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1 to stimulate vitamin D receptor targets and osteoblastogenesis.
2 osteoclastogenesis and a smaller increase in osteoblastogenesis.
3 othesized that estrogen loss also stimulates osteoblastogenesis.
4 plained, at least in part, by an increase in osteoblastogenesis.
5 to enhanced osteoclastogenesis and decreased osteoblastogenesis.
6 on stiff substrates and to cells undergoing osteoblastogenesis.
7 s positive for Runx2, a master regulator for osteoblastogenesis.
8 differentiation, while also contributing to osteoblastogenesis.
9 nesis and coordinates osteoclastogenesis and osteoblastogenesis.
10 neage determination between adipogenesis and osteoblastogenesis.
11 ntly inhibited adipogenesis whereas promoted osteoblastogenesis.
12 NFATc1 regulates both osteoclastogenesis and osteoblastogenesis.
13 nd increasing adipogenesis while suppressing osteoblastogenesis.
14 1 isoform transcripts is a hallmark of early osteoblastogenesis.
15 ells and represents a primary determinant of osteoblastogenesis.
16 promoted enhanced adipogenesis and decreased osteoblastogenesis.
17 ctivator critically mediates Ihh function in osteoblastogenesis.
18 expression along various lineages including osteoblastogenesis.
19 ormation of osteoblast precursors to promote osteoblastogenesis.
20 interrelated network of miRNAs that control osteoblastogenesis.
21 of action of this antiosteoporotic agent in osteoblastogenesis.
22 and hyperactivation of p38 MAPK that favors osteoblastogenesis.
23 erostin expression by the osteocyte favoring osteoblastogenesis.
24 contrast, deletion of Tie2 has no effect on osteoblastogenesis.
25 udies, we evaluated the role of Wnt11 during osteoblastogenesis.
26 ize Wnt signaling, an essential stimulus for osteoblastogenesis.
27 HES-1 appears to mediate effects of Notch on osteoblastogenesis.
28 1 interacts with RUNX2, a master molecule of osteoblastogenesis and a regulator of chondrocyte matura
32 , identify Bicc1 as a genetic determinant of osteoblastogenesis and BMD and suggest that it does so b
33 amin C's epigenetic functions are central to osteoblastogenesis and bone formation and may be leverag
34 nt, at least in part, for the attenuation of osteoblastogenesis and bone formation by the age-depende
35 eoclastosis, and angiogenesis and stimulated osteoblastogenesis and bone formation, whereas ephrinB2-
37 togenesis in a cell-autonomous manner and in osteoblastogenesis and chondrogenesis in non-cell-autono
38 one mass through a dual mechanism: increased osteoblastogenesis and decreased osteoclastogenesis.
41 t indispensable for Avp action in inhibiting osteoblastogenesis and gene expression, Avp-stimulated g
42 ticoids depress bone formation by inhibiting osteoblastogenesis and increasing osteoblast apoptosis.
43 s bone resorption over formation by lowering osteoblastogenesis and increasing osteoclastogenesis.
44 he bisphosphonate group, is known to enhance osteoblastogenesis and inhibit osteoclastic bone resorpt
46 t homeostasis, resulting in the promotion of osteoblastogenesis and inhibition of osteoclastogenesis,
47 rate that canonical Wnt signaling stimulates osteoblastogenesis and inhibits adipogenesis of bipotent
49 ghly expressed during osteoclastogenesis and osteoblastogenesis and is dramatically upregulated in th
50 close to TMEM135, a gene recently linked to osteoblastogenesis and longevity) significantly associat
51 in vivo, the agomir significantly increased osteoblastogenesis and mineralization, reversed bone los
53 eptor, EphB4, is involved in the coupling of osteoblastogenesis and osteoclastogenesis and in angioge
54 plays a pivotal role in the disregulation of osteoblastogenesis and osteoclastogenesis induced by ovx
55 he Phe377del mutation in ANK causes impaired osteoblastogenesis and osteoclastogenesis resulting in h
56 tetracycline-labeled vertebrae, and impaired osteoblastogenesis and osteoclastogenesis, as determined
58 obiota has anti-anabolic effects suppressing osteoblastogenesis and pro-catabolic effects enhancing o
60 gests that some miRs play important roles in osteoblastogenesis and skeletal homeostasis, much less i
62 with severe osteopenia because of defective osteoblastogenesis and subsequent impaired osteocalcin p
64 scle dedifferentiation with manifestation of osteoblastogenesis and ultimately endovascular calcium p
67 whereas ephrinB2-Fc stimulated angiogenesis, osteoblastogenesis, and bone formation but had no effect
