ライフサイエンスコーパス: Shh

1 Shh also inhibited enteric neural crest-derived cell (EN

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

3 Shh mediates activity-dependent and injury-induced hippo

4 Shh overexpression, achieved in ovo using Shh-encoding r

5 Shh signaling is impaired in null embryos and primary ci

6 Shh strongly induced the expression of versican and coll

7 Shh-dependent suprabasal cell shape suggests convergent

8 Shh-type medulloblastoma displays distinct H3K27me3 prop

9 Shh/ZRS colocalisation, therefore, correlates with the s

10 Eya1 drives the growth of medulloblastoma, a Shh-dependent hindbrain tumor.

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

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

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

14 In microcultures, soluble FGFR3 abolishes Shh without affecting Gsc expression.

15 S-causing mutations in Arl13b did not affect Shh signaling in these same assays, suggesting these mut

16 Finally, although Shh regulates taste placode patterning, we find that it

17 r subjects had somatic mutations in GLI3, an Shh pathway gene associated with HH.

18 ased when ND2:WIP1 mice were crossed with an Shh-activated MB mouse model.

19 es and at all developmental stages analysed, Shh-ZRS spatial distances were still consistently shorte

20 r reduction in K8/18/Ub+ foci (P < 0.08) and Shh+ hepatocytes (P < 0.05) than the placebo group, effe

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

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

23 Inhibition of Fgf and Shh signaling disrupted the oriented migration of cells,

24 domains by the opposing actions of Fgfs and Shh emanating from dorsal and ventral domains of the for

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

26 of Shh-dependent (posterior mesenchyme) and Shh-independent, cilium-based (anterior mesenchyme) Hedg

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

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

29 diated regulation of apical Par proteins and Shh signaling.

30 ng an increase in the expression of Sox2 and Shh.

31 key processes such as tubulin transport and Shh signaling.

32 odysplasin A receptor (EDAR) and the Wnt and Shh pathways.

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

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

35 mic region and enriched interactions between Shh and ZRS throughout E11.5 embryos.

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

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

38 n those to a neural enhancer located between Shh and ZRS in the genome.

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

40 Both Shh and HGF were heterogeneously expressed in PDAC strom

41 eals that Nodal is required to maintain both Shh and Gsc expression, but whereas Gsc is largely maint

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

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

44 The inhibition of Gli activity by Shh operates at multiple levels.

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

46 ll as in other malignancies characterized by Shh overexpression.

47 erty of lens epithelial cells, controlled by Shh.

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

49 w for the first time that YB-1 is induced by Shh in CGNPs.

50 ation of isolated ENCCs was not inhibited by Shh protein.

51 is selected by repressive input provided by Shh-induced transcription factors that act as the key no

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

53 e effective down-regulation of the canonical Shh signaling as spinal cord development progresses.

54 limb bud-specific Shh expression, but close Shh and ZRS proximity in the nucleus occurs regardless o

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

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

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

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

59 hese results suggest that epithelial-derived Shh acts indirectly on the developing ENS by regulating

60 f both genes depends on epithelially derived Shh signaling, with additional modulation by Bmp, Wnt, a

61 hese findings demonstrate that nerve-derived Shh is a critical regulator of lineage-specific stem cel

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

63 rved in these mice, demonstrating diminished Shh signaling.

64 Understanding how disrupted Shh signaling protects against BPI could uncover variant

65 romotes progenitor differentiation, elevated Shh signaling.

66 Furthermore, enhanced Shh signaling through activated Smo cannot overcome impa

67 Epidermal Shh stimulates proliferation of the papillary fibroblast

68 rk of active promoters H3K4me3, for example, Shh and Gdnf, and the reduction of H3K27me3 results in i

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

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

71 Regenerated spinal cords expressed Shh, and cyclopamine inhibited CT induction.

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

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

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

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

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

77 r results suggest a neuroprotective role for Shh signaling in the context of HIV infection, underscor

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

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

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

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

82 ggest that proNodal/FGFR3 signalling governs Shh duration by repressing canonical BMP signalling, and

83 edulloblastoma, is driven by Sonic hedgehog (Shh) and insulin-like growth factor (IGF) in the develop

84 The presence of Sonic Hedgehog (Shh) and its signaling components in the neurons of the

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

86 thelial-specific deletion of sonic hedgehog (Shh) during postnatal homeostasis in the murine lung res

87 ss transcription through the sonic hedgehog (Shh) endoderm-specific enhancer MACS1 and that GATA-bind

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

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

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

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

92 Activation of sonic hedgehog (Shh) in cancer stem cell (CSC) has been demonstrated wit

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

94 Sonic hedgehog (Shh) is a mitogen for spinal cord progenitors, but how c

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

96 Sonic Hedgehog (Shh) is abnormally expressed in pancreatic cancer and is

97 Notochord-derived Sonic Hedgehog (Shh) is essential for dorsoventral patterning of the ove

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 limb defects that phenocopy Sonic Hedgehog (Shh) mutants.

