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1  its complex actions in bone to cells of the osteoblast lineage.
2  dependent upon expression of Gsalpha in the osteoblast lineage.
3 rentiation of mesenchymal stem cells towards osteoblast lineage.
4  accompanied by reduced Wnt signaling in the osteoblast lineage.
5 of mesenchymal cell differentiation into the osteoblast lineage.
6 lls, which some evidence suggests are of the osteoblast lineage.
7 es of these pathways in specification of the osteoblast lineage.
8 sB mice is independent of the changes in the osteoblast lineage.
9 ions downstream of Ihh in development of the osteoblast lineage.
10                                 Cells of the osteoblast lineage affect the homing and the number of l
11 blasts, allowing the conditional ablation of osteoblast lineage after treatment with ganciclovir (GCV
12 we identify two distinct roles for RA in the osteoblast lineage: an early role in blocking the recrui
13 ons in BMP receptor function targeted to the osteoblast lineage and demonstrate a necessary role of B
14 skeletal phenotype is cell autonomous to the osteoblast lineage and independent of adipocyte formatio
15 he mesenchymal maturation program toward the osteoblast lineage and is mechanistically distinct from
16 senchymal stem cell (hMSC) commitment to the osteoblast lineage and modulates Wnt/beta-catenin signal
17       Signals that govern development of the osteoblast lineage are not well understood.
18 ell migration and differentiation toward the osteoblast lineage as measured by mineralized nodule for
19  the effects of the NOTCH3 activation in the osteoblast lineage, BGLAP-Cre or Dmp1-Cre transgenics we
20 ated RUNX2 expression for differentiation to osteoblast lineages but failed to induce downstream RUNX
21 ises from mesenchymal cells induced into the osteoblast lineage by essential transcription factors an
22           Wnt10b shifts cell fate toward the osteoblast lineage by induction of the osteoblastogenic
23  the mouse osteocalcin 2 promoter in several osteoblast lineage cell lines.
24 e production of trophic factors required for osteoblast lineage cell maintenance, ultimately leading
25 dherin expression was efficiently ablated in osteoblast lineage cells as assessed by mRNA expression
26 C/EBP transcription factors was disrupted in osteoblast lineage cells by overexpressing a naturally o
27 lized 3.6Col1a1-tk mice in which replicating osteoblast lineage cells can be ablated in an inducible
28  on the skeleton, but the role of ERalpha in osteoblast lineage cells has remained elusive.
29    Our objective was to ablate proliferating osteoblast lineage cells in order to investigate the imp
30  (rAAV9) is highly effective for transducing osteoblast lineage cells in the bone.
31      In conclusion, N-cadherin expression in osteoblast lineage cells is dispensable for HSC maintena
32    Recently, we showed that Wnts produced by osteoblast lineage cells mediate the osteo-anabolic resp
33 nce suggesting that N-cadherin expression on osteoblast lineage cells regulates hematopoietic stem ce
34  receptor (EGFR) specifically inactivated in osteoblast lineage cells revealed that EGFR stimulates b
35 1 is a mechanosensitive ion channel by which osteoblast lineage cells sense and respond to changes in
36                         Osteoclasts act upon osteoblast lineage cells throughout their differentiatio
37 nesis indirectly by enhancing the ability of osteoblast lineage cells to stimulate osteoclastogenesis
38           By deleting the receptor Bmpr1a in osteoblast lineage cells with Dmp1-Cre, we observed a dr
39 lucose consumption in the primary culture of osteoblast lineage cells, and deletion of Glut1 diminish
40  Additional interactions of osteoclasts with osteoblast lineage cells, including interactions with ca
41 ugh PHEX/Phex expression occurs primarily in osteoblast lineage cells, transgenic Phex expression in
42 on of osteoclasts secondary to activation of osteoblast lineage cells, which expressed increased RANK
43 ressed by a variety of cell types, including osteoblast lineage cells.
44 ifferent stages of differentiation in murine osteoblast lineage cells.
45 llow the fates of stage-selective subsets of osteoblast lineage cells.
46  CXCL12 expression is secondary to a loss of osteoblast lineage cells.
47  in osteoclast precursors and indirectly via osteoblast lineage cells.
48 nsgenic mice that express Cre recombinase in osteoblast lineage cells.
49 rt through stimulating glucose metabolism in osteoblast lineage cells.
50 tion factor that is first expressed in early osteoblast-lineage cells and represents a primary determ
51 nce suggests that only a minuscule number of osteoblast-lineage cells are present in peripheral blood
52 Conditional Wnt16 inactivation revealed that osteoblast-lineage cells are the principal source of WNT
53                                              Osteoblast-lineage cells circulate in physiologically si
54 ne-specific proteins to identify circulating osteoblast-lineage cells in 11 adolescent males and 11 a
55                                 However, the osteoblast-lineage cells isolated from these mice exhibi
56  have been shown to disrupt Wnt signaling in osteoblast-lineage cells, but the efficacy for Wnt prote
57 nistically, YAP and TAZ regulate a subset of osteoblast-lineage cells, identified by single-cell RNA
58 ivated by either tamoxifen or doxycycline in osteoblast-lineage cells, we show that WNT7B recovers bo
59 ociated athanogene-1 (BAG-1) is expressed by osteoblast-lineage cells; early embryonic lethality in B
60 S immobilizes secreted OPG at the surface of osteoblasts lineage cells, which facilitates binding of
61 poietic (e.g. T and B-cell) and mesenchymal (osteoblast lineage, chondrocyte) cell types.
