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1 -induced maternal obesity can regulate fetal bone development.
2 fferentiation, mineralization, and calvarial bone development.
3 ritional exposures may permanently influence bone development.
4 intake and vitamin D status may affect fetal bone development.
5 teoblast differentiation during endochondral bone development.
6 ities, suggesting its essential role in long bone development.
7 isruption of the gut microbiota on long-term bone development.
8 ticular and growth plate regions crucial for bone development.
9 ates Ihh responsiveness during cartilage and bone development.
10 molecular program required for endochondral bone development.
11 e, regulates a number of processes including bone development.
12 hich is in the sensing of weight load during bone development.
13 kinase that plays an important role in long bone development.
14 I exposure may compromise fetal and neonatal bone development.
15 ealing recapitulates aspects of endochondral bone development.
16 (PTH) treatment during the 4-week course of bone development.
17 that they function independently in skin and bone development.
18 ulatory machinery to control intramembranous bone development.
19 unx2 gene product is essential for mammalian bone development.
20 leading to lower levels of C20 homologs and bone development.
21 s indicated that irradiation retarded normal bone development.
22 y regulates multiple aspects of endochondral bone development.
23 growth and may have advantages in promoting bone development.
24 l requirement of functional Runx2 for normal bone development.
25 GKII signaling in cartilage and endochondral bone development.
26 and Wnt signals are both critical for proper bone development.
27 ls regulating osteoblast differentiation and bone development.
28 x/flox mice partially rescues supraoccipital bone development.
29 hlight the role of this ribosomal protein in bone development.
30 otic disorder and its crucial role in normal bone development.
31 ar resolution available for the endochondral bone development.
32 te hypertrophy is essential for endochondral bone development.
33 -Raf and B-Raf exhibited normal endochondral bone development.
34 l and lipid metabolism, immune function, and bone development.
35 at p53 blocks osteoblast differentiation and bone development.
36 ures and also control cartilage, tendon, and bone development.
37 ts signaling pathways that are essential for bone development.
38 y intact skeleton with impaired endochondral bone development.
39 a major function of GSK3 during endochondral bone development.
40 ichondrium, and vascular endothelium to long bone development.
41 egulator of chondrocyte proliferation during bone development.
42 suppression of adrenal function, growth, and bone development.
43 ion factor with a well-characterized role in bone development.
44 ents to investigate its role in endochondral bone development.
45 (ECM) molecules are crucial processes during bone development.
46 upport chondrocyte survival during embryonic bone development.
47 ndrocyte differentiation during endochondral bone development.
48 both the CNC- and mesoderm-derived calvarial bone development.
49 s of the Wnt family, Wnt5a and Wnt5b in long bone development.
50 in individual muscle cell size, and impaired bone development.
51 nscription factors that control endochondral bone development.
52 of-function phenotype highlighted by ectopic bone development.
53 ality, and identifies a new role for Cbfb in bone development.
54 lization, osteoporosis, and abnormal compact bone development.
55 ondrogenesis to osteogenesis in endochondral bone development.
56 e to spatiotemporal expression of BSP during bone development.
57 ntiation of chondrocytes during endochondral bone development.
58 d its deficiency is associated with abnormal bone development.
59 f proteins involved in blood coagulation and bone development.
60 template in a process known as endochondral bone development.
61 id axis, impaired weight gains, and abnormal bone development.
62 mental pathways, including hematopoiesis and bone development.
63 g extracellular matrix by osteoblasts during bone development.
64 es, periosteal cells, and osteoblasts during bone development.
65 sses in mammals, including hematopoiesis and bone development.
66 ause CDPX2 and suggest a role for sterols in bone development.
67 implicated in regulating multiple stages of bone development.
68 implicated in pigmentation, mast cells, and bone development.
69 Stat1 as a mediator of growth retardation in bone development.
70 extracellular matrix remodeling important to bone development.
71 plate differentiation and thus abnormal long bone development.
72 potential roles in brown adipose tissue and bone development.
73 acilitating future in vitro studies on early bone development.
74 the bones of zebrafish, leading to impaired bone development.
75 ant function of intracellular cholesterol in bone development.
76 as a critical amino acid transporter during bone development.
77 and migration, independent of its effects on bone development.
78 tegral roles in carpal/tarsal and epiphyseal bone development.