68 , for 1alpha,25(OH)(2)D(3) biosynthesis, for osteoblastogenesis, and for small interfering RNA for me
69 n of preosteoblast replication, induction of osteoblastogenesis, and inhibition of osteoblast and ost
73 is by regulating both osteoclastogenesis and osteoblastogenesis, and they serve as inhibitors for cal
74 he principal site for osteoclastogenesis and osteoblastogenesis; and an increase in the former has be
75 genes that are capable of further affecting osteoblastogenesis, angiogenesis, and the deposition of
76 iously shown that cellular proliferation and osteoblastogenesis are important in the development of v
77 tagonists, namely SR49059 or ADAM, increased osteoblastogenesis, as did the genetic deletion of Avpr1
78 ignaling shifts mesenchymal cell fate toward osteoblastogenesis at the expense of adipogenesis; howev
81 he lineage determination of adipogenesis and osteoblastogenesis by demethylating Wnt10a gene and upre
84 vivo, cells from these mice showed enhanced osteoblastogenesis concordant with their high bone mass
85 associated with the post-commitment stage of osteoblastogenesis, demonstrated by impaired ECM mineral
88 hanced adipogenesis and consequently reduced osteoblastogenesis from MSCs, thus suppressing bone form
89 demonstrate that miR-34c is critical during osteoblastogenesis in part by regulating Notch signaling
90 adipogenic potential and causes spontaneous osteoblastogenesis in ST2 cells and mouse embryonic fibr
91 tween low bone mineral density and decreased osteoblastogenesis in the bone marrow and validate the s
94 elta signaling is required for Wnt3a-induced osteoblastogenesis in these cells, and PKCdelta homozygo
97 mal bone mass or osteopenia due to defective osteoblastogenesis increased bone formation without affe
100 (SAMP6) to test the hypothesis that reduced osteoblastogenesis is linked with decreased bone mass.
102 on factor proven essential for commitment to osteoblastogenesis, is also expressed in response to BMP
103 another mesenchymal differentiation process, osteoblastogenesis, is enhanced upon HDAC inhibition.
104 ctivated Fz2 does not influence apoptosis or osteoblastogenesis, it inhibits adipogenesis through a m
106 Runx2, a transcription factor essential for osteoblastogenesis, negatively regulates expression of t
107 pression in multiple myeloma cells inhibited osteoblastogenesis of bone marrow-derived osteoblast pro
108 n in a cellular in vivo context during early osteoblastogenesis of MC3T3-E1 cultures and BMSCs induce
111 ich p38 signaling in myeloma cells regulates osteoblastogenesis, osteoclastogenesis, and bone destruc
112 sal microbiota's immunoregulatory effects on osteoblastogenesis, osteoclastogenesis, marrow T-cell he
113 lpha,25(OH)(2)D(3) and 25(OH)D(3) stimulated osteoblastogenesis (P < 0.05), but only 1alpha,25(OH)(2)
114 d that DeltaFosB transcriptionally regulates osteoblastogenesis, possibly at the expense of adipogene
119 tructure, increased bone turnover, depressed osteoblastogenesis (Runx2, Sparc), and increased both os
120 e progression, immune system activation, and osteoblastogenesis suggest, respectively, that MM-MSC ar
121 ntiated mesenchyme and a marked reduction in osteoblastogenesis that resulted in a high incidence of
122 accumulating evidence has implicated BMPs in osteoblastogenesis, the mechanisms by which BMPs regulat
123 ecution and completion of BMP2 signaling for osteoblastogenesis through a mechanism that requires RUN
124 enitor cells toward adipogenesis rather than osteoblastogenesis through inhibiting Wnt/B-catenin sign
125 take place with the parallel enhancement of osteoblastogenesis, thus providing a novel therapeutic a
126 or followed by osteogenic challenge impaired osteoblastogenesis via suppressing Osx expression, sugge
127 essential role in cellular proliferation and osteoblastogenesis via the beta-catenin signaling pathwa
129 echanism involved in reduced bone formation, osteoblastogenesis was studied in bone marrow stromal ce
131 n, indicating that the stimulatory effect on osteoblastogenesis was unrelated to BMP and Wnt signalin
132 ate the potential role of Notch signaling in osteoblastogenesis, we used conditional alleles to genet
134 cription factor complex that is required for osteoblastogenesis, while antagonizing PPARgamma-mediate
135 reduced osteolytic lesion area and enhanced osteoblastogenesis, while loss of Notch3 in osteoblastic