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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
16 y analyzing the potential miRNAs that target BMP-7/6 in silica, we identified miR-22 as a potent miRN
19 ck circuit, whereby not only miR-22 inhibits BMP-7/6, but miR-22 by itself is induced by BMP-7/6.
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
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
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
40 ssay, complex formation was demonstrated for BMP-7 and growth and differentiation factor-8 (GDF-8), w
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
50 c potential of bone morphogenetic protein 7 (BMP-7) and transforming growth factor beta1 (TGFbeta1)-i
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
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.
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
69 ect on the affinity of chordin for BMP-4 and BMP-7 but C-terminal cleavage increases the efficacy of
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
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
82 t upon prodomain binding to fibrillin-1, the BMP-7 complex undergoes a conformational change, which d
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
88 It is concluded that maintenance of renal BMP-7 during the evolution of diabetic nephropathy reduc
90 cific expression profile of genes, including Bmp-7, EphA5/Cek-7, EphA4/Cek-8, and several chick homol
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
105 arent, suggesting that immunolocalization of BMP-7 in certain tissues represents specific extracellul
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
114 s ameliorated by the skeletal anabolic agent BMP-7, in part through deposition of phosphate and incre
116 In vitro lineage tracing confirmed that BMP-7-induced insulin-expressing cells arise mainly from
123 re, through a cell-autonomous loop BMP-4 and BMP-7 intensified Smad1/5 signaling though a feedforward
129 -7 significantly inhibit glomerular lesions, BMP-7 is most effective in the inhibition of tubular inf
131 nd biophysical methods are used to show that BMP-7 is secreted as a stable complex consisting of the
133 systemic administration of recombinant human BMP-7 leads to repair of severely damaged renal tubular
135 he ability of THR-123, a cyclic peptide with BMP-7-like activity, to regenerate beta-cell mass in dia
138 lular hyaluronan-cell interactions inhibited BMP-7-mediated Smad1 phosphorylation, nuclear translocat
140 we hypothesized that systemic treatment with BMP-7 might induce MET involving adult renal fibroblasts
144 3'UTR were necessary for recruitment of the BMP-7 mRNA to polysomes and sufficient to direct the add
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
151 1 (IGF-1) and bone morphogenetic protein 7 (BMP-7) on bovine spine discs and by elucidating the rele
153 protein (Ad-GFP or control virus), BMP-7 (Ad-BMP-7), or an antagonist of BMP bioactivity, noggin (Ad-
155 ssion of bone morphogenetic protein (BMP)-2, BMP-7, osteopontin, and bone sialoprotein were evaluated
161 tivity of chimeric precursors containing the BMP-7 prodomain and BMP-4 mature domain, or vice versa,
164 We present the nanoscale structure of the BMP-7 prodomain-growth factor complex using electron mic
168 hat neutralization of circulating endogenous BMP-7 results in significantly impaired regeneration of
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
175 n other tissues known to be active sites for BMP-7 signaling is not apparent, suggesting that immunol
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
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
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
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
203 us BMP-7 treatment, and CM plus TGFbeta1 and BMP-7 treatment (compared with CM treatment alone).
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
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