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1              Remarkably, for our purpose, an osteoblast-specific ablation of sympathetic signaling re
2 ice that were genetically altered to produce osteoblast-specific, activated PTH/PTHrP receptors (PPRs
3        In contrast, the AP1 site mediates an osteoblast-specific activation caused by the preferentia
4 steoblasts abolishes the binding of OSF2, an osteoblast-specific activator of transcription that bind
5          When multimerized, CE1 conferred an osteoblast-specific activity to a heterologous promoter
6 er, multimers of this OSE2 at -1347bp confer osteoblast-specific activity to a minimum alpha1(I) coll
7 timers of this alpha2(I) OSE2 element confer osteoblast-specific activity to the minimum alpha1(I) co
8                                      Through osteoblast-specific alteration of p53 status, we develop
9 To address this mechanism, we generated late-osteoblast-specific and osteocyte-specific WNT1 loss- an
10                  These results indicate that osteoblast-specific aptamer-functionalized LNPs could ac
11  generation and analysis of chondrocyte- and osteoblast-specific Bmp2 conditional knockout (cKO) mice
12 subunit in osteoblasts in vivo, we generated osteoblast-specific Capn4 knock-out mice using the Cre-L
13  proliferation, resulted in the induction of osteoblast-specific cell death in vitro.
14 ly of transcription factors that binds to an osteoblast-specific cis-acting element (OSE2) activating
15                                         This osteoblast-specific cis-acting element binds Osf2, a rec
16 transcription that binds to OSE2, a critical osteoblast-specific cis-acting element present in OG1 an
17                  We previously identified an osteoblast-specific cis-acting element, termed OSE2, in
18 is study indicates the existence of multiple osteoblast-specific cis-acting elements of equal importa
19  two mouse osteocalcin genes, identified two osteoblast-specific cis-acting elements, OSE1 and OSE2,
20 aPPR), whose expression was regulated by the osteoblast-specific Col1a1 promoter (Col1a1-caPPR), supp
21 blasts from Col-luc transgenic mice carrying osteoblast-specific Col1alpha1 promoter reporter, lucife
22                                 Furthermore, osteoblast-specific Col2.3-Cre(+)/OTR(fl/fl) mice, but n
23 nction in the hypothalamus, pair-feeding and osteoblast-specific conditional deletion of Ksr2 reveals
24                           Our data show that osteoblast-specific CXCR4 deletion has profound effects
25                                              Osteoblast-specific deletion of Hnf4alpha resulted in im
26                                              Osteoblast-specific deletion of PPARdelta in mice, in tu
27                                              Osteoblast-specific deletion of Tak1 resulted in clavicu
28                                 Accordingly, osteoblast-specific deletion of TC-PTP promotes insulin
29                   Using transgenic mice with osteoblast-specific deletion of Vegfa, we demonstrated t
30 es still exist because of the lack of direct osteoblast-specific delivery systems for osteogenic siRN
31 oximal OSE2 element is critical to confer an osteoblast-specific, developmentally regulated pattern o
32 Although Lrp5 is viewed as a Wnt coreceptor, osteoblast-specific disruption of beta-Catenin does not
33 ng bone remodeling, we generated a postnatal osteoblast-specific disruption of Bmpr1a that encodes th
34         Of particular interest is the single osteoblast specific element known as osteocalcin specifi
35 sence of 12 putative Cbfa1 binding elements (osteoblast-specific element 2 (OSE(2))), suggesting a po
36  Cbfa1-binding site (-248 base pairs) termed osteoblast-specific element 2 (OSE2) decreased ameloblas
37 to -113, the OCFRE is juxtaposed to OSE2, an osteoblast-specific element that binds Runx2 (Osf2, Cbfa
38 e data represent the first description of an osteoblast-specific element within the bone sialoprotein
39      The runt domain site is identical to an osteoblast-specific element-2 or acute myelogenous leuke
40         In summary, this study identified an osteoblast-specific enhancer in the Cbfa1 promoter whose
41 ased binding to OSE1, a previously described osteoblast-specific enhancer in the mOG2 promoter.
42 sis mapped the PC1-responsive region to the "osteoblast-specific" enhancer element between -420 and -
43 rs C/EBPb, TEAD1, FOSL2 and JUND at putative osteoblast-specific enhancers.
44 fa1 is one of the positive regulators of the osteoblast-specific expression of both type I collagen g
45 -acting element as important as OSE2 for the osteoblast-specific expression of OG2 in cell culture an
46                                          The osteoblast-specific expression of the HGPS mutation incr
47 tive in transgenic mice and unable to direct osteoblast-specific expression.
48  and increased trabecular bone mass from pre-osteoblast specific Ezh2 deletion (Ezh2(flox/flox) Osx-C
49 rated that TNF-alpha enhanced DNA binding of osteoblast specific factor (Osf2), AP1, and CREB, transc
50                                   Two genes, osteoblast-specific factor 2 and corneal-derived transcr
51    Periostin was originally identified as an osteoblast-specific factor and is highly expressed in th
52 ated by members of Sp1 family instead of the osteoblast-specific factor Osf1.
