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1                                              Ihh deficiency caused condylar disorganization and growt
2                                              Ihh is normally downregulated in regions that will becom
3                                              Ihh regulates cartilage development through PTHrP-indepe
4                                              Ihh regulates ISC self-renewal and differentiation.
5                                              Ihh signaling mediates gastrin-induced proliferation of
6                                              Ihh-overexpressing transgenic animals were generated and
7 sing new experimental approaches that ablate Ihh specifically in Pgr-positive uterine cells of the mo
8 processes during post-natal life, we ablated Ihh in cartilage of neonatal mice and assessed the conse
9 Indian hedgehog (Ihh) signaling and abnormal Ihh protein distribution in the extracellular matrix.
10 stric epithelial proliferation by activating Ihh signaling in mice.
11                                 In addition, Ihh signaling can inhibit chondrocyte hypertrophy and sy
12   Although it is generally believed that all Ihh functions are mediated by the Gli family of transcri
13                                     Although Ihh(-/-) cells organize into chondrogenic condensations
14 ression in proliferating chondrocytes via an Ihh-independent pathway; phospho-CREB levels were compar
15 ebra periosteal cells in response to BMP and Ihh signaling, whereas distal CTs form from blastema cel
16 tic interaction between Wnt/beta-catenin and Ihh signaling in regulating synovial joint formation.
17                Both the Wnt/beta-catenin and Ihh signaling pathways play essential roles in crucial a
18 s of Atf4(-/-) bone marrow stromal cells and Ihh-blocking antibody eliminates this effect.
19 e P16/Ink4a, P21, GSK-3beta, Il-6, Ffg3, and Ihh were overexpressed.
20 ances in cross-talk between the BMP, FGF and Ihh/PTHrP pathways.
21                                Thus, IGF and Ihh signaling appear to control the growth of the skelet
22 e, we report that disruption of both IGF and Ihh signaling resulted in additive reduction in the size
23               Remarkably, in both Ihh-/- and Ihh-/-; Gli3-/- embryos, vascularization promoted osteob
24 Gli2, were up-regulated in Spop mutants, and Ihh target genes Patched 1 (Ptch1) and parathyroid hormo
25 hanical activation of cell proliferation and Ihh gene expression.
26              However, the roles of PTHrP and Ihh in regulating earlier steps in chondrocyte different
27 is controlled at multiple steps by PTHrP and Ihh through the mutual regulation of their activities.
28 ties were accompanied by increased Runx2 and Ihh expression and increased Indian hedgehog signaling.
29                  Interestingly, both Shh and Ihh are only expressed in the regenerating and developin
30  conditional approach to remove both Shh and Ihh functions from early mouse gut endoderm.
31      To examine the combined role of Shh and Ihh in intestinal morphogenesis, we generated transgenic
32                    The expression of Shh and Ihh is quite unique since these genes have never been de
33 ial for long-range signaling by both Shh and Ihh ligands.
34 nto the distant past, revealing that Shh and Ihh must once have shared responsibilities in establishi
35 mo acts epistatic to Ptc1 to mediate Shh and Ihh signaling in the early mouse embryo.
36 that Disp1 function is essential for Shh and Ihh signaling in the mouse, and Disp1 gene dose regulate
37 n an ex vivo environment, both wild-type and Ihh mutant vessels invade the Ihh(-/-) cartilage, though
38      More importantly, we found that Wnt and Ihh signaling interact with each other in distinct ways
39 hondrocyte differentiation markers Col X and Ihh.
40 me impairs Gli2-Foxc1 association as well as Ihh function.
41 that TGFbeta2 acts as a signal relay between Ihh and PTHrP in the regulation of cartilage hypertrophi
42 nstrates that Ihh is distributed well beyond Ihh expressing cells though the range of movement and si
43                                     Blocking Ihh function in primitive endoderm inhibits activation o
44 tero-posterior axis are orchestrated by both Ihh and Shh.