62                   Runx2 is indispensable for osteoblast lineage commitment and early differentiation
63 BPD transcriptomic networks in driving human osteoblast lineage commitment.
64 ctor Maf (also known as c-Maf) is central to osteoblast lineage commitment.
65 ncluding minimal association with osterix(+) osteoblast-lineage committed mesenchymal cells in wild-t
66 an important role in regulating BMP9-induced osteoblast lineage differentiation of MSCs.
67 coordinate beta-catenin signaling within the osteoblast lineage during embryonic and postnatal bone d
68 rect pluripotent mesenchymal cells toward an osteoblast lineage, exert their osteoinductive effects t
69       Mice lacking G(s)alpha in cells of the osteoblast lineage exhibit a reduction in pro-B and pre-
70 oth Malat1 KO and conditional KO mice in the osteoblast lineage exhibit significant osteoporosis.
71  active G alpha(q) transgene in cells of the osteoblast lineage exhibited severe osteopenia in cortic
72 dependent signaling pathways in cells of the osteoblast lineage extrinsically regulate bone marrow B
73          In the absence of Ihh, cells of the osteoblast lineage fail to activate the expression of Ru
74 ndifferentiated MPCs and MPCs induced to the osteoblast lineage for 1-7 days by cDNA microarray analy
75 ubunit G(s)alpha is required in cells of the osteoblast lineage for normal postnatal B lymphocyte pro
76 l and signaling mechanisms that regulate the osteoblast lineage for the calvaria, which forms the roo
77 otency, we measured the expression levels of osteoblast lineage genes in synovial and periosteal clon
78      Donor cells found in the bone expressed osteoblast lineage genes, and produced the extracellular
79 oreover, mice with loss of RNF146 within the osteoblast lineage had increased fat stores and were glu
80              Mice lacking Atg7 in the entire osteoblast lineage had low bone mass and fractures assoc
81 teriparatide's actions on early cells of the osteoblast lineage has been demonstrated.
82  increases the numbers of early cells of the osteoblast lineage, hastens their differentiation into o
83 hondrium; the latter were early cells of the osteoblast lineage immediately descended from their prog
84 omoter-driven cre to mark early cells of the osteoblast lineage in adult mice.
85 commitment of mesenchymal progenitors to the osteoblast lineage in association with enhanced Wnt sign
86 t Ihh signaling is directly required for the osteoblast lineage in the developing long bones and that
87 Ihh) is indispensable for development of the osteoblast lineage in the endochondral skeleton.
88 modulates cellular functions in cells of the osteoblast lineage in vitro and in vivo.
89 e of Gsalpha signaling in cells of the early osteoblast lineage in vivo by conditionally deleting Gsa
90                       Differentiation in the osteoblast lineage initiates with Runx2 expression, whic
91 n of osteoclast precursors with cells of the osteoblast lineage is a prerequisite for osteoclast form
92 these results suggest that commitment to the osteoblast lineage is not a requirement for RANKL gene t
93 ession in cells from different stages of the osteoblast lineage isolated by FACS sorting showed that
94 tivation of Wnt/betacatenin signaling in the osteoblast lineage leads to an increase in bone mass thr
95 tion of Tsc1 using the mesenchymal stem cell-osteoblast lineage markers induced cystogenesis in mice.
96       Taken together, our data indicate that osteoblast lineage maturation is a critical aspect under
97 le of RUNX2 activity and its function during osteoblast lineage maturation.
98 mmitment of mesenchymal cells ex vivo to the osteoblast lineage occurred in Runx2-II(-/-) mice, but o
99  family member 7B (Wnt7b) transiently in the osteoblast lineage of postnatal mice, with or without co
100          Postnatal removal of Gsalpha in the osteoblast lineage (P-Gsalpha(OsxKO) mice) yielded marke
101 ents may be necessary to regulate Osx during osteoblast lineage progression.
102 P-2 and IGF-1 regulate Osx expression during osteoblast lineage progression.
103          Selective deletion of Smurf2 in the osteoblast lineage recapitulates the phenotype of germli
104  data demonstrate that commitment within the osteoblast lineage requires sequential, stage-specific,
105           Deletion of G(s)alpha early in the osteoblast lineage results in a 59% decrease in the perc
106 Id expression may be critical to BMP-induced osteoblast lineage-specific differentiation of mesenchym
107                                              Osteoblast lineage-specific differentiation of mesenchym
108 ated by applying it to an important study of osteoblast lineage-specific differentiation.
109 kers [alkaline phosphatase, osteopontin, and osteoblast lineage-specific transcription factor (Cbfa-1
110  activity of this suppressor in cells of the osteoblast lineage suggest that it is expressed with oth
111 iption factor required for commitment to the osteoblast lineage, supporting the idea that osteoclast-
112                                 Cells of the osteoblast lineage that reside in the endosteal niche ha
113 eton, is strictly restricted to cells of the osteoblast lineage thereafter, and is regulated by BMP7
114              Although differentiation of the osteoblast lineage was not disturbed, the proliferation
115 es cell-specific gene expression in cells of osteoblast lineage, we constructed a recombinant adenovi
116 hown that Sox2 maintains self-renewal in the osteoblast lineage while inhibiting differentiation.

 
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