ライフサイエンスコーパス: Shh

1 Shh expression specifies the odontogenic epithelium duri

2 Shh has been shown to undergo injury-induced upregulatio

3 Shh induces the oncogene Yes-associated protein (YAP), w

4 Shh is located within a TAD known to contain all its enh

5 Shh mediates activity-dependent and injury-induced hippo

6 Shh signaling is impaired in null embryos and primary ci

7 Shh signaling is lost in reactive astrocytes at the lesi

8 Shh signaling reduced AD pathology and the levels of Shh

9 Shh signaling was impaired in gigaxonin-null zebrafish a

10 Shh-type medulloblastoma displays distinct H3K27me3 prop

11 ing the growth and transcription factors: 1) Shh and Bmp4, required for stomach outgrowth; 2) Barx1,

12 fibroblasts from patients with GAN and in a Shh activity reporter line depleted in gigaxonin.

13 in humans and mice and that Foxf2 acts in a Shh-Foxf-Fgf18-Shh molecular network controlling palatal

14 Mice lacking a Shh cis-enhancer, MFCS4 (ShhMFCS4/-), with reduced SHH i

15 also reduced in this region, suggestive of a Shh-Vax1 feedback loop during early development of the f

16 ed the turning of commissural axons toward a Shh gradient.

17 at the turning of rat commissural axons up a Shh gradient requires protein synthesis.

18 pathway components as measured by Gli-1 and Shh at transcriptional and translational levels.

19 are essential for zli enhancer activity and Shh expression in the mouse embryo.

20 nce related gene expression (Bmp2, GDNF, and Shh) in Acomys compared to Mus (p < .05).

21 A reduction of Hand2 and Shh gene dosage improves the integrity of anterior limb

22 on promotes ciliary localization of mSmo and Shh pathway activity.

23 mutant analysis supports that FP-netrin1 and Shh collaborate to attract at long range.

24 nes including Cdkn2a (p16), Cdkn2b (p15) and Shh.

25 key processes such as tubulin transport and Shh signaling.

26 dicates a strong association between Wnt and Shh signaling pathways in cusp patterning.

27 Scube2, a glycoprotein regulating astrocyte Shh release was decreased, inhibiting Shh delivery to br

28 PBO attenuated Shh signaling in vitro through a mechanism similar to th

29 We propose that Inpp5e attenuates Shh signaling in the neural tube through regulation of t

30 Because Shh reception occurs at primary cilia, which are positio

31 This regulatory link between Shh and planar cell polarity (PCP) signaling may also oc

32 Collectively our data suggest a link between Shh pathway activity and the physiological properties of

33 bserve a decreased spatial proximity between Shh and its enhancers during the differentiation of embr

34 e inhibitor (HL2-m5) was obtained that binds Shh with a KD of 170 nM, which corresponds to a 120-fold

35 Both Shh and HGF were heterogeneously expressed in PDAC strom

36 In the adult brain, Shh has neurotrophic function and is implicated in hippo

37 ngly active in the human fetal neocortex but Shh signaling was not strongly active in the mouse embry

38 ay was downregulated by Mtb-stimulation, but Shh levels in astrocytes were unchanged.

39 Here, we show that the guidance of axons by Shh requires protein synthesis.

40 ta suggest that direct targeting of Foxf2 by Shh signaling drives cNCC mesenchyme proliferation durin

41 of patterned apical constriction governed by Shh signaling that generates structural changes in the d

42 is induced by Wnt signaling but inhibited by Shh signaling, and epithelial Fgf10 signaling activates

43 rkhead box (Fox) genes that are regulated by Shh signaling during lip morphogenesis.