79 blast lineage during embryonic and postnatal bone development.
80 -related peptide (PTHrP), a key regulator of bone development.
81 x3 and Irx5, are crucial for heart, limb and bone development.
82 gh regulating Gli2/PTHrP during endochondral bone development.
83 f FGF signaling on downstream targets during bone development.
84 that RIP plays a fundamental role in normal bone development.
85 etromer mediated transport of PTHR in normal bone development.
86 ulogenesis, angiogenesis, haematopoiesis and bone development.
87 eoblasts is required for normal endochondral bone development.
88 buted to an improved understanding of normal bone development.
89 l retinol and carotenoid status on offspring bone development.
90 reased number of osteoblasts and accelerated bone development.
91 steoblast differentiation at early stages of bone development.
92 dral ossification, consistent with a role in bone development.
93 ce are associated with beneficial effects on bone development.
94 tion factor 2 (Runx2), a master regulator of bone development.
95 erences in vascularity correlated with later bone development.
96 relatively little is known about its role in bone development.
97 has been suggested that AMBN may function in bone development.
98 to cleft palate and defects in craniofacial bone development.
99 ondrocytes, play major roles in endochondral bone development.
100 mutations suggest its essential role in long bone development.
101 y transcription factor that is essential for bone development.
102 cells and the rate and pattern of calvarial bone development.
105 gnificantly ameliorated the impaired growth, bone development and adipogenesis of Thra1(PV/+) mice.
108 ence for neogenin in regulating endochondral bone development and BMP (bone morphogenetic protein) si
109 th plate activity is essential for postnatal bone development and body stature, yet the systems regul
110 blast gene regulatory network induced during bone development and bone repair, which acts upstream of
111 study uncovered an important role of SHP2 in bone development and cartilage homeostasis by influencin
114 letes, as adolescence is a critical time for bone development and failure to intervene can lead to lo
116 ummarize current knowledge related to normal bone development and fracture repair, and will describe
119 sis and homeostasis by negatively regulating bone development and growth and by suppressing bone neop
121 Wnt/beta-catenin signaling is central to bone development and homeostasis in adulthood and its de
122 we show here plays no apparent role in early bone development and homeostasis, but which is required
124 ation between the Wnt signaling pathways and bone development and homeostasis, we generated osteoblas
128 function of osteocytes as a source of Wnt in bone development and homoeostasis, complementing their k
129 ly, we find that genes involved in heart and bone development and immune responses are enriched in bo
130 tion of miR-34 and Notch signaling in normal bone development and in bone cancer could potentially le
131 that pVHL has a crucial role in endochondral bone development and is necessary for normal chondrocyte
132 PEBP2alphaA) gene plays an essential role in bone development and is one of a three-member family of
134 ytes and bone-forming osteoblasts to control bone development and maintenance, but the signaling path
139 ts suggest that high-fat feeding may disrupt bone development and modeling; high concentrations of NE
141 abnormal white adipose tissue physiology and bone development and morphology as important contributor
142 n and mechanism underlying PKD1-mediated the bone development and osteoblast differentiation are not
144 e that loss of PKD1 function led to impaired bone development and osteoblast differentiation through
148 role of NFATc1 downstream of BMP-2 in mouse bone development and provide novel evidence for the pres
149 own, its unique pattern of expression during bone development and regeneration, absence in adult tiss
152 elial cells (VEC) are critically involved in bone development and remodeling and influence OC recruit
153 Angiogenesis plays an important role in bone development and remodeling and is mediated by a ple
154 he molecular links between Wnt signaling and bone development and remodeling since initial reports th
155 macrophages and they play a central role in bone development and remodeling via the resorption of bo
158 odel allowed distinguishing, by analogy with bone development and repair, an outer, cortical-like per
160 CYPOR have been shown to lead to defects in bone development and steroidogenesis, resulting in sexua
161 neural tube, biliary duct, limb patterning, bone development and the kidney that mirror the human sy
162 f and A-Raf are dispensable for endochondral bone development and they indicate that the main role of
166 post-weaning growth is a critical window for bone development, and diet plays a central role in estab
167 to numerous physiologic processes including bone development, and its activation is controlled by IK
168 disrupted placental architecture, imbalanced bone development, and losses of functional neurons.