101 mote Smo phosphorylation and Sonic hedgehog (Shh) pathway activation.

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

103 involving regulation of the sonic hedgehog (Shh) pathway in 14/38 individuals (37%).

104 Stimulation of the sonic hedgehog (Shh) pathway in vertebrates results in accumulation and

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

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

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

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

109 d that constitutively active Sonic hedgehog (Shh) signaling expanded bRGs and IPCs and induced foldin

110 d to establish that impaired Sonic hedgehog (Shh) signaling is associated with loss of BBB function a

111 Sonic hedgehog (Shh) signaling is critical in development and oncogenesi

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

113 in a proliferative state by sonic hedgehog (Shh) signaling, and Aspm is expressed in Shh-driven medu

114 at higher or lower levels of sonic hedgehog (Shh) signaling, respectively.

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

116 transcription activation in Sonic hedgehog (Shh) signaling.

117 ry cilia, where it regulates Sonic hedgehog (Shh) signaling.

118 ern formation, a gradient of Sonic hedgehog (Shh) signalling in the chick wing bud specifies cells wi

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

120 ong with a downregulation of sonic hedgehog (Shh) transcription, but not in the equally proliferative

121 We hypothesized that sonic hedgehog (Shh), a secreted intestinal epithelial protein not expre

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

123 H3K27 in many genes, such as Sonic hedgehog (Shh), which is silenced throughout Schwann cell developm

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

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

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

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

128 controlled by the morphogen Sonic hedgehog (Shh).

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

130 t via the secreted morphogen Sonic hedgehog (Shh).

131 o the N-terminal cysteine of Sonic Hedgehog (Shh).

132 ugh the morphogen actions of Sonic hedgehog (Shh).

133 rapod limbs are patterned by asonic hedgehog(Shh)-expressing signalling centre known as the zone of p

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

135 Exposure to higher Shh levels, and collecting GFP-expressing precursors at

136 How Shh elicits changes in the growth cone cytoskeleton that

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

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

139 g1-regulated pathways are conserved in human Shh-type medulloblastoma, and Brg1 is important for the

140 Impaired Shh signaling may contribute to the pathogenesis of seve

141 ng is required for the patterning defects in Shh mutants.

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

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

144 og (Shh) signaling, and Aspm is expressed in Shh-driven medulloblastoma in mice.

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

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

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 We show that, instead, Shh signalling is necessary for, and promotes, invaginat

152 nt for PV interneurons was produced by lower Shh and by collecting mCherry-expressing cells after 17

153 ls through a non-canonical route to maintain Shh.

154 Mechanistically, Shh signaling increased the initial generation and self-

155 and neurological damage, and that modulating Shh signaling can rescue these detrimental effects.

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

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

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

159 rozygosity (LOH) variants involving multiple Shh genes, as well as other genes without an obvious bio

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

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

162 of this regulatory lexicon, we discover new Shh zli enhancers in mice and a functionally equivalent

163 is a critical mediator linking noncanonical Shh pathway to Warburg-like glycolysis in satellite cell

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

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

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

167 Administration of Shh mimetic, smoothened agonist (SAG) restored BBB integ

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

169 ermore, Mang-NPs inhibited the components of Shh pathway and Gli targets.

170 d the higher-order chromatin conformation of Shh in expressing and non-expressing tissues, both by fl

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

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

173 Depletion of Shh from HF-TACs abrogates both dermal adipogenesis and

174 notype results from severe downregulation of Shh expression in the rostral diencephalon ventral midli

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

176 eural progenitor specification downstream of Shh signaling, in which Nkx2.2 and Olig2 direct repressi

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

178 contribute to the intracellular dynamics of Shh signalling, resulting in different signalling dynami

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

180 insensitive to the proliferative effects of Shh is not well understood.

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

182 ay in drug resistance and tumor evolution of Shh pathway-dependent tumors.

183 SCLC tumor samples feature co-expression of Shh and BBS-cognate receptor (gastrin-releasing peptide

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

185 Importantly, reduced expression of Shh and Gli1 was also observed in these mice, demonstrat

186 ed increased proliferation and expression of Shh downstream targets.

187 f miR-219 depletion and forced expression of Shh phenocopied miR-219 deficiency.

188 WIP1 overexpression increased expression of Shh target genes and cell proliferation in response to S

189 er to locate and instigate the expression of Shh.

190 tified significantly elevated frequencies of Shh/ZRS colocalisation only in the Shh-expressing region

191 nto Shh, is a novel target for inhibition of Shh signaling in pancreatic cancer cells.