44 ), the key regulator for Wnt trafficking, by Shh-Cre to investigate how the Wnt ligands produced in t

45 We find that conditional knockout of Wls by Shh-Cre leads to defective ameloblast and odontoblast di

46 ion of Hedgehog signaling pathway components Shh, Gli1, and Patched1 was greatly decreased in Wls(Shh

47 ngtt in cultured mammalian cells compromised Shh pathway activity, suggesting that RNGTT is functiona

48 We conclude Shh supplied by taste nerves and local taste epithelium

49 Conversely, we show that conditional Shh overexpression activates canonical Hh signaling in S

50 In the postnatal cortex, Shh signaling is active in a subpopulation of mature ast

51 sets are useful entry points for deciphering Shh-dependent regulatory mechanisms involved in cochlear

52 Our findings indicate that defective Shh signaling is responsible for abnormal morphogenesis

53 s that these defects are caused by deficient Shh, we found that CBs reduced Shh signaling by inhibiti

54 However, although neurally derived Shh is in part responsible for the dependence of taste c

55 These studies uncover that tubule-derived Shh triggers the early activation of fibroblasts, which

56 localized to the primary cilia, dysregulated Shh and Wnt signaling and inhibited cell proliferation i

57 y, pMN cells of mutant embryos have elevated Shh signaling, coincident with the motor neuron to OPC s

58 together, these data suggest that endogenous Shh signaling in astrocytes is dynamically regulated in

59 oothened agonist or by addition of exogenous Shh, or neutralizing MMP-9 activity, decreased permeabil

60 architecture, whereas embryos with expanded Shh signaling, including the IFT-A complex mutants Ift12

61 ly, epithelial taste precursor cells express Shh transiently, and provide a local supply of Hh ligand

62 mice and that Foxf2 acts in a Shh-Foxf-Fgf18-Shh molecular network controlling palatal shelf growth.

63 ating palatal shelf growth through the Fgf18-Shh signaling network, Foxf2 controls palatal shelf morp

64 nexpected given the requirement of cilia for Shh transduction.

65 Cilia are essential for Shh signal transduction and the ciliary phosphatidylinos

66 se formation in dentate granule cells or for Shh-dependent neuronal precursor proliferation.SIGNIFICA

67 Therefore, ZBP1 is required for Shh to guide commissural axons.

68 To test whether Ptchd1 is required for Shh-dependent signaling, we examined two Shh-dependent c

69 We demonstrate that ZBP1 is required for Shh-mediated axon guidance, identifying a new member of

70 r Atonal homologue 1 (Atoh1) is required for Shh-type medulloblastoma development in mice.

71 , consistent with a neuroprotective role for Shh signaling after injury.

72 These data identify a critical role for Shh signaling in astrocyte-mediated modulation of neuron

73 on defined by Fgf10 and highlight a role for Shh signalling in the integrated development of the hypo

74 Our findings establish an important role for Shh upregulation in preventing AD, by increased Gli-driv

75 insight into several unanticipated roles for Shh, including priming the cochlear epithelium for subse

76 non-motile organelle that is specialized for Shh signal transduction and responsible, when defective,

77 NDCs were isolated from Shh-cre;ROSA:YFP mice at embryonic day 12.5 and postnata

78 Mitochondria from Shh-treated neurons were more electron-dense, as reveale

79 tants exhibiting loss (Smo(ecko) ) and gain (Shh-P1) of Shh signaling reveal a set of Shh-responsive

80 riven activation of the Sonic hedgehog gene (Shh), we have identified a change in chromosome conforma

81 cell layer demonstrating that MCs-generated Shh is a key modulator of hippocampal neurogenesis.

82 th these defects reproduced following global Shh deletion from E10.5 in pCag-CreERTM; Shhflox/flox em

83 re, we provide evidence that Sonic hedgehog (Shh) activates Gli2 by stimulating its phosphorylation o

84 Here, we investigated how Sonic hedgehog (Shh) and Fibroblast growth factor (Fgf) signaling regula

85 Sonic hedgehog (Shh) attracts spinal cord commissural axons toward the f

86 ion around the lesion allows Sonic hedgehog (Shh) binding and favors the local enrichment of this mor

87 at on induction of mouse AD, Sonic Hedgehog (Shh) expression in skin, and Hh pathway action in skin T

88 Sonic hedgehog (Shh) expression in the limb bud organizing centre called

89 In Ftm (-/-) embryos, Sonic hedgehog (Shh) expression was virtually lost in the ventral forebr

90 observed including decreased Sonic hedgehog (Shh) expression, abnormal cell adhesion, and altered rad

91 atory nerves are a source of sonic hedgehog (Shh) for taste bud renewal.

