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1 tegral roles in carpal/tarsal and epiphyseal bone development.
2 ticular and growth plate regions crucial for bone development.
3 ates Ihh responsiveness during cartilage and bone development.
4 molecular program required for endochondral bone development.
5 hich is in the sensing of weight load during bone development.
6 kinase that plays an important role in long bone development.
7 ealing recapitulates aspects of endochondral bone development.
8 (PTH) treatment during the 4-week course of bone development.
9 that they function independently in skin and bone development.
10 ulatory machinery to control intramembranous bone development.
11 unx2 gene product is essential for mammalian bone development.
12 leading to lower levels of C20 homologs and bone development.
13 s indicated that irradiation retarded normal bone development.
14 y regulates multiple aspects of endochondral bone development.
15 growth and may have advantages in promoting bone development.
16 l requirement of functional Runx2 for normal bone development.
17 GKII signaling in cartilage and endochondral bone development.
18 and Wnt signals are both critical for proper bone development.
19 ls regulating osteoblast differentiation and bone development.
20 x/flox mice partially rescues supraoccipital bone development.
21 blast lineage during embryonic and postnatal bone development.
22 otic disorder and its crucial role in normal bone development.
23 ar resolution available for the endochondral bone development.
24 te hypertrophy is essential for endochondral bone development.
25 -Raf and B-Raf exhibited normal endochondral bone development.
26 l and lipid metabolism, immune function, and bone development.
27 at p53 blocks osteoblast differentiation and bone development.
28 ures and also control cartilage, tendon, and bone development.
29 -related peptide (PTHrP), a key regulator of bone development.
30 ts signaling pathways that are essential for bone development.
31 y intact skeleton with impaired endochondral bone development.
32 a major function of GSK3 during endochondral bone development.
33 ichondrium, and vascular endothelium to long bone development.
34 egulator of chondrocyte proliferation during bone development.
35 suppression of adrenal function, growth, and bone development.
36 ion factor with a well-characterized role in bone development.
37 ents to investigate its role in endochondral bone development.
38 (ECM) molecules are crucial processes during bone development.
39 upport chondrocyte survival during embryonic bone development.
40 ndrocyte differentiation during endochondral bone development.
41 both the CNC- and mesoderm-derived calvarial bone development.
42 s of the Wnt family, Wnt5a and Wnt5b in long bone development.
43 in individual muscle cell size, and impaired bone development.
44 nscription factors that control endochondral bone development.
45 of-function phenotype highlighted by ectopic bone development.
46 ality, and identifies a new role for Cbfb in bone development.
47 gh regulating Gli2/PTHrP during endochondral bone development.
48 lization, osteoporosis, and abnormal compact bone development.
49 f FGF signaling on downstream targets during bone development.
50 ondrogenesis to osteogenesis in endochondral bone development.
51 e to spatiotemporal expression of BSP during bone development.
52 ntiation of chondrocytes during endochondral bone development.
53 d its deficiency is associated with abnormal bone development.
54 f proteins involved in blood coagulation and bone development.
55 template in a process known as endochondral bone development.
56 id axis, impaired weight gains, and abnormal bone development.
57 mental pathways, including hematopoiesis and bone development.
58 g extracellular matrix by osteoblasts during bone development.
59 es, periosteal cells, and osteoblasts during bone development.
60 sses in mammals, including hematopoiesis and bone development.
61 ause CDPX2 and suggest a role for sterols in bone development.
62 implicated in regulating multiple stages of bone development.
63 implicated in pigmentation, mast cells, and bone development.
64 Stat1 as a mediator of growth retardation in bone development.
65 extracellular matrix remodeling important to bone development.
66 plate differentiation and thus abnormal long bone development.
67 that RIP plays a fundamental role in normal bone development.
68 etromer mediated transport of PTHR in normal bone development.
69 ulogenesis, angiogenesis, haematopoiesis and bone development.
70 eoblasts is required for normal endochondral bone development.
71 buted to an improved understanding of normal bone development.
72 l retinol and carotenoid status on offspring bone development.
73 reased number of osteoblasts and accelerated bone development.
74 steoblast differentiation at early stages of bone development.
75 dral ossification, consistent with a role in bone development.
76 ce are associated with beneficial effects on bone development.
77 tion factor 2 (Runx2), a master regulator of bone development.
78 erences in vascularity correlated with later bone development.
79 relatively little is known about its role in bone development.
80 has been suggested that AMBN may function in bone development.
81 ondrocytes, play major roles in endochondral bone development.
82 mutations suggest its essential role in long bone development.
83 y transcription factor that is essential for bone development.
84 cells and the rate and pattern of calvarial bone development.
85 fferentiation, mineralization, and calvarial bone development.
86 ritional exposures may permanently influence bone development.
87 intake and vitamin D status may affect fetal bone development.
88 teoblast differentiation during endochondral bone development.
89 ities, suggesting its essential role in long bone development.
92 gnificantly ameliorated the impaired growth, bone development and adipogenesis of Thra1(PV/+) mice.
