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1 hange associated with repression of terminal chondrocyte differentiation.
2 tween different epigenetic mechanisms during chondrocyte differentiation.
3 f Sox9, a transcription factor essential for chondrocyte differentiation.
4 about the cytoskeletal components regulating chondrocyte differentiation.
5 lates chondrocyte proliferation but inhibits chondrocyte differentiation.
6 h) and of collagen type X--all indicative of chondrocyte differentiation.
7 ecific inhibitor of PHD2, promoted articular chondrocyte differentiation.
8 f columns, and acceleration of periarticular chondrocyte differentiation.
9 inase-13 (MMP-13) expression during terminal chondrocyte differentiation.
10 ession of different types of collagen during chondrocyte differentiation.
11 nitor cell to promote osteoblast and prevent chondrocyte differentiation.
12 and redundant in major steps of growth plate chondrocyte differentiation.
13  these factors are central to the control of chondrocyte differentiation.
14 iferation, its inactivation is essential for chondrocyte differentiation.
15 artilage tissue-specific gene expression and chondrocyte differentiation.
16 elopment, where c-Maf is required for normal chondrocyte differentiation.
17 nail-related transcription repressors during chondrocyte differentiation.
18 n the regulation of Agc expression following chondrocyte differentiation.
19 gnals are essential for repressing articular chondrocyte differentiation.
20 dicating that Cbfa1 may control hypertrophic chondrocyte differentiation.
21 tion between these signaling pathways during chondrocyte differentiation.
22 ignaling regulation of the cell cycle during chondrocyte differentiation.
23 s have established that Sox9 is required for chondrocyte differentiation.
24 molecules have been implicated in regulating chondrocyte differentiation.
25 MAPK in transmitting PTH signals to regulate chondrocyte differentiation.
26 letal element length due to an inhibition of chondrocyte differentiation.
27 esignated HiPER1, has a role in growth plate chondrocyte differentiation.
28 hat PTHrP and its receptor are essential for chondrocyte differentiation.
29 ing chondrocyte proliferation and by slowing chondrocyte differentiation.
30 iption factor SOX-9 lead to abnormalities in chondrocyte differentiation.
31 ion caused by delayed cell cycle exit during chondrocyte differentiation.
32 ive feedback loop that modulates the rate of chondrocyte differentiation.
33  the effects of Indian Hedgehog and PTHrP on chondrocyte differentiation.
34  for PTHrP as an inhibitor of the program of chondrocyte differentiation.
35 or probing regulatory interactions governing chondrocyte differentiation.
36 etic program that induces chondrogenesis and chondrocyte differentiation.
37  TGF-beta1-induced Smad2 phosphorylation and chondrocyte differentiation.
38 nces collagen fibrillogenesis, and modulates chondrocyte differentiation.
39 cle and entered the prehypertrophic phase of chondrocyte differentiation.
40 ep1, Hivep2, and Hivep3 in osteoblast and/or chondrocyte differentiation.
41  downstream mediator of Wnt in repression of chondrocyte differentiation.
42 s the TGFbeta pathway to efficiently promote chondrocyte differentiation.
43 h factor beta (TGFbeta), a potent agonist of chondrocyte differentiation.
44  miR-365 abolishes mechanical stimulation of chondrocyte differentiation.
45 ortant in the early stages of osteoblast and chondrocyte differentiation.
46 ssion is regulated in vitro as a function of chondrocyte differentiation.
47 rpolarized to depolarized state during early chondrocyte differentiation.
48 important transcription factors that control chondrocyte differentiation.
49 in promoting both growth plate and articular chondrocyte differentiation.
50 is one of key downstream molecules of GEP in chondrocyte differentiation.
51 s therefore to control general regulators of chondrocyte differentiation.
52 roles as both a regulator and an effector of chondrocyte differentiation.
53  study, we established a role for lncRNAs in chondrocyte differentiation.
54 f BMP2, and it is required for BMP2-mediated chondrocyte differentiation.
55  full proteolytic activity and inhibition of chondrocyte differentiation.
56 ein and subsequently disrupting hypertrophic chondrocyte differentiation.
57 nces osteoblast differentiation and inhibits chondrocyte differentiation.
58 sor proliferation and inhibited hypertrophic chondrocyte differentiation.
59 verexpression of Wdr5 in osteoblasts affects chondrocyte differentiation.
60 f GSK-3alpha induced markers of neuronal and chondrocyte differentiation.
61 CDS-associated abnormalities in hypertrophic chondrocyte differentiation.
62 o repress transcription of genes involved in chondrocyte differentiation.
63 ntagonizes the Wnt/beta-catenin signaling in chondrocyte differentiation.
64 ial cartilage proteoglycan and key marker of chondrocyte differentiation.