92 equirement for the Hh ligand Sonic Hedgehog (Shh) for the progression of SCLC.

93 dance.SIGNIFICANCE STATEMENT Sonic hedgehog (Shh) guides axons via a noncanonical signaling pathway t

94 aKO interstitium and ectopic sonic hedgehog (Shh) in subsets of non-dilated P7 mutant proximal tubule

95 howed that gigaxonin governs Sonic Hedgehog (Shh) induction, the developmental pathway patterning the

96 Sonic hedgehog (Shh) is a multifunctional signaling protein governing pa

97 Sonic hedgehog (Shh) is a secreted protein that controls the patterning

98 arly limb bud, for instance, Sonic hedgehog (Shh) is expressed in the distal posterior mesenchyme, wh

99 Smoothened Agonist (SAG), a Sonic Hedgehog (Shh) mimetic in order to fortify blood brain barrier (BB

100 Treatment with the Sonic hedgehog (Shh) pathway agonist purmorphamine or cyclin-dependent k

101 ression was regulated by the Sonic Hedgehog (Shh) pathway.

102 brane protein related to the Sonic hedgehog (Shh) receptor, Patched, and involved in intracellular tr

103 Sonic hedgehog (Shh) signal transduction specifies ventral cell fates in

104 Sonic hedgehog (Shh) signal transduction was downregulated in the mutant

105 ypothesized to contribute to Sonic hedgehog (Shh) signaling and synapse formation.

106 Here, we show that Sonic hedgehog (Shh) signaling in mature astrocytes is required for esta

107 In the healthy, adult CNS, Sonic hedgehog (Shh) signaling is active in mature, differentiated astro

108 l neurons, activation of the Sonic hedgehog (Shh) signaling pathway affects multiple aspects of mitoc

109 as recently found to inhibit Sonic hedgehog (Shh) signaling, a key developmental regulatory pathway.

110 In the ventral neural tube, sonic hedgehog (Shh) signaling, together with broadly expressed transcri

111 pled receptor that regulates Sonic Hedgehog (Shh) signaling.

112 l constriction controlled by Sonic hedgehog (Shh) signaling.

113 ing pathogenic mechanisms on Sonic Hedgehog (Shh) signaling.

114 Here, we show that Sonic hedgehog (Shh) signalling in the embryonic chick wing bud specifie

115 ansgenic mouse model for the sonic hedgehog (Shh) subgroup of medulloblastoma, here we evaluated the

116 P expression is regulated by Sonic hedgehog (Shh) through transcription factor Gli-1.

117 of netrin1 (FP-netrin1) and Sonic hedgehog (Shh), that can attract the axons at a distance in vitro.

118 Here, we show that Sonic hedgehog (Shh), which encodes a secreted protein signal, is expres

119 ibroblasts was identified as sonic hedgehog (Shh), which was rapidly induced in renal tubules and cou

120 rowth factor-beta (Tgfbeta), sonic hedgehog (Shh), wingless-integrated site (Wnt)/beta-catenin, bone

121 de was designed based on the sonic hedgehog (Shh)-binding loop of hedgehog-interacting protein (HHIP)

122 cycle timer that operates in Sonic hedgehog (Shh)-expressing polarising region cells of the chick win

123 Here, we show in mice that sonic hedgehog (Shh)-induced proliferation of cranial neural crest cell

124 We report here that Sonic Hedgehog (Shh)-Smoothened signaling downregulates Shisa2, which in

125 urvival as low as 50-60% for Sonic Hedgehog (Shh)-type medulloblastoma.