45                          Remarkably, in both Ihh-/- and Ihh-/-; Gli3-/- embryos, vascularization prom
46                  Indian hedgehog (encoded by Ihh) has been shown to be expressed in the uterine epith
47 upted in about 30% of columnar chondrocytes, Ihh action in the periarticular chondrocytes was upregul
48  livers, and some of these cells coexpressed Ihh, Ptc, and/or Gli2.
49 a shows, for the first time, that continuous Ihh action is required for completion of post-natal TMJ
50                                   Decreasing Ihh action in these mice reduced elongation of columns,
51 rst time, that postnatal chondrocyte-derived Ihh is essential for maintaining the growth plate and ar
52                          Ovaries lacking Dhh/Ihh exhibit theca layer loss, blunted steroid production
53                            Production of Dhh/Ihh in granulosa cells requires growth differentiation f
54  a growth-plate-like structure with distinct Ihh, collagen X, and osteopontin expression patterns.
55 Proliferation was partially restored in dual Ihh;Gli3 mutants, suggesting that Gli3 is normally a neg
56                             Although ectopic Ihh does not induce overt ossification along the entire
57 gesting a synergistic effect between ectopic Ihh and endogenous factors such as the bone morphogeneti
58 lin D1 is markedly downregulated when either Ihh or Smo activity is removed from chondrocytes, indica
59 n of Atf4 in chondrocytes induces endogenous Ihh mRNA, and Atf4 directly binds to the Ihh promoter an
60 th factor-evoked ERK activation and enhanced Ihh and Pthrp expression, whereas fibroblast growth fact
61            Deletion of intestinal epithelial Ihh disrupted the intestinal mesenchymal architecture, d
62                        Intestinal epithelial Ihh signals to the mesenchymal compartment to regulate f
63 genitor cell population to prevent excessive Ihh production.
64                     Treatment with exogenous Ihh did not fully restore normal proteoglycan levels in
65  cells that accumulate in PBC livers express Ihh or Hh-target genes including the Hh-receptor, Patche
66       Scattered stromal cells also expressed Ihh.
67 phenotypes of embryo yolk sacs deficient for Ihh or SMO: Whereas Ihh(-/-) yolk sacs can form blood ve
68 amined the ability of ES cells deficient for Ihh or smoothened (Smo), which encodes a receptor compon
69 ly establish Gli3 as a critical effector for Ihh activity in the developing skeleton, but also identi
70 ng a transmembrane protein indispensable for Ihh signaling) has been only partially successful, due t
71                                   A role for Ihh in yolk sac function is suggested by the observation
72  hedgehog (Shh), a functional substitute for Ihh, stimulates expression of Tgfb2 and Tgfb3 mRNA in th
73 REB levels were comparable in cartilage from Ihh(-/-) and wild-type mice.
74 signed to segregate the activity of Shh from Ihh.
75                                 Furthermore, Ihh mediates the mechanotransduction process in a bone m
76  by increased expression of Indian Hedgehog (Ihh) and hyperproliferation of surface mucous cells.
77 nied by an up-regulation of Indian Hedgehog (Ihh) and maintenance of Hh pathway activity.
78 olume, and up-regulation of Indian hedgehog (Ihh) and of collagen type X--all indicative of chondrocy
79 signaling cascade involving Indian hedgehog (Ihh) and parathyroid hormone related peptide (PTHrP) has
80 thway activation, increased Indian hedgehog (Ihh) and parathyroid hormone-related protein (Pthrp, als
81                             Indian hedgehog (Ihh) and PTHrP signaling play crucial roles in regulatin
82 s, sonic hedgehog (Shh) and indian hedgehog (Ihh) are secreted by the endoderm of the mammalian gut,
83                 We identify Indian hedgehog (Ihh) as a novel downstream target of AR in external geni
84                             Indian hedgehog (Ihh) controls multiple aspects of endochondral skeletal
85                             Indian hedgehog (Ihh) controls multiple aspects of endochondral skeletal
86                             Indian hedgehog (Ihh) critically regulates multiple aspects of endochondr
87 s Desert hedgehog (Dhh) and Indian hedgehog (Ihh) from granulosa cells.
