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1 r undergoing adipogenesis, osteogenesis, and chondrogenesis).
2 ed key regulatory networks prominent in hESC chondrogenesis.
3 rning and at later post-patterning stages of chondrogenesis.
4 v3.2 is responsible for Ca(2+) influx during chondrogenesis.
5 smic reticulum stress transducer crucial for chondrogenesis.
6 ch mimics the function of nSMase2, inhibited chondrogenesis.
7 lreticulin-deficient ESCs, while suppressing chondrogenesis.
8 2+) channel Cav3.2 is essential for tracheal chondrogenesis.
9 ng a secreted factor during TGF-beta-induced chondrogenesis.
10 naling proteins including BMPs, and restrict chondrogenesis.
11 nally shifted phalangeal joints and impaired chondrogenesis.
12 etas (TGFbeta), regulate multiple aspects of chondrogenesis.
13 contribution of these N-cadherin peptides to chondrogenesis.
14 erformed on distinct stages of hESC-directed chondrogenesis.
15 signaling required for joint patterning and chondrogenesis.
16 te decisions from osteogenesis to adipo- and chondrogenesis.
17 ractions during mesenchymal condensation and chondrogenesis.
18 s a regulator of mesenchymal stem cell (MSC) chondrogenesis.
19 and Sox9 may determine the earliest steps of chondrogenesis.
20 al activity of Sox9, the master regulator of chondrogenesis.
21 Canonical Wnt signaling strongly inhibits chondrogenesis.
22 d transforming growth factor beta to support chondrogenesis.
23 collagen content, and mineralization during chondrogenesis.
24 are known to regulate gene expression during chondrogenesis.
25 owth plate chondrocytes where it facilitates chondrogenesis.
26 ssion of several miRNAs was regulated during chondrogenesis.
27 ypertrophic chondrocytes and is required for chondrogenesis.
28 maintenance and the suppression of in vitro chondrogenesis.
29 Edn1 signaling and NC differentiation during chondrogenesis.
30 -associated proteins, similar to its role in chondrogenesis.
31 nd that Alcama interacts with Nadl1.1 during chondrogenesis.
32 n to activate downstream target genes during chondrogenesis.
33 addition to its previously described role in chondrogenesis.
34 thritis arises from abnormal and accelerated chondrogenesis.
35 ned the role of receptor Smads 1, 5 and 8 in chondrogenesis.
36 cts miR-199a(*)-mediated repression of early chondrogenesis.
37 e RhoA in such cultures can markedly enhance chondrogenesis.
38 lycan desulfation is a critical regulator of chondrogenesis.
39 ix (ECM) components normally associated with chondrogenesis.
40 d H3K27ac were de-methylated during in vitro chondrogenesis.
41 that NF-kappaB-p65 facilitates growth plate chondrogenesis.
42 wn-regulation of Sox9, a master regulator of chondrogenesis.
43 e now identify a possible role for GATA-6 in chondrogenesis.
44 ally regulated exon 2 splicing switch during chondrogenesis.
45 o affected as a result of the delay in early chondrogenesis.
46 not from migration defect, but from impaired chondrogenesis.
47 tissue, creating the correct environment for chondrogenesis.
48 le in the TRANSFAC database, as important to chondrogenesis.
49 criptional regulatory networks that regulate chondrogenesis.
50 Runx2 fulfills antagonistic functions during chondrogenesis.
51 lop normally until the onset of craniofacial chondrogenesis.
52 efect under a periosteal flap into goats for chondrogenesis.
53 gnaling pathways are essential regulators of chondrogenesis.
54 nts for BMP signaling in multiple aspects of chondrogenesis.
55 fering RNA inhibits Col2a1 expression during chondrogenesis.
56 genesis and in the activation of Sox9 during chondrogenesis.
57 g is essential for multiple aspects of early chondrogenesis.
58 (COL2A1) is developmentally regulated during chondrogenesis.
59 and in concert with Sox proteins to regulate chondrogenesis.
60 PGC-1alpha) as a coactivator for Sox9 during chondrogenesis.
61 ctivates Sox9-dependent transcription during chondrogenesis.