126 controlled by the morphogen Sonic hedgehog (Shh).

127 long-range limb enhancer of Sonic hedgehog (Shh).

128 Normally silent heterozygous Shh null mutations exacerbated PBO teratogenicity at all

129 iple stages, whereas the Sonic hedgehog (Hh [Shh])-deficient FL showed increased B cell development,

130 How Shh elicits changes in the growth cone cytoskeleton that

131 s known about the molecular mechanism of how Shh orchestrates changes in the growth cone cytoskeleton

132 However, Shh was also reduced in this region, suggestive of a Shh

133 e an integrated genomic approach to identify Shh-dependent genes and associated regulatory sequences

134 of ARL13B do not underlie the alterations in Shh transduction, which is unexpected given the requirem

135 preformed interaction and a 50% decrease in Shh expression but no phenotype, suggesting an additiona

136 lting in developmental patterning defects in Shh signaling-dependent tissues such as the limb and neu

137 y effects of SHH pathway-inhibiting drugs in Shh-activated MB cells in vitro.

138 Epithelial Wls loss of function in Shh lineage also leads to aberrant cell proliferation in

139 ells from Gli3-deficient FL but increased in Shh-deficient FL, and in vitro Shh treatment or neutrali

140 erein we show that several genes involved in Shh and Wnt signaling were differentially expressed in t

141 nitor cells accompanied by cartilage loss in Shh-Cre;Gpr177(loxp/loxp) mutants.

142 we studied Atoh1 dosage and modifications in Shh-type medulloblastoma.

143 lls are co-present with cartilage nodules in Shh-Cre;Ctnnb1(DM/loxp) mutants, which maintain partial

144 astrocytes exhibit a pronounced reduction in Shh activity in a spatiotemporally-defined manner.

145 Shh-ZRS contacts and a moderate reduction in Shh transcription.

146 that Inpp5e plays a more complicated role in Shh signaling than previously appreciated.

147 e of the dorsal mesocardium was validated in Shh(-/-) mutants, which recapitulate heart shape changes

148 t of the core signalling circuitry including Shh, Wnt, Hippo, PI3K and MAPK pathways.

149 expression of repair cell markers, including Shh, GDNF, and BDNF.

150 rocyte Shh release was decreased, inhibiting Shh delivery to brain endothelial cells.

151 he most posterior digit, and that inhibiting Shh-signaling inhibited Fgf8 expression, anteroposterior

152 Mouse embryos lacking Shh or its essential signal transduction components disp

153 entally important, but contentious, lineages-Shh and Cux2.

154 cifically targeting the intrafollicular MAPK-Shh axis may provide a promising strategy to manage CIA.

155 Moreover, Shh and Gli1 expression was increased in Tmem107(-/-) an

156 ch drives IGF2 expression in CGNPs and mouse Shh-associated medulloblastomas.

157 The previously unreported Msi2-Shh-Gli1 pathway adds to the growing understanding of th

158 , and that experimental ablation of neuronal Shh expression causes loss of taste receptor cells (TRCs

159 regeneration of TRCs thus requires neuronal Shh, illustrating the principle that neuronal delivery o

160 ifies ZBP1 as a new mediator of noncanonical Shh signaling in axon guidance.SIGNIFICANCE STATEMENT So

161 identifying a new member of the noncanonical Shh signaling pathway.

162 58A) mice are viable and fertile with normal Shh signal transduction.