65 id changes in PTHrP expression and articular chondrocyte differentiation.
66 in B is a regulator of Runx2 function during chondrocyte differentiation.
67 to osteoblasts or by a specific hypertrophic chondrocyte differentiation ability of Cbfa1, we used th
68                           Moreover, abnormal chondrocyte differentiation affects mineralization of ca
69 trophic phenotype characterized by premature chondrocyte differentiation and accelerated bone formati
70 alyses of growth plates demonstrated delayed chondrocyte differentiation and accelerated mineralizati
71 rly in mesenchymal progenitor cells promoted chondrocyte differentiation and blocked the activity of
72 lated during chondrocyte hypertrophy, normal chondrocyte differentiation and bone development were ob
73 ow-grade joint inflammation promotes altered chondrocyte differentiation and cartilage catabolism.
74 containing transcription factor required for chondrocyte differentiation and cartilage formation.
75 t transcription factor that is essential for chondrocyte differentiation and cartilage formation.
76 ed high mobility group-Box gene 9) regulates chondrocyte differentiation and cartilage-specific expre
77 y transcription factor that is essential for chondrocyte differentiation and chondrocyte-specific gen
78 eservation of postnatal growth plate through chondrocyte differentiation and Col II deposition and fu
79                    As calcium also instructs chondrocyte differentiation and collagen synthesis, calc
80 arch cartilage elements due to reductions in chondrocyte differentiation and condensation.
81 e report that ADAMTS-7 is upregulated during chondrocyte differentiation and demonstrates the tempora
82  cartilaginous inflammation in OA to altered chondrocyte differentiation and disease progression thro
83                  Here, we show that aberrant chondrocyte differentiation and ectopic cartilage format
84                   ADAMTS-7 potently inhibits chondrocyte differentiation and endochondral bone format
85 t inppl1a is also important for hypertrophic chondrocyte differentiation and endochondral bone length
86 -like signals with the potential to modulate chondrocyte differentiation and function in OA progressi
87 that Foxc1 and Foxc2 are required for normal chondrocyte differentiation and function, as loss of bot
88                              Pthlh regulates chondrocyte differentiation and Gli activity in a Sufu-d
89            However, Stat3 loss did not alter chondrocyte differentiation and hypertrophy in embryonic
90 esses, whereas suppression of ECM1 enhances, chondrocyte differentiation and hypertrophy in vitro and
91        Cell cycle regulation is critical for chondrocyte differentiation and hypertrophy.
92                     This features a delay in chondrocyte differentiation and in bone collar formation
93 t coordinated levels of MGP are required for chondrocyte differentiation and matrix mineralization.
94  by Hedgehog and beta-catenin signalling, to chondrocyte differentiation and matrix synthesis by SoxE
95  suggest that cartilage matrix has a role in chondrocyte differentiation and maturation.
96 ith achondroplasia, RBM-007 rescued impaired chondrocyte differentiation and maturation.
97       Low oxygen tension (hypoxia) regulates chondrocyte differentiation and metabolism.
98    Our protocol should facilitate studies of chondrocyte differentiation and of cell replacement ther
99                    By 7 weeks, the delays in chondrocyte differentiation and ossification have largel
100 ding to a seeming reversal in the pattern of chondrocyte differentiation and ossification.
101 /-) embryos exhibited delays in hypertrophic chondrocyte differentiation and osteoblast differentiati
102 tion of the skeleton is complex, and impacts chondrocyte differentiation and osteoclast formation in
103 nockdown of SMAD 1/5/8 impaired NICD-induced chondrocyte differentiation and p57 expression.
104                  Similarly, cilia facilitate chondrocyte differentiation and production of a cartilag
105 alance in the regulatory network controlling chondrocyte differentiation and proliferation.
106                           Rapamycin promotes chondrocyte differentiation and restores these defects i
107 the zebrafish craniofacial skeleton precedes chondrocyte differentiation and restricts where cells un
108            Cell-matrix interactions regulate chondrocyte differentiation and survival.
109 indings that PHD2 is a negative regulator of chondrocyte differentiation and that hypoxia signaling i
110  novel critical role of GEP growth factor in chondrocyte differentiation and the molecular events bot
111  directly controls the pace and synchrony of chondrocyte differentiation and thereby coordinates deve
112 ular to columnar chondrocytes (periarticular chondrocyte differentiation) and thereby regulates the l
113 te proliferation, inhibition of hypertrophic chondrocyte differentiation, and a delay in the formatio
114 volved in extracellular matrix organization, chondrocyte differentiation, and connective tissue devel
115 rtant in the regulation of limb development, chondrocyte differentiation, and degeneration of articul
116  upregulation, acceleration of periarticular chondrocyte differentiation, and elongation of the colum
117 ndrocyte proliferation, delayed hypertrophic chondrocyte differentiation, and endochondral bone forma
118 racteristic concave shape, exhibited ectopic chondrocyte differentiation, and occasionally adhered to
119 ter activity was detectable at all stages of chondrocyte differentiation, and Sdc4 deficiency inhibit
