                          The BMP-7 prodomain and BMP-7 complex, but not the separated
163                                              BMP-7 prodomain variants were used to map the critical e
164    We present the nanoscale structure of the BMP-7 prodomain-growth factor complex using electron mic
165                Bone morphogenetic protein 7 (BMP-7) regulates cellular metabolism in embryonic and ad
166 P-7 in reproductive tissues, and the role of BMP-7 remains unclear.
167                                              BMP-7 restores skeletal anabolic balance in animal model
168 hat neutralization of circulating endogenous BMP-7 results in significantly impaired regeneration of
169                          Here we report that BMP-7 reverses TGF-beta1-induced epithelial-to-mesenchym
170 rapeutic administration of recombinant human BMP-7 (rhBMP-7) significantly enhances liver regeneratio
171 systemic administration of recombinant human BMP-7 (rhBMP-7) significantly inhibited EndMT and the pr
172 mutant/KRAS-dependent cells, KRAS stimulates BMP-7 secretion and BMP signaling, leading to TAK1 activ
173 morphogenetic protein (BMP) such as BMP-2 or BMP-7 sets in motion a cascade of cellular events result
174 ol 3-kinase/Akt pathway and thus potentiated BMP-7 signaling in bovine NP cells.
175 n other tissues known to be active sites for BMP-7 signaling is not apparent, suggesting that immunol
176 teraction between Fbn2-rich microfibrils and BMP-7 signaling.
177  ACVR1 is the major receptor for transducing BMP-7 signals in osteoclasts.
178                                              BMP-7 significantly improved the total neurological scor
179                               Interestingly, BMP-7 significantly increased TH-ir in the SN of the non
180 ous locomotor activity was observed, however BMP-7 significantly increased the density of tyrosine hy
181 t although aminoguanidine, pyridoxamine, and BMP-7 significantly inhibit glomerular lesions, BMP-7 is
182 ent caused further downregulation of Klotho, BMP-7, Smad7, and E-cadherin, all of which are associate
183                                              BMP-7 specifically limited Smad3 but not Smad2 signaling
184 r exhibited Smad1 nuclear translocation upon BMP-7 stimulation.
185 the effect of a potent osteoinductive agent (BMP-7), suggesting a synergism between the soluble facto
186 7, and noggin was substantially increased by BMP-7, suggesting a negative feedback regulatory mechani
187 1/5/9 levels when induced either by BMP-2 or BMP-7, suggesting that ACVR1 is the major receptor for t
188 al skeletal histomorphometry was reversed by BMP-7 therapy to normal values and significantly improve
189  be re-engaged by systemic administration of BMP-7 to mediate repair of tubular injury in a fibrotic
190  search of a mechanism behind the ability of BMP-7 to repair damaged renal tubules, we hypothesized t
191         We therefore tested the potential of BMP-7 to reverse TGF-beta1-induced de novo EMT in a mous
192                   The ossicles formed by the BMP-7-transduced HOKC were smaller and more dense than t
193  smaller and more dense than those formed by BMP-7-transduced human gingival fibroblasts (HGF).
194 ty was limited to fibroblasts, we found that BMP-7-transduced human oral keratinocyte cells (HOKC) al
195 hoenolpyruvate carboxykinase promoter-driven BMP-7 transgene and nondiabetic, transgenic mice as well
196                         These effects of the BMP-7 transgene occur without changing renal TGF-beta le
197  of messenger RNA levels, was highest in the BMP-7-treated group.
198 is as compared to the control-treated and Ad-BMP-7-treated specimens.
199  29.0+/-4.9 O.D. control vs. 64.4+/-6.9 O.D. BMP-7-treated, p<0.001).
200 lso noted (113.2 ng/g control vs. 198.2 ng/g BMP-7-treated, p<0.01).
201 : 14.8+/-1.19 O.D. control vs. 36+/-2.6 O.D. BMP-7-treated, p<0.05; pars compacta: 29.0+/-4.9 O.D. co
202 arbitrary units) control vs. 50.2+/-4.3 O.D. BMP-7-treated; p<0.05].
203 us BMP-7 treatment, and CM plus TGFbeta1 and BMP-7 treatment (compared with CM treatment alone).
204                                              BMP-7 treatment corrected the hyperphosphatemia, correct
205                     No significant effect of BMP-7 treatment on spontaneous locomotor activity was ob
206                                     However, BMP-7 treatment reduced Smad3 DNA binding to a consensus
207 ved with CM plus TGFbeta1 treatment, CM plus BMP-7 treatment, and CM plus TGFbeta1 and BMP-7 treatmen
208  at limiting fibrosis of the kidney when the BMP-7 was administered during the progression of fibroti
209  and a treatment protocol used to examine if BMP-7 was beneficial at limiting fibrosis of the kidney
210 ricularly administered neurotrophic factors, BMP-7 was not associated with an increase in the sensiti
211 mologous to the fibrillins, the prodomain of BMP-7 was tested for binding to fibrillin-1 or to LTBP-1
212 ellet was in the group in which TGFbeta1 and BMP-7 were added to the medium.
213                       Here, we observed that BMP-7, which preferentially binds to ACVR1, promotes ost
214  structure of the antagonist Noggin bound to BMP-7, which shows that Noggin inhibits BMP signalling b
215 ansforming growth factor-beta (TGF-beta) and BMP-7 with high affinity, suggesting that it may be an i

 
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