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1 homozygous mutant mice demonstrated delayed endochondral and intramembranous bone formation, whereas
4 in Sox9-expressing cells exhibited a lack of endochondral and intramembranous ossification and a lack
6 pair, but inefficient fibrinolysis decreases endochondral angiogenesis and ossification, thereby inhi
7 tron, is a layered structure formed by basal endochondral axial skeletal elements (ribs, vertebrae) a
8 ories of a phylogenetically deeper origin of endochondral bone and its absence in chondrichthyans as
10 provide evidence for neogenin in regulating endochondral bone development and BMP (bone morphogeneti
13 ate that B-Raf and A-Raf are dispensable for endochondral bone development and they indicate that the
15 feration and delay chondrocyte maturation in endochondral bone development at least partly through cy
18 ompensate for the lack of C-P4H-II in proper endochondral bone development, but their combined partia
19 expression that was associated with impaired endochondral bone development, defective osteoblast-medi
20 issue growth and perfusion, ossification and endochondral bone development, leading to radiographic c
21 We have also shown that VHL is important for endochondral bone development, since loss of VHL in chon
24 tudy the requirement for GSK activity during endochondral bone development, we inhibited GSK3 in cult
25 asculature is also known to be essential for endochondral bone development, yet the underlying mechan
39 considered as two separate processes during endochondral bone formation after birth, recent studies
43 Loss of JNK signaling results in abnormal endochondral bone formation and subsequent severe scolio
44 ement of neurofibromin and ERK1/2 for normal endochondral bone formation and support the notion that
46 get of PTHrP signaling, negatively regulates endochondral bone formation by associating with and inac
48 l II) and displayed chondrodysplasia with no endochondral bone formation even though the molecular pr
49 rylation; however, a role for Raf kinases in endochondral bone formation has not been identified.
56 seous junction, leading to partial rescue of endochondral bone formation shown by proper bone length.
57 t that Dym-deficient mice display defects in endochondral bone formation similar to that of Dyggve-Me
58 and the donor cells directly participated in endochondral bone formation via their differentiation in
59 ilage in the hypertrophic zone, few signs of endochondral bone formation, and large regions of disorg
60 tly inhibits chondrocyte differentiation and endochondral bone formation, and this inhibition depends
61 tics did not influence osteoblastogenesis or endochondral bone formation, but notably enhanced osteoc
64 der characterized by extensive extraskeletal endochondral bone formation, share a recurrent mutation
65 ed CSPGs in signaling paradigms required for endochondral bone formation, the brachymorphic (bm) mous
66 To investigate the in vivo role of P63 upon endochondral bone formation, we have established transge
87 al defects, reduced body size, and defective endochondral bone growth due to impaired BMP-mediated ch
88 a key driving mechanism responsible for poor endochondral bone growth in achondroplasia disorders cau
90 of growth plate chondrocytes is required for endochondral bone growth, but the mechanisms and pathway
99 Here we report the discovery of extensive endochondral bone in Minjinia turgenensis, a new genus a
103 hanism of valvular heart disease involves an endochondral bone process that is expressed as cartilage
104 mice showed delayed initiation and impaired endochondral bone repair, accompanied by a severe angiog
107 ralized area, and an inner, trabecular-like, endochondral bone, generated mainly by the human cells a
111 (FGFR3) is expressed in the growth plate of endochondral bones and serves as a negative regulator of
113 esenchymal condensations that give origin to endochondral bones are hypoxic during fetal development,
114 premature fusion of growth plates of various endochondral bones was evident, resulting in dwarfism in
120 ssion of a dominant-negative MEF2C mutant in endochondral cartilage impairs hypertrophy, cartilage an
121 nd that local beta-NGF injections during the endochondral/cartilaginous phase promoted osteogenic mar
122 racellular matrix deposition in proximity to endochondral condensations (Sox9+) on the CAM-implanted
124 FV 108) is represented by fin rays and three endochondral elements: other elements are not preserved.
125 on program analogous to that observed during endochondral embryonic skeletal development, with the po
131 and radiological assessment evidenced marked endochondral new bone formation leading to joint ankylos
132 ts within the CD9(+) population that lead to endochondral or intramembranous-like bone formation.
135 terminal phalanx forms late in gestation by endochondral ossification and continues to elongate unti
136 e for pRB and p107 in cartilage development, endochondral ossification and enchondroma formation that
137 e for pRB and p107 in cartilage development, endochondral ossification and enchondroma formation that
138 vo system to unlink the processes initiating endochondral ossification and establish more precisely t
139 ificial tissue undergoes intramembranous and endochondral ossification and forms a trabecular-like bo
140 ides in vivo evidence for the role of p38 in endochondral ossification and suggests that Sox9 is a li
142 that syndecan 4 is functionally involved in endochondral ossification and that its loss impairs frac
143 rview of the processes of chondrogenesis and endochondral ossification and their control at the molec
144 els of active canonical Wnt signaling enable endochondral ossification and therefore PF-suture closur
145 ical Wnt signaling in the PF suture inhibits endochondral ossification and therefore, suture closure,
147 ority of skeletal elements that form through endochondral ossification are absent, and the ones that
150 n and Has2 expression to control the rate of endochondral ossification as a negative feedback mechani
151 (P < 0.05), and had enhanced early and late endochondral ossification as demonstrated by Safranin O,
152 coagulation, Osteoclast differentiation and endochondral ossification as the major pathways associat
153 dentified a previously unrecognized delay in endochondral ossification associated with the loss of Gp
154 ion in hypertrophic chondrocytes accelerates endochondral ossification at both E17.5 and P1 stages.