95 ence for neogenin in regulating endochondral bone development and BMP (bone morphogenetic protein) si
96 blast gene regulatory network induced during bone development and bone repair, which acts upstream of
97 study uncovered an important role of SHP2 in bone development and cartilage homeostasis by influencin
100 letes, as adolescence is a critical time for bone development and failure to intervene can lead to lo
102 ummarize current knowledge related to normal bone development and fracture repair, and will describe
105 sis and homeostasis by negatively regulating bone development and growth and by suppressing bone neop
107 Wnt/beta-catenin signaling is central to bone development and homeostasis in adulthood and its de
108 we show here plays no apparent role in early bone development and homeostasis, but which is required
110 ation between the Wnt signaling pathways and bone development and homeostasis, we generated osteoblas
114 function of osteocytes as a source of Wnt in bone development and homoeostasis, complementing their k
115 tion of miR-34 and Notch signaling in normal bone development and in bone cancer could potentially le
116 that pVHL has a crucial role in endochondral bone development and is necessary for normal chondrocyte
117 PEBP2alphaA) gene plays an essential role in bone development and is one of a three-member family of
119 ytes and bone-forming osteoblasts to control bone development and maintenance, but the signaling path
123 ts suggest that high-fat feeding may disrupt bone development and modeling; high concentrations of NE
125 n and mechanism underlying PKD1-mediated the bone development and osteoblast differentiation are not
127 e that loss of PKD1 function led to impaired bone development and osteoblast differentiation through
131 role of NFATc1 downstream of BMP-2 in mouse bone development and provide novel evidence for the pres
132 own, its unique pattern of expression during bone development and regeneration, absence in adult tiss
135 elial cells (VEC) are critically involved in bone development and remodeling and influence OC recruit
136 Angiogenesis plays an important role in bone development and remodeling and is mediated by a ple
137 he molecular links between Wnt signaling and bone development and remodeling since initial reports th
138 macrophages and they play a central role in bone development and remodeling via the resorption of bo
141 odel allowed distinguishing, by analogy with bone development and repair, an outer, cortical-like per
143 CYPOR have been shown to lead to defects in bone development and steroidogenesis, resulting in sexua
144 neural tube, biliary duct, limb patterning, bone development and the kidney that mirror the human sy
145 f and A-Raf are dispensable for endochondral bone development and they indicate that the main role of
147 to numerous physiologic processes including bone development, and its activation is controlled by IK
148 disrupted placental architecture, imbalanced bone development, and losses of functional neurons.
149 ellular processes, including cardiac growth, bone development, and specification of skeletal muscle f
150 chondrogenesis, and cartilage growth during bone development, and that mTOR is an essential mechanot
152 enesis, wound healing, defense/immunity, and bone development are enriched during blastema formation
153 iologies that include hemostasis, apoptosis, bone development, arterial calcification, signal transdu
155 F-I reinforce the essential role of IGF-I in bone development at both the embryonic and postnatal sta
156 delay chondrocyte maturation in endochondral bone development at least partly through cyclic AMP (cAM
159 was conditionally disrupted during embryonic bone development, bone mass surprisingly was increased w
160 the perisinusoidal space and are needed for bone development, bone remodeling, and fracture repair.
162 ch occurs not only during cranial and facial bone development but also in the surface periosteum of m
163 t that PGHS-2 is not necessary for wild-type bone development but plays a critical role in bone resor
164 Wnt signaling is a critical regulator of bone development, but the identity and role of the Wnt-p
165 which is involved in endocrine function and bone development, but the roles for the other transcript
166 the lack of C-P4H-II in proper endochondral bone development, but their combined partial and complet
167 cle and cardiovascular development, controls bone development by activating the gene program for chon
168 broblast growth factors (FGFs) regulate long bone development by affecting the proliferation and diff
169 o evidence that CXCR4 functions in postnatal bone development by regulating osteoblast development in
170 r intracellular degradation occurring during bone development, cancer invasion, and fibrosis protecti
172 at was associated with impaired endochondral bone development, defective osteoblast-mediated bone for
173 naling pathways that have important roles in bone development, discuss emerging areas such as the rol
174 rent abnormalities were observed in prenatal bone development, Dmp1-deficient (Dmp1(-/-)) mice unexpe
175 any of the predictor genes are implicated in bone development, drug resistance, and tumorigenesis.
176 ignal in patterning anterior pharyngeal arch bone development during the first week after fertilizati
177 -1 target genes, including genes involved in bone development (e.g. Col1a1, Postn/Osf2, and the bone
178 Here we show that an essential regulator of bone development, FGF18, is a direct target of canonical
183 e of lysyl oxidase enzyme activity to normal bone development has long been appreciated, but regulati
184 r b, encoded by Cbfb), a role for Cbfbeta in bone development has not been demonstrated owing to leth
185 ween maternal vitamin A status and offspring bone development have not previously been elucidated.