88           We identified the Indian hedgehog (Ihh) gene as a target of BMP signaling.
89 in (Ocn) in osteoblasts and indian hedgehog (Ihh) in chondrocytes.
90     We examined the role of Indian hedgehog (Ihh) in mesenchymal organization and the mechanisms by w
91  to mechanical induction of Indian hedgehog (Ihh) in primary chicken chondrocytes cultured in 3-dimen
92                             Indian hedgehog (Ihh) is essential for chondrocyte and osteoblast prolife
93                             Indian hedgehog (Ihh) is essential for embryonic mandibular condylar grow
94 ous studies have shown that Indian hedgehog (Ihh) is expressed in the visceral endoderm both in the v
95                             Indian hedgehog (Ihh) is expressed normally in the growth plates of Evc(-
96                             Indian hedgehog (Ihh) is indispensable for development of the osteoblast
97                             Indian hedgehog (Ihh) is indispensable for osteoblast differentiation dur
98           The expression of Indian hedgehog (Ihh) is markedly decreased, whereas the expression of ot
99 ly secreted Sonic (Shh) and Indian hedgehog (Ihh) proteins that directly signal to adjacent mesoderm.
100 tes that also expressed the Indian hedgehog (Ihh) receptor and transcriptional target Patched 1(Ptch1
101                             Indian Hedgehog (Ihh) regulates chondrocyte and osteoblast differentiatio
102                             Indian hedgehog (Ihh) regulates endochondral ossification in both a parat
103       Here we asked whether Indian hedgehog (Ihh) regulates symphyseal cartilage development and grow
104                             Indian Hedgehog (Ihh) regulates tissue morphogenesis.
105                     Loss of Indian hedgehog (Ihh) results in reduction in pancreas size, indicating a
106 th plates showed diminished Indian hedgehog (Ihh) signaling and abnormal Ihh protein distribution in
107 igated the role of Disp1 in Indian hedgehog (Ihh) signaling in the developing bone bypassing the leth
108                             Indian hedgehog (Ihh) signaling is indispensable for osteoblast different
109 d that most likely reflects Indian hedgehog (Ihh) signaling originating from the underlying gut endod
110 related peptide (PTHrP) and Indian hedgehog (Ihh) signaling tightly regulates chondrocyte proliferati
111  reduced Ihh expression and Indian hedgehog (Ihh) signaling.
112 ndral skeleton, a target of Indian hedgehog (Ihh) signaling.
113 on of either Sonic (Shh) or Indian Hedgehog (Ihh) under control of the human Pax4-promoter.
114 ondrogenic genes, including Indian hedgehog (Ihh), a critical mediator of mechanotransduction.
115 ts genetically with that by Indian hedgehog (Ihh), a locally produced growth signal for the endochond
116                             Indian hedgehog (Ihh), a member of the hedgehog (Hh) family of proteins,
117 ly detectable expression of Indian hedgehog (Ihh), collagen X (Col10a1), Vegf (Vegfa), MMP-13 (Mmp13)
118                             Indian hedgehog (Ihh), one of the three mammalian hedgehog (Hh) proteins,
119                             Indian hedgehog (Ihh), patched (Ptc), and Gli3 are expressed at low level
120 otein (PTHrP), regulated by Indian hedgehog (Ihh), prevents premature hypertrophic differentiation, t
121 ), sonic hedgehog (Shh) and Indian hedgehog (Ihh), we demonstrate that Disp1 genetically interacts wi
122                             Indian hedgehog (Ihh), which is predominantly expressed in prehypertrophi
123 omain typically occupied by Indian hedgehog (Ihh).
124 nied by early activation of Indian hedgehog (Ihh).