169 ellular processes, including cardiac growth, bone development, and specification of skeletal muscle f
170 chondrogenesis, and cartilage growth during bone development, and that mTOR is an essential mechanot
172 enesis, wound healing, defense/immunity, and bone development are enriched during blastema formation
173 ubfamily (V) 4 mutations that interfere with bone development are Y602C or R616Q at the S4-S5 linker.
174 iologies that include hemostasis, apoptosis, bone development, arterial calcification, signal transdu
177 F-I reinforce the essential role of IGF-I in bone development at both the embryonic and postnatal sta
178 delay chondrocyte maturation in endochondral bone development at least partly through cyclic AMP (cAM
181 was conditionally disrupted during embryonic bone development, bone mass surprisingly was increased w
182 the perisinusoidal space and are needed for bone development, bone remodeling, and fracture repair.
185 ch occurs not only during cranial and facial bone development but also in the surface periosteum of m
186 t that PGHS-2 is not necessary for wild-type bone development but plays a critical role in bone resor
187 Wnt signaling is a critical regulator of bone development, but the identity and role of the Wnt-p
188 which is involved in endocrine function and bone development, but the roles for the other transcript
189 the lack of C-P4H-II in proper endochondral bone development, but their combined partial and complet
190 cle and cardiovascular development, controls bone development by activating the gene program for chon
191 broblast growth factors (FGFs) regulate long bone development by affecting the proliferation and diff
192 o evidence that CXCR4 functions in postnatal bone development by regulating osteoblast development in
193 r intracellular degradation occurring during bone development, cancer invasion, and fibrosis protecti
195 at was associated with impaired endochondral bone development, defective osteoblast-mediated bone for
196 naling pathways that have important roles in bone development, discuss emerging areas such as the rol
197 ment for genes underlying monogenic forms of bone development diseases, and for the collagen formatio
198 rent abnormalities were observed in prenatal bone development, Dmp1-deficient (Dmp1(-/-)) mice unexpe
199 any of the predictor genes are implicated in bone development, drug resistance, and tumorigenesis.
200 ignal in patterning anterior pharyngeal arch bone development during the first week after fertilizati
201 -1 target genes, including genes involved in bone development (e.g. Col1a1, Postn/Osf2, and the bone
202 Here we show that an essential regulator of bone development, FGF18, is a direct target of canonical
207 e of lysyl oxidase enzyme activity to normal bone development has long been appreciated, but regulati
208 r b, encoded by Cbfb), a role for Cbfbeta in bone development has not been demonstrated owing to leth
209 ween maternal vitamin A status and offspring bone development have not previously been elucidated.
210 ignalling transduction that is essential for bone development, however, how IFT proteins regulate Hh
211 beta-catenin signaling, a major regulator of bone development; however, the ability of PEDF to restor
212 /PEG paste formulation augments high-density bone development in a defect model (~2.4-fold increase i
213 ells in newborn mice is sufficient to rescue bone development in early-onset autosomal recessive oste
216 nd lifestyle counseling provided to maximize bone development in individuals assigned male at birth.
219 ral to the coupling of angiogenesis and long bone development in mice (see the related article beginn
221 wn as Cbfa1, Osf2 and AML3) is essential for bone development in mice, and mutations in RUNX2 are fou
223 chick cranial skeleton, especially parietal bone development in the presence of high glucose levels,
224 3 has been shown to play important roles in bone development in vitro by mediating multiple signalin
225 tal MR imaging allows visualization of human bone development in vivo by means of epimetaphyseal char
226 impairment of chondrocyte proliferation and bone development in wild-type, but not in STAT-1(-/-) ru
227 ibit abnormalities in embryonic endochondral bone development, including delayed ossification and inc
228 keletal fractures is essentially a replay of bone development, involving the closely regulated, inter
229 which further supports the notion that long bone development is a modular process.This article has a
234 es strongly support a hypothesis that dermal bone development is modular, with different gene sets fu
235 osteoblasts demonstrates that ihha-dependent bone development is not only region specific, but also b
237 and perfusion, ossification and endochondral bone development, leading to radiographic changes observ
238 vels by 3- or 6-fold caused abnormalities in bone development, megakaryocytes, granulocytes, and T ce
239 ow these high-fat, energy-dense diets affect bone development, morphology, and modeling is poorly und
240 ract the effects of a high-fat diet (HFD) on bone development, morphology, and remodeling remains poo