120              Similar changes in endochondral chondrocyte differentiation are essential for physiologi
121 PTHrP and Ihh in regulating earlier steps in chondrocyte differentiation are unclear.
122 sion of collagen X, a marker of growth plate chondrocyte differentiation (assessed by immunohistochem
123 hibitor, was able to induce pre-hypertrophic chondrocyte differentiation both in vitro and in vivo.
124 hedgehog are implicated in the regulation of chondrocyte differentiation, but the specific cellular t
125 nail (Sna) and Slug (Slugh), are involved in chondrocyte differentiation by controlling the expressio
126                               LOXL2 promotes chondrocyte differentiation by mechanisms that are likel
127 ession of Wdr5 in the perichondrium promotes chondrocyte differentiation by modulating the expression
128      Mutations in SOX9, a gene essential for chondrocyte differentiation cause the human disease camp
129                                              Chondrocyte differentiation controls skeleton developmen
130           In addition to the acceleration of chondrocyte differentiation, conventional transgenic mic
131 cription factor c-Maf is required for normal chondrocyte differentiation during endochondral bone dev
132 ese results identify Cbfa1 as a hypertrophic chondrocyte differentiation factor and provide a genetic
133                                              Chondrocyte differentiation factor Sox-9 was detected in
134         Herein we report that GEP stimulates chondrocyte differentiation from mesenchymal stem cells
135                      In an in vitro model of chondrocyte differentiation, human dermal fibroblasts (h
136 collagen II, an early and abundant marker of chondrocyte differentiation, identified a minimal DNA el
137 ive activation of the BMP receptor-IA blocks chondrocyte differentiation in a similar manner as misex
138 ophic chondrocyte phenotypes revealed normal chondrocyte differentiation in c-Raf(f/f);ColII-Cre(+) m
139 vels of Col2a1 and other specific markers of chondrocyte differentiation in culture, we then asked wh
140 e that elevated expression of Foxc1 promotes chondrocyte differentiation in mouse embryonic stem cell
141 as uncoupled from the usual tight linkage to chondrocyte differentiation in the epiphyseal growth pla
142 t proliferation of prechondrogenic cells and chondrocyte differentiation in the phalangeal region are
143 BX1 is crucial for the normal progression of chondrocyte differentiation in the spheno-occipital sync
144  of columns and stimulation of periarticular chondrocyte differentiation in these models were still o
145              Wdr5 accelerates osteoblast and chondrocyte differentiation in vitro, and is development
146 BP1 mRNA expression was downregulated during chondrocyte differentiation in vitro.
147 induction of sclerotomal gene expression and chondrocyte differentiation in vitro.
148 THrP) has also been demonstrated to regulate chondrocyte differentiation in vivo.
149  mice, we reveal a role for these factors in chondrocyte differentiation in vivo.
150                                      Altered chondrocyte differentiation, including development of ch
151 -regulates expression of genes essential for chondrocyte differentiation, including Sox9, Col2a1, and
152 ted markers of chondrocyte proliferation and chondrocyte differentiation increased, although these ch
153 information on transcriptional regulation of chondrocyte differentiation induced by DBP.
154 d for the normal progression of hypertrophic chondrocyte differentiation into bone in the developing
155                                              Chondrocyte differentiation is abnormal in the Six2-null
156                                        Thus, chondrocyte differentiation is controlled at multiple st
157                         Proper regulation of chondrocyte differentiation is necessary for the morphog
158 ecreased approximately 10%, and hypertrophic chondrocyte differentiation is perturbed.
159 sis and of the genes expressed as markers of chondrocyte differentiation is poorly understood.
160  AGGRECAN, a matrix protein expressed during chondrocyte differentiation, is also expressed.
161 x9 cooperatively activated expression of the chondrocyte differentiation marker Col2a1 in 10T1/2 and
162 ration, and the expression of mRNAs encoding chondrocyte differentiation markers and growth factors.
163 ression of HDAC4 reverses miR-1 induction of chondrocyte differentiation markers Col X and Ihh.
164 ion of HDAC4 reverses miR-365 stimulation of chondrocyte differentiation markers including Ihh, Col X
165 he small molecule kartogenin, which promotes chondrocyte differentiation (median effective concentrat
166 nt for a common regulation of osteoblast and chondrocyte differentiation mediated by Cbfa1.