62 model for the initial events of mesenchymal chondrogenesis.
63 marrow mesenchymal stem/stromal cell (BMSC) chondrogenesis.
64 and one from the oral ectoderm that promotes chondrogenesis.
65 ing limb, suggesting that it plays a role in chondrogenesis.
66 ndroprogenitors and has an essential role in chondrogenesis.
67 mesenchymal stem cells (MSCs) improves their chondrogenesis.
68 ature of human mesenchymal stem cells during chondrogenesis.
69 tant degradation of the nanoparticles during chondrogenesis.
70 g and pathway analysis of the process of MSC chondrogenesis.
71 density micromass' using TGF-beta3 to induce chondrogenesis.
72 more widely used chemical induced method for chondrogenesis.
73 ommit to an osteogenic identity and suppress chondrogenesis.
74 ocytes and mesenchymal stem cells undergoing chondrogenesis.
75 1) is a previously unrecognized regulator of chondrogenesis.
76 ction of osteogenesis and the suppression of chondrogenesis.
77 nhibitor (SST0001), which strongly inhibited chondrogenesis.
78 he chondrocyte differentiation programme and chondrogenesis.
79 genesis, patterning of the oral skeleton and chondrogenesis.
80 suppresses osteogenesis, whereas it promotes chondrogenesis.
81 eurin/NFAT signaling pathway during tracheal chondrogenesis.
82 mimic mesenchymal condensation leading into chondrogenesis.
83 of chondrocyte hypertrophy and growth plate chondrogenesis, although the specific molecular mechanis
84 e-specific lncRNA, is upregulated during MSC chondrogenesis and appears to act directly downstream of
86 eta1 is a growth factor that is critical for chondrogenesis and binds to both biglycan and fibromodul
87 with exogenous heparanase greatly stimulated chondrogenesis and bone morphogenetic protein signaling
88 nction and that its absence leads to ectopic chondrogenesis and cartilage formation in conjunction wi
90 tides and evaluated their role in regulating chondrogenesis and cartilage matrix deposition by encaps
92 tes therefore offer a unique model for adult chondrogenesis and cartilage repair and may serve as ins
94 that Twist1 contributes to the repression of chondrogenesis and chondrocyte gene expression resulting
97 romodulin as novel key players in regulating chondrogenesis and ECM turnover during temoporomandibula
99 cle provides an overview of the processes of chondrogenesis and endochondral ossification and their c
102 ormone-related peptide, negatively regulates chondrogenesis and endochondral ossification via associa
104 nservation of SOX9's regulatory functions in chondrogenesis and gonad development among species, we p
106 t within an arthritic joint may also inhibit chondrogenesis and induce degradation of native and engi
108 In addition, the involvement of Nell-1 in chondrogenesis and its relevant pathologies have been re
111 plate chondrocytes facilitates growth plate chondrogenesis and longitudinal bone growth by inducing
112 Growth hormone (GH) stimulates growth plate chondrogenesis and longitudinal bone growth with its sti
115 cascades in response to TGF-beta to control chondrogenesis and osteogenesis during mandibular develo
117 in human chondrocytes and potently inhibited chondrogenesis and osteogenesis using in vitro models.
118 ral bone growth due to impaired BMP-mediated chondrogenesis and osteogenesis, recapitulating the huma
122 involvement of actin binding proteins during chondrogenesis and provide a molecular basis to a human
125 P-4 by genetically engineered MDSCs enhanced chondrogenesis and significantly improved articular cart
127 trast, treatment with TGFbeta also supported chondrogenesis and stimulated Sox9 expression, but faile
128 findings identify JAWS as a key regulator of chondrogenesis and synovial joint positioning required f
129 PR1B are functionally redundant during early chondrogenesis and that BMP signaling is required for ch
130 ore suggest that GATA-6 also plays a role in chondrogenesis and that Gpr49 is a potential direct targ
131 novel genes that regulate human growth plate chondrogenesis and thereby contribute to the normal vari
133 of mTOR is necessary for cell proliferation, chondrogenesis, and cartilage growth during bone develop
135 transcription factor germane to osteogenesis/chondrogenesis, and increased migratory ability in KFs.