125  zones independently of the Indian hedgehog (Ihh)/parathyroid hormone-related peptide (PTHrP) negativ
126                                           In Ihh(-/-) embryos, skeletal muscle development appears ab
127                                           In Ihh-null mice, however, symphyseal development was defec
128 4(-/-) embryos and rectifies the decrease in Ihh expression, Hh signaling, proliferation and accelera
129 stly, we studied postnatal mice deficient in Ihh in cartilage; their cranial base defects only minima
130 e for the failure of osteoblast formation in Ihh-null embryos.
131        Here, we show that removal of Gli3 in Ihh-null mouse embryos restored normal proliferation and
132                       Loss of muscle mass in Ihh null mouse embryos is accompanied by a dramatic incr
133 ses were accompanied by marked reductions in Ihh and PTHrP as well as sFRP-1, an endogenous Wnt signa
134 skeletal muscle mass similar to that seen in Ihh(-/-) mouse embryos.
135 ophy, we have both activated and inactivated Ihh signaling in the absence of PTHrP during endochondra
136 on of its epithelial target genes, including Ihh, in the Wnt7a-Cre(+)PR(f/-) mice.
137 hondrocyte differentiation markers including Ihh, Col X, and Runx2.
138 bitor treatment of chondroid cells increased Ihh and Pthrp expression.
139                      Sonic (Shh) and Indian (Ihh) hedgehog are expressed in the epithelium throughout
140 reduction in the combined epithelial Indian (Ihh) and Sonic (Shh) hedgehog signal leads to mislocaliz
141                         Sonic (Shh), Indian (Ihh), and Desert (Dhh) hedgehog constitute the repertoir
142              In this negative-feedback loop, Ihh inhibits hypertrophic differentiation by regulating
143 he role of Ihh in myogenesis, we manipulated Ihh expression in the developing chick hindlimb.
144  transcription activator critically mediates Ihh function in osteoblastogenesis.
145  been established which Gli protein mediates Ihh activity in skeletal development.
146 n important function for CSPGs in modulating Ihh signaling in the developing growth plate, and highli
147 Our results demonstrate that neither Shh nor Ihh is required for mammary gland morphogenesis and func
148  Atf4 in chondrocytes is required for normal Ihh expression and for its paracrine effect on osteoblas
149 ested by the observation that roughly 50% of Ihh(-/-) mice die at mid-gestation, potentially owing to
150 the hypertrophic cartilage in the absence of Ihh but requires simultaneous removal of Gli3 to restore
151                            In the absence of Ihh, cells of the osteoblast lineage fail to activate th
152 red for normal transcriptional activation of Ihh target genes.
153 Atf4 as a novel transcriptional activator of Ihh in chondrocytes that paces longitudinal bone growth
154 at cholesterol, by modifying the activity of Ihh (another of the Hedgehog family proteins) in the gro
155  possibly by altering the normal activity of Ihh, results in suppressed longitudinal bone growth and
156                           Direct analysis of Ihh trafficking in the target field demonstrates that Ih
157 i3 collectively mediate all major aspects of Ihh function during endochondral skeletal development.
158 els in mutant cultures, but a combination of Ihh and BMP-2 did.
159 italia and show that conditional deletion of Ihh inhibits penile masculinization.
160 atial-specific manner; postnatal deletion of Ihh resulted in loss of columnar structure, premature va
161 sed with mice with conditional disruption of Ihh in the small intestine epithelium.
162  outgrowth were due in part to disruption of Ihh signaling during endochondral bone formation.
163 intestinal epithelial-specific disruption of Ihh.
164 sed a model where TGFbeta acts downstream of Ihh and upstream of PTHrP in a cascade of signals that r
165 e that Wnt signaling functions downstream of Ihh in development of the osteoblast lineage.
166       Beta-catenin is required downstream of Ihh signaling and osterix expression for osteoblast diff
167 muscle mass appears to be a direct effect of Ihh since ectopic expression of Ihh by RCAS retroviral i
168 vious efforts to delineate direct effects of Ihh on chondrocytes by Col2-Cre-mediated ablation of Smo
169        Despite the pro-osteogenic effects of Ihh on periosteal cell differentiation, mechanical artic
170 s important role by dampening the effects of Ihh-PTHrP together with sFRP-1.