241 resulting tissue recapitulates the stages of bone development observed in vivo, including phenotypic
242 provide a rational explanation for abnormal bone development occurring in humans or mice with consti
245 tions include the regulation of endochondral bone development, of hair follicle formation, and of bra
246 of chondrogenesis and vascularization during bone development, on the structure and function of the p
247 in a mouse LBP model, but it did not affect bone development or homeostasis of bone mass in adult mi
248 processes such as optic-fissure closure and bone development or homeostasis, which go beyond what is
250 and humans include defects in cartilage and bone development, our study suggests that Rab23 is invol
251 sx2 is believed to play a role in regulating bone development, particularly in sutures of cranial bon
252 r results suggest that altered cartilage and bone development play a significant role in the pathogen
253 hree such connections, linking dementia with bone development, polycystic ovary syndrome with cardiov
254 ription factor that plays a critical role in bone development, postnatal bone formation, and chondroc
255 length may indicate a role for VDR in fetal bone development, potentially by mediating transplacenta
256 c mutant and implicate NF-kappaB proteins in bone development, raising new directions in the treatmen
262 at control calcium/phosphate homeostasis and bone development, respectively, through activation of th
263 mutant rapunzel has heterozygous defects in bone development, resulting in skeletal overgrowth, thus
265 d chondrocyte growth, defective endochondral bone development, shortened limbs, and neonatal lethalit
266 shown that VHL is important for endochondral bone development, since loss of VHL in chondrocytes caus
267 t cells, and malignant cells), haemopoiesis, bone development, spermatogenesis, embryogenesis, and ov
268 ride intake from birth to age 15 yr for Iowa Bone Development Study cohort members with age 15 yr dua
269 ers in the prospective population-based Iowa Bone Development Study participated in MVPA assessments
270 FGF signaling cascade in regulating frontal bone development, suggests that TGFbeta functions as a m
271 are well-studied regulators of cartilage and bone development that have been Food and Drug Administra
272 ant human disorder characterized by abnormal bone development that is mainly due to defective intrame
274 rphogenetic proteins (BMPs) are required for bone development, the repair of damage skeletal tissue,
275 findings compliment previous studies linking bone development to locomotor mechanics by providing a f
276 stigate the role of Wdr5 during endochondral bone development, transgenic mice overexpressing Wdr5 un
277 ibutes to the osteoblast differentiation and bone development via elevation of osteoblast markers thr
279 ding of Notch signaling during cartilage and bone development we generated and compared general Notch
280 e the physiological role of Wnt signaling in bone development, we analyzed FABP4-Wnt10b mice, which e
281 ow PTEN functions in osteoprogenitors during bone development, we conditionally deleted Pten in mice
282 egulating mineralization/osteogenesis during bone development, we devised a coculture system in which
283 aining could also be used to detect abnormal bone development, we ectopically expressed BMP2 in zebra
284 stigate the in vivo impact of mutant DLX3 on bone development, we established transgenic (TG) mice ex
285 mine the requirement of S1P in cartilage and bone development, we have created cartilage-specific S1P
286 irement for GSK activity during endochondral bone development, we inhibited GSK3 in cultured metatars
287 ophy, normal chondrocyte differentiation and bone development were observed in Minpp1-deficient mice.
288 re retarded growth, infertility, and delayed bone development were partially reverted in Thra1(PV/+)
289 during embryonic and perinatal craniofacial bone development, where it localizes to the skeletogenic
290 ation of calvarial cells, as well as in vivo bone development, whereas dominant-negative MEK1 was inh
291 both isoforms results in complete arrest of bone development, whereas selective loss of Runx2-II is
292 ngitudinal and appositional murine postnatal bone development, which involves proper timing of chondr
293 provide a framework for understanding dermal bone development with an aim of bringing it closer to th
294 hese changes will help us understand cranial bone development with respect to the brain, as well as d
295 anisms governing muscle, cardiovascular, and bone development with respect to their regulation by MEF
296 to underlie several hereditary disorders of bone development, with specific FGFR3 mutations causing
298 istic pathway for regulating intramembranous bone development within the skull that involves Runx2- a
299 tor proliferation and differentiation during bone development, yet how the receptor elicits these dis
300 also known to be essential for endochondral bone development, yet the underlying mechanism has remai