53              Overexpression of c-Fos, c-Jun, osteoblast-specific factor-2, and core binding factor-be
54                               The ability of osteoblast-specific FoxO1 deficiency to affect metabolic
55                                              Osteoblast-specific G(s)alpha deficiency leads to reduce
56                                     In vivo, osteoblast-specific gain of miR-34c in mice leads to an
57                           Here, we show that osteoblast-specific gain of Notch function causes severe
58                                              Osteoblast-specific gain- and loss-of-function experimen
59 struct encoding p204 antisense RNA inhibited osteoblast-specific gene activation by Cbfa1 in an osteo
60                       The molecular basis of osteoblast-specific gene expression and differentiation
61 ivation and reduced its ability to stimulate osteoblast-specific gene expression and differentiation
62  LCMV and PVM infections resulted in reduced osteoblast-specific gene expression in bone, loss of ost
63 Runx2 and Osterix, has the ability to induce osteoblast-specific gene expression in non-osteoblastic
64  displayed enhanced osteogenic potential and osteoblast-specific gene expression in vitro and in vivo
65 t the skeleton early during development, and osteoblast-specific gene expression occurs only after th
66 anscription factor, TFIIA gamma, facilitates osteoblast-specific gene expression through interactions
67               To elucidate the mechanisms of osteoblast-specific gene expression we are studying the
68 - and NH(2)-terminated surfaces up-regulated osteoblast-specific gene expression, alkaline phosphatas
69 Atf4 in non-osteoblastic cells would lead to osteoblast-specific gene expression, one of the most imp
70 hway has an important role in the control of osteoblast-specific gene expression.
71 teocalcin genes are excellent tools to study osteoblast-specific gene expression.
72 ired for activation of Osf2 and induction of osteoblast-specific gene expression.
73 e through the ERK/MAPK pathway can stimulate osteoblast-specific gene expression.
74 to bone lineages and is a major regulator of osteoblast-specific gene expression.
75 on with DLX5 or a related factor to activate osteoblast-specific gene expression.
76 nt model for studying mechanisms controlling osteoblast-specific gene expression.
77 inal differentiation of osteoblasts, and for osteoblast-specific gene expression.
78        We have studied the regulation of the osteoblast-specific gene osteocalcin (OC) by FGF2 in phe
79 e state, while in bone marrow pericytes, the osteoblast-specific gene Runx2 was primed for expression
80 nce to the promoter for osteocalcin, another osteoblast-specific gene with a loss-of-function phenoty
81 ying the regulation of osteocalcin, the most osteoblast-specific gene.
82 activating the expression of osteocalcin, an osteoblast-specific gene.
83 t OSE1 is present in the promoter of several osteoblast-specific genes including Cbfa1 itself.
84  transcriptional component for activation of osteoblast-specific genes like osteocalcin.
85  complexes containing the BRM ATPase repress osteoblast-specific genes to maintain the precursor stat
86  activation of Runx2 activity, expression of osteoblast-specific genes, and calcium deposition.
87 ostate cancer cells can induce expression of osteoblast-specific genes.
88 ells induces the expression of the principal osteoblast-specific genes.
89 oreover, the impact of postnatally acquired, osteoblast-specific insulin deficiency on the pancreas-t
90                     The relationship between osteoblast-specific insulin signaling, osteocalcin activ
91 function of osteoblast-derived Jagged1 using osteoblast-specific Jagged1 transgenic mouse model.
92 ass in Lrp5-deficient mice, and gut- but not osteoblast-specific Lrp5 inactivation decreases bone for
93 ptors, Bmpr1a and Acvr1, respectively, in an osteoblast-specific manner, increased bone mass in mice.
94 abecular bone and/or stromal cells increases osteoblast-specific marker expression in hyperactive Gja
95 keleton but fail to form bone and to express osteoblast-specific marker genes.
96 nesis in MSCs and therefore functioned as an osteoblast-specific marker.
97 ontributed to the up-regulated expression of osteoblast-specific markers (e.g., Bsp and Ocn) in Gja1(
98                                              Osteoblast-specific miR-23a cluster gain-of-function mic
99 igated the role of IL-3 on the regulation of osteoblast-specific molecules, receptor activator of NF-
100 e the role of osteocalcin, the most abundant osteoblast-specific non-collagenous protein, we have gen
101 tions between ATF4 and Runx2/Cbfa1 stimulate osteoblast-specific Ocn expression and suggests that thi
102 on of the Adar1 gene decreased expression of osteoblast-specific osteocalcin and bone sialoprotein ge
103  homeoprotein, which is able to regulate the osteoblast-specific osteocalcin promoter, can bind this
104 mic and transmembrane domains, driven by the osteoblast-specific osteocalcin promoter.