163 AAV-Cre mediated ablation of Shh in the adult dentate gyrus led to a marked degenerat

164 In addition, ablation of Shh in the adult dentate gyrus led to increased neural p

165 s posterior digit identity in the absence of Shh signalling, thus indicating that it specifies antero

166 Activation of Shh receptors in the dendrites of hippocampal neurons en

167 e utilize a gene expression tracer allele of Shh (Shh-nlacZ) which allowed the identification of a su

168 cell markers (CD24 and CD133), components of Shh pathway (Gli1, Gli2, Patched1/2, and Smoothened), Gl

169 and a previously unrecognized convergence of Shh agonism and cyclin-dependent kinase inhibition as po

170 First, we show that conditional deletion of Shh in the anterior hypothalamus results in a fully pene

171 Genetic deletion of Shh, the primary Hh ligand expressed in the lung, in Kra

172 all effective doses disrupted development of Shh-dependent transient forebrain structures that genera

173 Selective disruption of Shh signaling in astrocytes produces a dramatic increase

174 Disruption of Shh signaling is linked to birth defects, including holo

175 in Npc1-/- mice due to the downregulation of Shh expression.

176 a mouse model of CIA, the downregulation of Shh signaling in the hair matrix is a critical early eve

177 al that Tbx2 and Tbx3 function downstream of Shh to maintain pro-proliferative mesenchymal Wnt signal

178 portant in understanding how the duration of Shh signaling regulates neural tube patterning.

179 61 mutations cause NTDs via dysregulation of Shh and Wnt signaling in mice, and novel rare variants o

180 The dysregulation of Shh signaling is associated with a shortening of the pri

181 h a WIP1 inhibitor suppressed the effects of Shh stimulation and potentiated the growth inhibitory ef

182 gic ablation requires neuronal expression of Shh and can be substantially enhanced by pharmacologic a

183 Shh(+) MCs indicating that the expression of Shh by MCs confers a survival advantage during the respo

184 Gigaxonin-dependent inhibition of Shh activation was also demonstrated in primary fibrobla

185 Inhibition of Shh signaling recapitulated key morphological and functi

186 Inhibition of Shh signaling restored the number of motor neurons to no

187 Likewise, pharmacologic inhibition of Shh signaling with cyclopamine also hindered fibroblast

188 e that positively controls the initiation of Shh transduction, and reveal the causal role of Shh dysf

189 Tubule-specific knockout of Shh in mice inhibited fibroblast activation and aggravat

190 euron-OPC switch by controlling the level of Shh activity in pMN progenitors, and also regulates the

191 e, we showed an elevated expression level of Shh-which is essential for development, homeostasis, and

192 aling reduced AD pathology and the levels of Shh expression determined disease severity.

193 fect on Shh expression patterns or levels of Shh expression during development - except where enhance

194 e expression and subcellular localization of Shh effectors and ciliary proteins are severely disturbe

195 nces between cusps were reduced in molars of Shh activity-suppressed mice in vivo.

196 ent kainic acid (KA) increased the number of Shh(+) MCs indicating that the expression of Shh by MCs

197 iting loss (Smo(ecko) ) and gain (Shh-P1) of Shh signaling reveal a set of Shh-responsive genes parti

198 ation specified by the projection pattern of Shh-expressing neurons.

199 g and highlight the therapeutic potential of Shh mimetics against CNS complications associated with H

200 xpectations, the developmental regulation of Shh expression is remarkably robust to TAD perturbations

201 transduction, and reveal the causal role of Shh dysfunction in motor deficits, thus highlighting the

202 se findings validate neuroprotective role of Shh signaling and highlight the therapeutic potential of

203 However, the in vivo role of Shh signaling in cusp pattern formation and the molecula

204 rted the stimulatory and inhibitory roles of Shh and Bmp, respectively; providing better insight into

205 in (Shh-P1) of Shh signaling reveal a set of Shh-responsive genes partitioned into four expression ca

206 mpal neurogenesis but the cellular source of Shh in the hippocampus remains ill defined.

207 s (MCs) as a prominent and dynamic source of Shh within the dentate gyrus.

208 hen both the epithelial and neural supply of Shh are removed, taste buds largely disappear.

209 lator of Wnt signaling, after suppression of Shh activity.