171 as is Bmp4, which may mediate the effects of Ihh.
172  PC-Shh(KO)/GKO mice increased expression of Ihh and proliferation within the surface epithelium comp
173              MiR-365 increases expression of Ihh and the hypertrophic marker type X collagen, whereas
174 cal stress greatly induces the expression of Ihh by chondrocytes.
175 ct effect of Ihh since ectopic expression of Ihh by RCAS retroviral infection of chicken embryo hindl
176      In contrast, chronic over-expression of Ihh in the intestinal epithelium leads to progressive ex
177  Lastly, AY 9944 decreased the expression of Ihh in the metatarsal growth plate.
178 ssification is delayed and the expression of Ihh target genes inhibited.
179               Foxc1 stimulates expression of Ihh target genes, including PTHrP and Col10a1, through i
180 e epithelium was collected and expression of Ihh was quantified by laser capture microdissection foll
181   In this study, we show a novel function of Ihh.
182                           Lower induction of Ihh, Ptc, and Hoxa10 is seen in response to progesterone
183 able to override the osteogenic influence of Ihh on the periosteum, but does not interfere with the c
184 rowth plates of these mice exhibit a lack of Ihh, PTHrP-R, and Col10 expression indicating a loss of
185 ts, the condyles displayed reduced levels of Ihh expression, H4C-positive proliferating chondroprogen
186                       Direct measurements of Ihh binding to defined GAG chains demonstrated that Ihh
187 r no Ptch1-lacZ staining and no migration of Ihh expressing cells into the developing placenta.
188 ndent upregulation but also misexpression of Ihh, leading to abnormal phalanges, fusion of sutures an
189                                The number of Ihh+ cells/portal triad was 6-fold greater in PBC livers
190                            Overexpression of Ihh caused PTHrP upregulation, elongation of columns, an
191 1 is an important transcriptional partner of Ihh-Gli2 signalling during endochondral ossification, an
192     In conclusion, the skeletal phenotype of Ihh(-/-) embryos represents the sum of disturbances in t
193 terior epiblasts cultured in the presence of Ihh protein, as is Bmp4, which may mediate the effects o
194 er distance, reflecting the reduced range of Ihh movement.
195                                 Reduction of Ihh in chicken embryo hindlimbs reduced skeletal muscle
196 R binding sites in the 5'-flanking region of Ihh.
197 cyte hypertrophy, while a down-regulation of Ihh expression may be responsible for a significant redu
198 S-PGs to exert their roles via regulation of Ihh signaling topography and action.
199 , Spop is an important positive regulator of Ihh signaling and skeletal development.
200               To further examine the role of Ihh in myogenesis, we manipulated Ihh expression in the
201 required for the paracrine signaling role of Ihh in the skeleton.
202         Our results revealed a novel role of Ihh signaling in promoting chondrocyte hypertrophy indep
203 whether there is a PTHrP-independent role of Ihh signaling in regulating chondrocyte hypertrophy, we
204  We uncovered previously unexpected roles of Ihh signaling in synovial joint formation and the essent
205                             Transcription of Ihh in ovariectomized mice is induced by progesterone bu
206                             Transcription of Ihh increases dramatically in the luminal epithelium and
207                               Transplants of Ihh-null anlagen also developed normally.
208             In these models, upregulation of Ihh action in the periarticular region was also observed
209 r in the growth plate caused upregulation of Ihh action, PTHrP upregulation, acceleration of periarti
210 rvival, beta-catenin is required upstream of Ihh signaling to inhibit chondrocyte apoptosis.
211                    Analysis was conducted on Ihh to determine whether PR directly regulates epithelia
212  and that FGF exerts antagonistic effects on Ihh expression.
213 ies arise following removal of either Shh or Ihh.
214 og (Shh) protein in vitro, or overexpressing Ihh in the cartilage of PTHrP(-/-) embryos or inactivati
215 fects are observed in both Pax4-Shh and Pax4-Ihh transgenic lines, suggesting that regulation of the
216 ous Wnt signaling antagonist and a potential Ihh signaling target.
