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

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