167          In vivo, early limb development and chondrocyte differentiation occurred normally in Tgfbr2-
168 vement of a MEK/ERK/Ets1 pathway in blocking chondrocyte differentiation of cardiac neural crest.
169  found that TGF-beta1 significantly inhibits chondrocyte differentiation of wild-type metatarsal rudi
170 he hypothesis that two critical steps of the chondrocyte differentiation pathway are sensitive to Sox
171 t SOX9 is essential for several steps of the chondrocyte differentiation pathway, we asked whether Ct
172 9 is required during sequential steps of the chondrocyte differentiation pathway.
173 ntrolling the progression of cells along the chondrocyte differentiation pathway.
174 hese and perhaps other genes involved in the chondrocyte differentiation pathway.
175  In contrast to Ihh mutants (Ihh(n)/Ihh(n)), chondrocyte differentiation proceeds normally.
176  and that Sox9 can subsequently initiate the chondrocyte differentiation program in a variety of cell
177 e and developing cartilage, can activate the chondrocyte differentiation program in somitic mesoderm
178 x3.2, Nkx3.2-N200Q is unable to activate the chondrocyte differentiation program in somitic mesoderm,
179 ned skeletal elements, without affecting the chondrocyte differentiation program.
180 y through SEs, to implement the growth plate chondrocyte differentiation program.
181 s are crucial regulators of the hypertrophic chondrocyte differentiation program.
182 ers concomitant with the reexpression of the chondrocyte differentiation program.
183 ox9 expression, suggestive of an accelerated chondrocyte differentiation program.
184 dlin-2 and a mechanism for regulation of the chondrocyte differentiation programme and chondrogenesis
185          This study shows that miR-140 has a chondrocyte differentiation-related expression pattern.
186                            BMPR-IA regulates chondrocyte differentiation, serving as a downstream med
187 d intramembranous ossification as well as in chondrocyte differentiation, similar to but less severe
188 w that the mutant receptor caused a block in chondrocyte differentiation specifically at the prehyper
189 n and the relationship of these effects with chondrocyte differentiation stage.
190 te dihydrate, underlying the significance of chondrocyte differentiation state and the factors regula
191 yte biology and investigated its role in the chondrocyte differentiation status, rRNA levels and prot
192 ssion of Wdr5 in the perichondrium regulates chondrocyte differentiation, studies were undertaken usi
193 he DNA enhancer element in genes involved in chondrocyte differentiation, such as Col11a2 and Col9a2,
194 blast differentiation as well as accelerated chondrocyte differentiation, suggesting that overexpress
195              We also show that GEP activates chondrocyte differentiation through Erk1/2 signaling and
196 signaling inhibits bone growth by inhibiting chondrocyte differentiation through the MAPK pathway and
197  (PTHrP) which negatively regulates terminal chondrocyte differentiation through the PTH/PTHrP recept
198 beta-catenin transcriptional activity during chondrocyte differentiation to ensure proper development
199 s (OA) pathogenesis by regulating a shift in chondrocyte differentiation to hypertrophy.
200 r of chondroprogenitor cells and accelerated chondrocyte differentiation to hypertrophy.
201 drogenesis, and reducing SOX9 dosage allowed chondrocyte differentiation to proceed and significantly
202 late endochondral ossification by inhibiting chondrocyte differentiation toward hypertrophy.
203 mesenchymal progenitor cells in vitro causes chondrocyte differentiation under conditions allowing on
204 e microRNA found to adversely regulate early chondrocyte differentiation via direct targeting of the
205 hanically responsive microRNA that regulates chondrocyte differentiation via directly targeting HDAC4
206 lation and mice with reduced PPR expression, chondrocyte differentiation was accelerated not only at
207 rowth in these animals, the role of Hdac3 in chondrocyte differentiation was evaluated.
208 ern of expression of genes known to regulate chondrocyte differentiation was not perturbed in Pbx1-de
209                      In contrast, suppressed chondrocyte differentiation was observed throughout the
210                                              Chondrocyte differentiation was promoted by Hivep3 overe
211 unx2, which plays a major role in late stage chondrocyte differentiation, was enhanced in Hmgb2(-/-)
212   The expression of Twist-1, which regulates chondrocyte differentiation, was increased in Col I-Wdr5
213 ssential role during the sequential steps of chondrocyte differentiation, we have used the Cre/loxP r
214                Because Sox9 is essential for chondrocyte differentiation, we propose that FGFs and th
215  -independent pathways, Runx2 expression and chondrocyte differentiation were analyzed using bones fr
216 tion, the expression patterns of markers for chondrocyte differentiation were not altered in vertebra
217 ccelerated mineralization due to accelerated chondrocyte differentiation, which is associated with ec
218 als at 7 days after injury revealed elevated chondrocyte differentiation within articular cartilage a

 
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