136 kewise, nMSCs presented compromised in vitro chondrogenesis, and Meckel's cartilage was underdevelope
138 expression of SOX9, the master regulator of chondrogenesis, and reducing SOX9 dosage allowed chondro
139 is a transcriptional activator required for chondrogenesis, and SOX5 and SOX6 are closely related DN
140 or), an important regulator of angiogenesis, chondrogenesis, and wound healing, is overexpressed in a
141 The abnormal progression of hypertrophic chondrogenesis appeared to be associated with the sustai
143 CPSC also display a higher commitment toward chondrogenesis as demonstrated by a higher expression of
144 tiviral HMGB2 transduction of MSC suppressed chondrogenesis as reflected by an inhibition of Col2a1 a
146 CM1 seems to be critical for PTHrP action in chondrogenesis, as blockage of ECM1 nearly abolishes PTH
147 miR-199a(*) significantly inhibited early chondrogenesis, as revealed by the reduced expression of
148 tant role of GRASLND in regulating stem cell chondrogenesis, as well as its therapeutic potential in
152 e to orchestrate spatiotemporal programs for chondrogenesis autonomously, and to implement cartilage
153 nstrate that FoxA factors are induced during chondrogenesis, bind to conserved binding sites in the c
154 ndicate that heparanase is able to stimulate chondrogenesis, bone morphogenetic protein signaling, ce
155 g the many factors involved in regulation of chondrogenesis, bone morphogenetic proteins (BMPs) and m
156 C3H10T1/2 cells can prevent the induction of chondrogenesis, but cannot reverse the chondrogenic phen
157 nt dimer when it activates genes involved in chondrogenesis, but functions as a monomer to activate g
158 scription factor Sox9 is necessary for early chondrogenesis, but its subsequent roles in the cartilag
159 redundant L-Sox5 and Sox6 proteins to effect chondrogenesis, but the mode of action of the trio remai
160 indicate that IGF-I stimulates growth plate chondrogenesis by activating NF-kappaB-p65 in chondrocyt
161 ore, previous investigations of induction of chondrogenesis by human ESCs required embryoid body form
163 g factor beta subunit (CBFbeta), and induces chondrogenesis by regulating the CBFbeta-RUNX1 transcrip
164 n OA mainly by having a beneficial effect on chondrogenesis by the donor and host cells as well as by
165 principal processes underlying growth plate chondrogenesis, chondrocyte proliferation and hypertroph
166 and integration of DNA methylation data with chondrogenesis chromatin states revealed that enhancers
167 esis RNA), by RNA interference disrupted MSC chondrogenesis, concomitant with reduced cartilage-speci
168 pendent and BMP-responsive manner to promote chondrogenesis, consistent with the ectopic endochondral
169 , decreased proliferation at early stages of chondrogenesis, delayed skeletal vascularization and del
171 limb bud patterning but defective or delayed chondrogenesis due to a lack of Sox9 and Col2a1 expressi
173 e the cellular function of key regulators of chondrogenesis found mutated in chondrodysplasia syndrom
174 mbers of the BMP family that are crucial for chondrogenesis, GDF5 and BMP4, regulate the pattern of B
177 r (GDF)-2) potently induces osteogenesis and chondrogenesis, has been implicated in the differentiati
180 ranscriptomes generated during hESC-directed chondrogenesis identified key functionally related clust
181 gs suggest that BMP-6 is a potent inducer of chondrogenesis in ADAS cells, in contrast to mesenchymal
182 dult growth, and we show that persistence of chondrogenesis in adult skates correlates with ability t
183 sectioning was used to investigate secondary chondrogenesis in disarticulated craniofacial elements o
185 results reveal that the genetic pathway for chondrogenesis in lampreys and gnathostomes is conserved
187 d Kartogenin (KGN) - that greatly stimulates chondrogenesis in marrow-derived mesenchymal stem cells
188 he skeleton and that Tgfbr2 can act to limit chondrogenesis in mesenchymal cells like the interzone.