217 te that BMP signaling is required to promote Ihh expression, and to inhibit activation of STAT and ER
218               Cotransfection of the proximal Ihh promoter with PR demonstrated that PR directly regul
219                        Consequently, a PTHrP-Ihh feedback loop is established, but over a shorter dis
220 titutive ERK1/2 activation, strongly reduced Ihh expression and decreased chondrocyte proliferation a
221 5(-/-) mice that are associated with reduced Ihh expression and Indian hedgehog (Ihh) signaling.
222 nding suggests that the hormone may regulate Ihh through both nuclear receptor-dependent and -indepen
223 h PR demonstrated that PR directly regulates Ihh transcription.
224 independent Notch signaling likely regulates Ihh responsiveness during cartilage and bone development
225 ey act, at least in part, by down-regulating Ihh signaling, Fgfr3, and Runx2 and by up-regulating Bmp
226 pregulate Cyclin D1 and to antagonize Runx2, Ihh, and collagen X expression when Zfp521 was absent.
227                      In the ex vivo setting, Ihh(-/-) cells differentiate into osteoblasts and deposi
228                       Here we show that Shh, Ihh, ptc-1, and ptc-2 are expressed during lens regenera
229                                  Smo and Shh/Ihh compound mutants have identical phenotypes: embryos
230  of the Hh pathway, such as Shh, Smo and Shh/Ihh compound mutants, also have laterality defects.
231 t arrest in cartilage differentiation, since Ihh(-/-) chondrocytes undergo hypertrophy and terminal d
232 ated by increased transcript levels of Sox9, Ihh, Col2a1, and Col10a1.
233 lineage requires sequential, stage-specific, Ihh and canonical Wnt/beta-catenin signaling to promote
234  These findings indicate that BMP stimulates Ihh expression.
235                                       Strong Ihh expression was detected in most bile ductular cells.
236  occur when Shh is not expressed, suggesting Ihh acts directly on fetal myoblasts to regulate seconda
237                                  In summary, Ihh is required for multiple processes during synchondro
238 ineage in the developing long bones and that Ihh functions in conjunction with other factors such as
239               These results demonstrate that Ihh acts on periarticular chondrocytes to stimulate thei
240 rine cells of the mouse, we demonstrate that Ihh is an essential mediator of Pgr action in the uterus
241 ken together, these results demonstrate that Ihh signaling is directly required for the osteoblast li
242 ding to defined GAG chains demonstrated that Ihh interacts with CS, particularly chondroitin-4-sulfat
243 icking in the target field demonstrates that Ihh is distributed well beyond Ihh expressing cells thou
244 nt study has not only provided evidence that Ihh signaling directly controls PTHrP expression and cho
245               Previous studies indicate that Ihh signaling in the long bones is essential for initial
246 s removed from chondrocytes, indicating that Ihh regulates chondrocyte proliferation at least in part
247 rter and genome-editing studies in mice that Ihh is regulated by a constellation of at least nine enh
248 erses transcription-PCR assays revealed that Ihh is up-regulated in embryonic cells upon BMP treatmen
249                                 We show that Ihh is a direct target of BMP pathways in chondrocytes,
250                            Here we show that Ihh stimulates differentiation of periarticular to colum
251 -immunoprecipitation experiments showed that Ihh binds to the major cartilage CSPG aggrecan via its C
252                              We suggest that Ihh acts in vivo on a potential progenitor cell to promo
253                        Our data suggest that Ihh may transduce mechanical signals during cartilage gr
254                      These data suggest that Ihh positively controls differentiation of periarticular
255                        Our data suggest that Ihh promotes fetal myoblast survival during their differ
256 essive Patched-1 expression, suggesting that Ihh distribution was wider and responsible for such exce
257 is in the adjacent epiblast, suggesting that Ihh is an endogenous signal that plays a key role in the
258                                          The Ihh(-/-) cranial bases displayed reduced growth and chon
259  absence of blood vessels is not because the Ihh(-/-) skeleton is anti-angiogenic; in fact, in an ex
260 natal life, mesenchymal cells expressing the Ihh receptor Patched1 were present anterior to the Ihh-e
261                       RT-PCR analysis in the Ihh(-/-) lines shows a substantial decrease in the expre
262  limited vascular remodeling observed in the Ihh(-/-) yolk sacs.