155 that Phd2 expressed in chondrocytes inhibits endochondral ossification at the epiphysis by suppressin
156 how that redifferentiation does not occur by endochondral ossification but by the direct ossification
158 Shn3 impairs growth plate maturation during endochondral ossification but simultaneously results in
159 minal differentiation of chondrocytes during endochondral ossification by activating the TGFalpha/EGF
160 , which drive the early steps of heterotopic endochondral ossification by lowering oxygen tension in
161 F signaling pathway plays essential roles in endochondral ossification by regulating osteoblast proli
164 re we hypothesized that hMSCs pushed through endochondral ossification can engineer a scaled-up ossic
165 the oc/oc mouse, a mouse model with impaired endochondral ossification caused by a loss of osteoclast
166 This is followed by the formation of a new endochondral ossification center at the distal end of th
168 mmalian limb structures by stimulating a new endochondral ossification center that utilizes an existi
173 data show that humans with CCD have altered endochondral ossification due to altered RUNX2 regulatio
175 ibit chondrodysplasia and a complete lack of endochondral ossification even though Runx2 expression,
176 ion from mesenchymal stem cells in vitro and endochondral ossification ex vivo, and GEP-knockdown mic
177 vertebral segmentation, joint formation and endochondral ossification for this ubiquitously expresse
178 tal mandible or calvaria that do not undergo endochondral ossification formed only bone without marro
181 in modern jawless fishes and the absence of endochondral ossification in early fossil gnathostomes a
183 ng of terminal cartilage differentiation and endochondral ossification in mandibular condylar cartila
188 loss of Foxc1 function mouse (Foxc1(ch/ch)), endochondral ossification is delayed and the expression
189 /-) mice during embryogenesis and found that endochondral ossification is significantly impaired due
192 analyze the functional role of syndecan 4 in endochondral ossification of mouse embryos and in adult
196 B-catalyzed proteoglycans regulate postnatal endochondral ossification partially through the mediatio
197 vidence for the association of these two key endochondral ossification pathway genes with BMD and ost
203 show a promotion in markers associated with endochondral ossification such as Ihh, Alpl, and Sdf-1.
205 wounds with BMP2 in neonatal mice stimulates endochondral ossification to regenerate the stump bone.
206 ide, negatively regulates chondrogenesis and endochondral ossification via associating with progranul
212 FR3) plays a critical role in the control of endochondral ossification, and bone growth and mutations
213 tional partner of Ihh-Gli2 signalling during endochondral ossification, and that disruption of the Fo
215 e regeneration via either intramembranous or endochondral ossification, both within and outside of th
216 bone marrow (BM) is tightly associated with endochondral ossification, but little is known about the
218 eoblasts and periosteal cells during primary endochondral ossification, consistent with a role in bon
219 hat Axin2(-/-) PF-sutures lack physiological endochondral ossification, contain ectopic cartilage and
221 , which contribute to suture closure through endochondral ossification, in a process regulated in par
222 ssion of Sox9, a major negative regulator of endochondral ossification, in Col2a1-TAP63alpha transgen
223 containing endothelial cell masses, abnormal endochondral ossification, leading to stunted long bone
224 thening, and repair of most bones proceed by endochondral ossification, namely through formation of a
226 roplasia is a genetic disorder that inhibits endochondral ossification, resulting in disproportionate
227 spatiotemporal regulation in vitro resisted endochondral ossification, retained the expression of ca
230 uppressing expression of factors involved in endochondral ossification, such as osterix and vascular
232 s to defects in cartilage development during endochondral ossification, the process by which long bon
233 e observed in the calvarium, indicating that endochondral ossification, the process needed for the fo
234 To investigate the role of this pathway in endochondral ossification, we generated transgenic mice
235 ouse posterior frontal (PF) suture closes by endochondral ossification, whereas sagittal (SAG) remain
236 elements blocks chondrocyte hypertrophy and endochondral ossification, whereas signaling starting at
237 ure (PF) of the cranial vault closes through endochondral ossification, while other sutures remain pa
283 s play essential roles in crucial aspects of endochondral ossification: osteoblast differentiation, c
285 al stem/stromal cells (hMSCs) can execute an endochondral program and ectopically generate mature bon
286 we demonstrate beta-NGF's ability to promote endochondral repair in a murine model and uncover mechan
287 hedgehog (Ihh) controls multiple aspects of endochondral skeletal development by signaling to both c
288 ling simultaneously in the same cells during endochondral skeletal development using beta-catenin and
289 hedgehog (Ihh) controls multiple aspects of endochondral skeletal development, including proliferati
293 rs that have previously been associated with endochondral skeleton development to define the cellular
300 ables the spatial and temporal prediction of endochondral tissue regeneration, assessed as areas of c