210 Suppression of Shh signaling activity in vitro in explant assays appear

211 nd on smoothened, the obligate transducer of Shh signaling, indicating that Inpp5e functions within t

212 ified inner ear enhancers in the vicinity of Shh-responsive genes.

213 cquisition of anterior identity dependent on Shh signalling.

214 ructure have no readily detectable effect on Shh expression patterns or levels of Shh expression duri

215 The influence of PBO on Shh pathway transduction was assayed in mouse and human

216 The impact of PBO on Shh signaling in vitro and forebrain and face developmen

217 ary cusp patterns of mice lacking Sostdc1 or Shh at embryonic day 15.5.

218 In mice predisposed to Wnt- or Shh medulloblastoma, Ddx3x sensed oncogenic stress and s

219 ndependent Smo mutant, tumors overexpressing Shh exhibited marked chromosomal instability and Smoothe

220 nd visceral metastases, activating paracrine Shh signaling in tumor-stromal interactions.

221 In particular, Shh stimulation increases beta-actin protein at the grow

222 -canonical Wnt/planar cell polarity pathway, Shh/BMP signalling, and the transcription factors Grhl2/

223 iofacial and brain development, phenocopying Shh mutations.

224 a therapeutic response in mice with primary, Shh-driven medulloblastoma.

225 Addition of recombinant Shh to cultures of naive human CD4+ T cells in iTreg cul

226 ctional features of CIA, whereas recombinant Shh protein partially rescued hair loss.

227 by deficient Shh, we found that CBs reduced Shh signaling by inhibiting Smoothened (Smo), while Shh

228 evolutionary-conserved mechanism regulating Shh signaling.

229 development, and Gli3 functioned to repress Shh transcription.

230 hypomorphic ZRS allele, resulting in severe Shh loss of function and digit agenesis.

231 lize a gene expression tracer allele of Shh (Shh-nlacZ) which allowed the identification of a subpopu

232 he mouse, limb bud-restricted spatiotemporal Shh expression occurs from approximately E10 to E11.5 at

233 ntly, HL2-m5 is able to effectively suppress Shh-mediated hedgehog signaling and Gli-controlled gene

234 By targeting Shh signaling as a sensitive mechanism of action and exa

235 romatin remodeling and activate the TGFbeta, Shh and Wnt signaling pathways.

236 presses Hedgehog signaling activity and that Shh is its direct target in the hair follicle.

237 We also provide evidence that Shh stimulates sumoylation of mammalian Smo (mSmo) and t

238 Interestingly, we find that Shh signaling is restored to baseline levels two weeks a

239 We found that Shh stimulation increases phospho-ZBP1 levels in the gro

240 We found that Shh-expressing cells contributed to the most posterior d

241 gs confirm and extend the previous idea that Shh acts as an inhibitor in the reaction-diffusion model

242 We also reveal that Shh signalling is interpreted into specific patterns of

243 Pharmacological approaches reveal that Shh signalling promotes the growth and differentiation o

244 Our work revealed that Shh signaling is an evolutionarily conserved key target

245 is of gene expression profiles, we show that Shh and Bmp4 signaling pathways are activated in a compl

246 Our previous studies show that Shh null mice have smaller, aparathyroid primordia in wh

247 We further show that Shh protects neurons against a variety of stresses, incl

248 fluorescence imaging analyses, we show that Shh signaling activity reduces mitochondrial fission and

249 We show that Shh signaling maintains Siah2 expression in CGN progenit

250 f a transgenic Hh-reporter mouse showed that Shh signals directly to developing B cells and that Hh p

251 These results suggest that Shh plays an inhibitory role in cusp pattern formation b

252 e that neuronal delivery of cues such as the Shh signal can pattern distant cellular responses to ass

253 d prolongs mouse survival by disengaging the Shh-IL6-RANKL signaling network in stromal cells in the

254 y prove a valuable PET imaging probe for the Shh subgroup of medulloblastoma and possibly other pedia