263  formation in the Runx2-null, but not in the Ihh-null embryo.
264 sely, a dominant negative Foxc1 inhibits the Ihh target gene expression.
265  wild-type and Ihh mutant vessels invade the Ihh(-/-) cartilage, though only wild-type vessels expand
266 ates of Evc(-/-) mice, but expression of the Ihh downstream genes Ptch1 and Gli1 was markedly decreas
267            We also suggest expression of the Ihh gene, which contains multiple Smad binding sites, mi
268              The BMP response element of the Ihh promoter contains multiple GC-rich motifs known as t
269 dral ossification was delayed in much of the Ihh(-/-) cranial bases but, surprisingly, was unaffected
270  mechanisms downstream or independent of the Ihh-PTHrP signaling pathway, a pivotal signaling system
271 ent manner, and have attempted to rescue the Ihh-null mouse with the Gli2 activator, either alone or
272 ous Ihh mRNA, and Atf4 directly binds to the Ihh promoter and activates its transcription.
273 ceptor Patched1 were present anterior to the Ihh-expressing secondary cartilage, proliferated, differ
274 aracterization of a mouse model in which the Ihh gene was successfully ablated from postnatal chondro
275 ation zone; this location coincides with the Ihh and Col X expression regions in vivo.
276 one of the growth plate, coinciding with the Ihh expression region in vivo.
277 the secondary chondrocytes derives from this Ihh source.
278                                        Thus, Ihh signaling is essential for symphyseal cartilage deve
279 o which different Gli proteins contribute to Ihh functions is not fully understood.
280 strated that these cells can also respond to Ihh, and do so both by enhanced proliferation and precoc
281 , a molecule necessary for responsiveness to Ihh, from the developing tendon and enthesis altered the
282                          Equally unexpected, Ihh(-/-) growth plates stained poorly with Alcian blue a
283 ivated the beta-catenin gene and upregulated Ihh signaling simultaneously in the same cells during en
284 , exited from the cell cycle and upregulated Ihh.
285 e may both mediate the effect of upregulated Ihh signaling in promoting chondrocyte hypertrophy.
286                   We found that upregulating Ihh signaling in the developing cartilage by treating PT
287               The early lethality of various Ihh-ablated mutant mice, however, prevented further anal
288 erence was seen in cultured wild-type versus Ihh(-/-) synchondrosis chondrocytes.
289 mbryos and continued Erg expression and weak Ihh expression in Sox5(-/-)6(-/-) growth plates suggest
290  yolk sacs deficient for Ihh or SMO: Whereas Ihh(-/-) yolk sacs can form blood vessels, the vessels a
291                   In order to assess whether Ihh is sufficient to induce bone formation in vivo, we h
292                In order to determine whether Ihh is directly required for osteoblast differentiation,
293 vely by the pmx through a mechanism in which Ihh and Bmp4 synergize to promote expansion of bone tiss
294 y forming a negative feedback loop, in which Ihh signaling regulates chondrocyte hypertrophy by contr
295 collar in the long bones of embryos in which Ihh was artificially expressed in all chondrocytes by th
296 ressor is the predominant mode through which Ihh controls chondrocyte proliferation and maturation, b
297            Thus, the mechanism through which Ihh induces osteoblast differentiation requires other ef
298 lature-derived signal, which integrates with Ihh and Wnt signals to determine the osteoblast versus c
299 ed in vitro by periosteal cells treated with Ihh and BMP-2.
300   Rather than forming a typical narrow zone, Ihh(-/-) hypertrophic chondrocytes occupied an elongated

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