105     In contrast, deletion of Ddrgk1 with the osteoblast-specific Osteocalcin-Cre and Leptin receptor-
106                                 As a result, osteoblast-specific overexpression of Hnf4alpha2 prevent
107       Here, we evaluated the consequences of osteoblast-specific overexpression of or loss of insulin
108                                              Osteoblast-specific overexpression of TGF-beta 2 from th
109 ion and repression of the Runx2 gene via its osteoblast-specific P1 promoter (encoding mRNA for the R
110 tions observed in mice heterozygous for both osteoblast-specific Pdk1 deletion and either Runx2 or Cr
111 capitulation of RTS spectrum phenotypes with osteoblast-specific Pdk1 deletion in mice (Pdk1osx mice)
112                            Osteocalcin is an osteoblast-specific peptide that is reported to be invol
113                                              Osteoblast-specific PGC-1alpha upregulation by 6-C-beta-
114 ly via macropinocytosis, and boosted in vivo osteoblast-specific Plekho1 gene silencing, which promot
115 scription factor, CBFA1, and associates with osteoblast-specific promoters in vivo in a CBFA1-depende
116 tic cells alters transcriptional activity of osteoblast-specific promoters, presumably via modulation
117 is activity was needed for the regulation of osteoblast-specific promoters.
118 A segment that abolished the binding of this osteoblast-specific protein also abolished lacZ expressi
119 as for examining factors which contribute to osteoblast-specific regulation of gene expression.
120 2 and MINT both target an information-dense, osteoblast-specific regulatory region of the OC proximal
121 results in synergistic transactivation of an osteoblast-specific reporter.
122                                          The osteoblast-specific secreted molecule osteocalcin behave
123 decreases the bioactivity of osteocalcin, an osteoblast-specific secreted molecule that enhances secr
124 SHP2's role in skeletal development, we made osteoblast-specific SHP2 deficient mice using Osterix (O
125 rBMPR-IB also blocked mRNA expression of the osteoblast specific transcription factor, Osf2/ Cbfa1, a
126 a 3/polyoma enhancer-binding protein 2alphaA/osteoblast-specific transcription factor 2 regulates ost
127       This study identifies Osf2/Cbfa1 as an osteoblast-specific transcription factor and as a regula
128 keletal dysplasia caused by mutations in the osteoblast-specific transcription factor CBFA1.
129 , osteocalcin, alkaline phosphatase, and the osteoblast-specific transcription factor Cbfa1.
130 eam signaling molecules Smad1 and -5 and the osteoblast-specific transcription factor core-binding fa
131 stent with an observed downregulation of the osteoblast-specific transcription factor core-binding fa
132                          Osterix (Osx) is an osteoblast-specific transcription factor essential for o
133 er being the binding site of Cbfa1, the only osteoblast-specific transcription factor known to date.
134                                    Since the osteoblast-specific transcription factor Osf2/Cbfa1 is i
135                     Here, we report that the osteoblast-specific transcription factor Osterix (Osx),
136                          Osterix (Osx) is an osteoblast-specific transcription factor required for bo
137                          Osterix (Osx) is an osteoblast-specific transcription factor required for os
138  that Foxo1 is a novel negative regulator of osteoblast-specific transcription factor Runx2 and modul
139 consensus sequences which bound CREB and the osteoblast-specific transcription factor Runx2, and when
140 urf1 mediates the protein degradation of the osteoblast-specific transcription factor Runx2/Cbfa1.
141                                  Cbfa1 is an osteoblast-specific transcription factor that is essenti
142           Although the CBFA1 gene encodes an osteoblast-specific transcription factor that regulates
143                          Osterix (Osx) is an osteoblast-specific transcription factor which is essent
144                                  Runx2 is an osteoblast-specific transcription factor whose steady-st
145 o demonstrate that phosphorylation of Cbfa1 (osteoblast-specific transcription factor) was not requir
146       Here, we studied the role of Cbfa1, an osteoblast-specific transcription factor, in the control
147 xpression of core binding factor alpha-1, an osteoblast-specific transcription factor, increased in p
148                          It is known that an osteoblast-specific transcription factor, Runx2, is esse
149 iochemical characterization of Osf1, a novel osteoblast-specific transcription factor.
150 fa1/AML3/PEBP2alphaA), a recently identified osteoblast-specific transcription factor.
151 element binds Osf2, a recently characterized osteoblast-specific transcription factor.
152 ase activity, and by increased expression of osteoblast-specific transcription factors (eg, runt-rela
153 g site is a regulatory element important for osteoblast-specific transcriptional activation of the rO
154 tagenesis established that both sites act as osteoblast-specific transcriptional enhancers and togeth
155 lls was associated with up-regulation of the osteoblast-specific transcriptor factor Cbfa1.
156 geted to osteoblasts using the murine 2.3-kb osteoblast-specific type I collagen promoter.
157 ne development and homeostasis, we generated osteoblast-specific Wls-deficient (Ocn-Cre;Wls-flox) mic
158              We developed a mouse model with osteoblast-specific Wnt16 overexpression (Obl-Wnt16).

 
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