186 ignalling transduction that is essential for bone development, however, how IFT proteins regulate Hh
187 beta-catenin signaling, a major regulator of bone development; however, the ability of PEDF to restor
192 ral to the coupling of angiogenesis and long bone development in mice (see the related article beginn
193 wn as Cbfa1, Osf2 and AML3) is essential for bone development in mice, and mutations in RUNX2 are fou
195 chick cranial skeleton, especially parietal bone development in the presence of high glucose levels,
196 3 has been shown to play important roles in bone development in vitro by mediating multiple signalin
197 tal MR imaging allows visualization of human bone development in vivo by means of epimetaphyseal char
198 impairment of chondrocyte proliferation and bone development in wild-type, but not in STAT-1(-/-) ru
199 ibit abnormalities in embryonic endochondral bone development, including delayed ossification and inc
200 keletal fractures is essentially a replay of bone development, involving the closely regulated, inter
205 es strongly support a hypothesis that dermal bone development is modular, with different gene sets fu
206 osteoblasts demonstrates that ihha-dependent bone development is not only region specific, but also b
208 and perfusion, ossification and endochondral bone development, leading to radiographic changes observ
209 vels by 3- or 6-fold caused abnormalities in bone development, megakaryocytes, granulocytes, and T ce
210 ow these high-fat, energy-dense diets affect bone development, morphology, and modeling is poorly und
211 resulting tissue recapitulates the stages of bone development observed in vivo, including phenotypic
212 provide a rational explanation for abnormal bone development occurring in humans or mice with consti
213 tions include the regulation of endochondral bone development, of hair follicle formation, and of bra
214 processes such as optic-fissure closure and bone development or homeostasis, which go beyond what is
216 and humans include defects in cartilage and bone development, our study suggests that Rab23 is invol
217 sx2 is believed to play a role in regulating bone development, particularly in sutures of cranial bon
218 r results suggest that altered cartilage and bone development play a significant role in the pathogen
219 hree such connections, linking dementia with bone development, polycystic ovary syndrome with cardiov
220 ription factor that plays a critical role in bone development, postnatal bone formation, and chondroc
221 length may indicate a role for VDR in fetal bone development, potentially by mediating transplacenta
222 c mutant and implicate NF-kappaB proteins in bone development, raising new directions in the treatmen
228 at control calcium/phosphate homeostasis and bone development, respectively, through activation of th
229 mutant rapunzel has heterozygous defects in bone development, resulting in skeletal overgrowth, thus
231 d chondrocyte growth, defective endochondral bone development, shortened limbs, and neonatal lethalit
232 shown that VHL is important for endochondral bone development, since loss of VHL in chondrocytes caus
233 t cells, and malignant cells), haemopoiesis, bone development, spermatogenesis, embryogenesis, and ov
234 ride intake from birth to age 15 yr for Iowa Bone Development Study cohort members with age 15 yr dua
235 ers in the prospective population-based Iowa Bone Development Study participated in MVPA assessments
236 FGF signaling cascade in regulating frontal bone development, suggests that TGFbeta functions as a m
237 are well-studied regulators of cartilage and bone development that have been Food and Drug Administra
238 ant human disorder characterized by abnormal bone development that is mainly due to defective intrame
240 rphogenetic proteins (BMPs) are required for bone development, the repair of damage skeletal tissue,
241 stigate the role of Wdr5 during endochondral bone development, transgenic mice overexpressing Wdr5 un
242 ibutes to the osteoblast differentiation and bone development via elevation of osteoblast markers thr
244 ding of Notch signaling during cartilage and bone development we generated and compared general Notch
245 e the physiological role of Wnt signaling in bone development, we analyzed FABP4-Wnt10b mice, which e
246 ow PTEN functions in osteoprogenitors during bone development, we conditionally deleted Pten in mice
247 egulating mineralization/osteogenesis during bone development, we devised a coculture system in which
248 aining could also be used to detect abnormal bone development, we ectopically expressed BMP2 in zebra
249 stigate the in vivo impact of mutant DLX3 on bone development, we established transgenic (TG) mice ex
250 mine the requirement of S1P in cartilage and bone development, we have created cartilage-specific S1P
251 irement for GSK activity during endochondral bone development, we inhibited GSK3 in cultured metatars
252 ophy, normal chondrocyte differentiation and bone development were observed in Minpp1-deficient mice.
253 re retarded growth, infertility, and delayed bone development were partially reverted in Thra1(PV/+)
254 during embryonic and perinatal craniofacial bone development, where it localizes to the skeletogenic
255 ation of calvarial cells, as well as in vivo bone development, whereas dominant-negative MEK1 was inh
256 both isoforms results in complete arrest of bone development, whereas selective loss of Runx2-II is
257 ngitudinal and appositional murine postnatal bone development, which involves proper timing of chondr
258 provide a framework for understanding dermal bone development with an aim of bringing it closer to th
259 anisms governing muscle, cardiovascular, and bone development with respect to their regulation by MEF
260 to underlie several hereditary disorders of bone development, with specific FGFR3 mutations causing
262 istic pathway for regulating intramembranous bone development within the skull that involves Runx2- a
263 tor proliferation and differentiation during bone development, yet how the receptor elicits these dis
264 also known to be essential for endochondral bone development, yet the underlying mechanism has remai
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