192 Wnt/beta-catenin signaling by LiCl enhances chondrogenesis in pericyte pellet cultures in the presen
193 itor of BMP receptors drastically attenuated chondrogenesis in recombinant human BMP 2-treated mutant
194 nexpected role of lipids as orchestrators of chondrogenesis in response to oxygen tension which is, a
195 the competence of somitic cells to initiate chondrogenesis in response to subsequent BMP signals by
197 I collagen were noted when pericytes undergo chondrogenesis in the hydrogel in the absence of inducti
198 with progressive loss of SSCs and diminished chondrogenesis in the joints of both mice and humans.
199 se data indicate that Osr1 normally prevents chondrogenesis in the mammalian tongue through repressio
200 cal mechanical environment promote secondary chondrogenesis in the mandibular adductor enthesis of du
201 rogenic genes, including Col2a1, followed by chondrogenesis in the MSC and developing chick limb.
203 steoprogenitor differentiation and perturbed chondrogenesis in the proximal region of the mandible.
204 ression of the myogenic factor Pax3 prevents chondrogenesis in these cells, while chondrogenic factor
205 our results indicate that neogenin promotes chondrogenesis in vitro and in vivo, revealing an unexpe
209 istology and expression of genes that affect chondrogenesis, including members of the FGF and BMP pat
210 ors have been identified that play a role in chondrogenesis, including the positive transacting facto
211 ion, which recapitulated the early stages of chondrogenesis, including transient vascularization.
212 iRNA targeting ANGPTL4 prior to induction of chondrogenesis increased expression of type II collagen
213 of precartilage condensations and subsequent chondrogenesis, indicating that downregulation of HA is
216 otides, nicotinamide, and IL-1beta inhibited chondrogenesis-induced down-regulation of cartilage-spec
217 nterior mesenchyme to undergo SOX9-dependent chondrogenesis, instead persisting as an interdigital-li
218 metabolic programming of the MSCs directing chondrogenesis into articular- or epiphyseal cartilage-l
219 rogramming of MSCs by oxygen tension directs chondrogenesis into either permanent or transient hyalin
221 and that repression of Runx2 at the onset of chondrogenesis is a prerequisite for the activation of a
222 n embryonic limb development have shown that chondrogenesis is initiated by cellular condensation, du
223 he transcriptional network that drives early chondrogenesis is intact, and that cell polarity within
225 ed in the developing tongue mesenchyme where chondrogenesis is subsequently activated to form the ect
226 Thus, one mechanism whereby Sox9 regulates chondrogenesis is to promote efficient beta-catenin phos
227 Sox9, a key transcriptional regulator of chondrogenesis, is required for TGF-beta-mediated regula
228 ining gene-9 (Sox9), the master regulator of chondrogenesis, is widely expressed in the nascent tongu
229 morphogenic protein (BMP) signaling promotes chondrogenesis, it is not clear whether BMP-induced chon
230 work and act in concert in the regulation of chondrogenesis.-Kong, L., Zhao, Y.-P., Tian, Q.-Y., Feng
231 blocks Wnt/beta-catenin signaling, inhibited chondrogenesis, leading to reduced Sox-9 and type II col
232 lular nanofiber scaffolds supported enhanced chondrogenesis marked by proteoglycan production minimal
233 come of this interaction improves viability, chondrogenesis, matrix formation, and homeostasis in the
234 hat laminins and nidogen-2 drive CPCs toward chondrogenesis may help in the elucidation of new treatm
236 ht of the inhibitory effects on growth plate chondrogenesis mediated by other FGFs, we hypothesized t
239 migration beneath the brain, requirements in chondrogenesis occur later, as cells form separate trabe
240 r thereafter in the course of BMP2-triggered chondrogenesis of a micromass culture of pluripotent C3H
242 e metabolism and is critical for accelerated chondrogenesis of ank/ank mesenchymal precursors and P(i
243 silencing suppressed Creb3l2 expression and chondrogenesis of ATDC5 cells, whereas infection of Alg2