255 Embryos lacking the Shh effector Gli2 fail to produce appropriate midline ce

256 tal gene regulation, we have manipulated the Shh TAD - creating internal deletions, deleting CTCF sit

257 nfiguration underlying the regulation of the Shh gene by its unique limb enhancer, the ZRS, in vivo d

258 TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the ne

259 hat the preformed chromatin structure of the Shh locus is sustained by multiple components and acts t

260 he BBB is disrupted by downregulation of the Shh pathway and breakdown of TJPs, secondary to increase

261 ed by both pharmacological activation of the Shh pathway and human gigaxonin, pointing to an evolutio

262 ess, local pharmacological activation of the Shh pathway in astrocytes mitigates inflammation, consis

263 In addition, exogenous activation of the Shh pathway promotes neuroprotection mediated by reactiv

264 ranscriptional response to activation of the Shh pathway.

265 togenesis as well as a downregulation of the Shh signaling pathway in the palatal mesenchyme.

266 tor population relies on the activity of the Shh, Wnt and Fgf signaling pathways.

267 scles, by controlling the degradation of the Shh-bound Patched receptor.

268 s around the ZRS resulted in the loss of the Shh-ZRS preformed interaction and a 50% decrease in Shh

269 Focusing on the Shh pathway, we demonstrate the importance of uORFs with

270 governing the formation of cusp pattern, the Shh pathway has been implicated as an important player.

271 t loss of apical characteristics reduces the Shh signaling response, causing cell cycle exit and diff

272 e detection circuit linking responses to the Shh mitogen and the extracellular matrix to control cere

273 ral forebrain and in regions adjacent to the Shh-expressing ZLI.

274 ing the ZRS region led to a shift within the Shh-ZRS contacts and a moderate reduction in Shh transcr

275 Therefore, Shh induces the local translation of beta-actin at the g

276 y, we discover that NKX2-1 binds directly to Shh and Wnt7b and regulates their expression to control

277 idylinositol phosphatase Inpp5e is linked to Shh regulation.

278 reduction in the transcriptional response to Shh pathway activation.

279 outgrowth of the otic vesicle in response to Shh signaling.

280 d ciliogenesis and reduced responsiveness to Shh signalling.

281 Similar to Shh inhibition, repression of gigaxonin in zebrafish imp

282 s of transcriptional and non-transcriptional Shh signaling.

283 for Shh-dependent signaling, we examined two Shh-dependent cell populations that express high levels

284 ction of Foxf2 expression was dependent upon Shh pathway effectors in cNCCs, while a functional GLI-b

285 Using Shh(Cre) to target the mandibular epithelium, we ablated

286 ronment interactions were investigated using Shh+/- mice, which model human HPE-associated genetic mu

287 increased in Shh-deficient FL, and in vitro Shh treatment or neutralization reduced or increased the

288 When Shh signalling is blocked, polarising region cells over-

289 Taste buds are minimally affected when Shh is lost from either tissue source.

290 Here, we investigated whether Shh signaling mediates astrocyte response to injury.

291 mation and the molecular mechanisms by which Shh regulates cusp patterning are not clear.

292 in vivo phenotypic analyses of mice in which Shh activity was suppressed and compared with wild-type

293 naling by inhibiting Smoothened (Smo), while Shh mRNA or a CB1 receptor antagonist attenuated CB-indu

294 ors, which engages the Ras/Mapk cascade with Shh, and that this niche interaction is essential for pr

295 Our data are consistent with Shh signalling stimulating polarising region cell prolif

296 reased significantly in neurons treated with Shh.

297 Wls(Shh-Cre) teeth display reduced canonical Wnt signaling a

298 ifferentiation that are downregulated in Wls(Shh-Cre) teeth, act as direct downstream targets of the

299 on of Wnt5a and Wnt10b is not changed in Wls(Shh-Cre) teeth.

300 1, and Patched1 was greatly decreased in Wls(Shh-Cre) teeth.