244 e methods are similar to those published for chondrogenesis of bone marrow-derived mesenchymal stem c
245 mportant to better understand signal-induced chondrogenesis of chondrogenic progenitors in physiologi
246 (PLL) molecular weight and concentration on chondrogenesis of cocultures of mesenchymal stem cells (
248 acterised the DNA methylation changes during chondrogenesis of mesenchymal stem cells (MSCs) by Infin
250 ptides onto HA hydrogels promotes both early chondrogenesis of MSCs and cartilage-specific matrix pro
251 at this 3D hydrogel environment supports the chondrogenesis of MSCs, and here we demonstrate through
252 s antagonist, soluble Flt-1 (sFlt-1), on the chondrogenesis of skeletal muscle-derived stem cells (MD
254 the underlying molecular pathways that drive chondrogenesis of these populations of adult stem cells
256 ACVR1 as the underlying cause of the ectopic chondrogenesis, osteogenesis and joint fusions seen in F
258 condensation and has key roles in regulating chondrogenesis, osteogenesis, and bone and mineral homeo
259 s (e.g., type X collagen) by MSCs undergoing chondrogenesis raises concern for a tissue engineering a
260 ntetheinase, which inhibits synthesis of the chondrogenesis regulator glutathione, since we observed
263 02723505, which we termed ROCR (regulator of chondrogenesis RNA), by RNA interference disrupted MSC c
264 udal (occipital) chondrocranium, followed by chondrogenesis rostrally to form the nasal capsule, and
268 reduced expression of early marker genes for chondrogenesis such as cartilage oligomeric matrix prote
269 lysis identified regulators of hESC-directed chondrogenesis such as miR-29c-3p with 10 of its establi
270 f Sox9 to both inhibit myogenesis and induce chondrogenesis, suggesting that Nkx3.2 is required for S
271 the 3'UTR of Sox9, the central initiator of chondrogenesis, suggesting that Twist1 might directly re
272 d that adopting an osteogenesis-inducing and chondrogenesis-suppressing cell fate in the ventral mese
274 ytes, a mechanism resembling in vivo somitic chondrogenesis that is not recapitulated with TGFbeta.
275 rk provides new insights into the control of chondrogenesis that may ultimately lead to a stem cell-b
276 in BMP-2-mediated initiation of mesenchymal chondrogenesis that results in activation of Sox9 at lea
278 The cells displayed a propensity to undergo chondrogenesis that was enhanced by treatment with exoge
279 ates one of the major pathways that promotes chondrogenesis, the transforming growth factor beta rece
280 RNAs was measured in the ATDC5 cell model of chondrogenesis using microarray and was verified using q
281 producible model system of human ESC-induced chondrogenesis, using a novel direct plating method in w
282 ndent on Vanin-1; however, Vanin-1 regulates chondrogenesis via glutathione metabolism and is critica
283 asia, identifying a mechanism that regulates chondrogenesis via modulation of SOX9 ubiquitination.
284 ese results demonstrate that Phlpp1 controls chondrogenesis via multiple mechanisms and that Phlpp1 i
289 pand our understanding of the role of VHL in chondrogenesis, we conditionally deleted VHL in mesenchy
290 ha in mesenchymal condensations and in early chondrogenesis, we conditionally inactivated Hif-1alpha
291 gain insight into the role of ANGPTL4 during chondrogenesis, we used recombinant ANGPTL4 as well as a
292 air, the effects of selective EP agonists on chondrogenesis were examined in E11.5 long-term limb bud
294 av3.2 overexpression in ATDC5 cells enhances chondrogenesis, which could be blunted by both blocking
295 evaluate the effects of STC on growth plate chondrogenesis, which is the primary determinant of long
296 ccurate predictor of the degree of long-term chondrogenesis, while the presence of PLL was shown to h
297 ional and post-transcriptional regulation of chondrogenesis will enable us to improve hESC chondrogen
298 essential role for barx1 at early stages of chondrogenesis within the developing zebrafish viscerocr
300 promoting effect on IGF-1 expression and on chondrogenesis, yet it is not known whether other signal