192 Inhibition of Shh signaling is thus an attractive clinical target for

193 Inhibition of Shh signaling reversed the effects of miR-219 depletion

194 Inhibition of Shh signaling, by addition of cyclopamine or a function-

195 Here, we show that inhibition of Shh signalling at a specific stage of chick wing develop

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

197 smooth mouse neocortex, whereas the loss of Shh signaling decreased the number of bRGs and IPCs and

198 , treatment response correlated with loss of Shh+ hepatocytes and improvement in Hh-regulated process

199 Manipulation of Shh signalling shows that Shh coordinates progenitor cel

200 Using a mouse model of Shh-type medulloblastoma, we deleted Brg1 in precancerou

201 ising from four independent murine models of Shh medulloblastoma, alongside any role in tumorigenesis

202 formation in two independent mouse models of Shh-activated MB.

203 ify Notch signalling as a novel modulator of Shh signalling that acts mechanistically via regulation

204 Treatment-related changes in the numbers of Shh+ hepatocytes correlated with changes in serum AST (p

205 s), regulate a dynamic expression pattern of Shh in the ectoderm covering the frontonasal (FNP) and m

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

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

208 d identified Eya1 as a positive regulator of Shh signaling.

209 To further explore the role of Shh and other factors in cIN fate determination, we gene

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

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

212 us, T-box3 controls digit number upstream of Shh-dependent (posterior mesenchyme) and Shh-independent

213 cquisition of anterior identity dependent on Shh signalling.

214 determine the effects of Arl13b mutations on Shh signaling.

215 onsible for the attachment of palmitate onto Shh, is a novel target for inhibition of Shh signaling i

216 nd IHH), the receptor SMO, and several other Shh downstream pathway members, including CREBBP and GLI

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

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

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

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

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

222 ilia interferes with its ability to regulate Shh-stimulated chemotaxis, despite previous evidence tha

223 iptional program that specifically regulates Shh-type medulloblastoma growth.

224 development, and Gli3 functioned to repress Shh transcription.

225 nalling, and that local BMPs rapidly silence Shh once endogenous Nodal-FGFR3 signalling is downregula

226 novel mESC lines in which Ptch1, Ptch2, Smo, Shh and 7dhcr were inactivated via gene editing in multi

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

228 e spatiotemporal domain of limb bud-specific Shh expression, but close Shh and ZRS proximity in the n

229 Limb-specific Shh expression is regulated by the ( approximately 1 Mb

230 Specifically, Shh produced in the dorsal region of the AGM, stem cell

231 Strikingly, Shh decreases Gli signaling in the embryonic spinal cord

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

233 al for therapeutic interventions that target Shh pathways.

234 wth, development and metastasis by targeting Shh pathway.

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 ches in the little skate to demonstrate that Shh secretion from a signalling centre in the developing

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

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

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

241 itch for rx3 Together, our studies show that Shh and Rx3 govern formation of a distinct progenitor do

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

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

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

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

246 Manipulation of Shh signalling shows that Shh coordinates progenitor cell selection and behaviour

247 Emerging findings suggest that Shh also has important roles in the formation and plasti

248 The Shh pathway genes in these large somatic lesions include

249 ation signal, or GTPase handling altered the Shh response in distinct assays of transcriptional or no

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

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

252 zing the cerebellar progenitor model for the Shh subgroup of medulloblastoma in mice, we show for the

253 llows the additional digit to arise from the Shh-producing cells of the polarizing region - an abilit

254 te measurement of the temporal change in the Shh morphogen is a plausible mechanism for determining p

255 ts against BPI could uncover variants in the Shh pathway that cause or increase risk for this and rel

256 nase that acts as a repressor protein in the Shh pathway, and four subjects had somatic mutations in

257 encies of Shh/ZRS colocalisation only in the Shh-expressing regions of the limb bud, in a conformatio

258 es not respond directly to Shh; instead, the Shh signal transduction originates from the somatodendri

259 Moreover, the Shh-induced upregulation of Gli2 transcription prevents

260 Interpretation of the Shh gradient depends on both the amount of ligand and du

261 for Notch shaping the interpretation of the Shh morphogen gradient and influencing cell fate determi

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

263 ther, our data implicate perturbation of the Shh pathway in at least 37% of individuals with the HH e

264 Sufu mutations lead to maintenance of the Shh pathway in the presence of Smo inhibitors.

265 ranscriptional response to activation of the Shh pathway.

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

267 ith these results, in vivo activation of the Shh signaling pathway rescued the semilobar phenotype bu

268 induction of higher expression levels of the Shh target gene Ptch1 and subsequently induction of more

269 ordates, indicating an ancient origin of the Shh zli regulatory network that predates the chordate ph

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

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

272 ologically associating domain (TAD) over the Shh/ZRS genomic region and enriched interactions between

273 Although no manipulation recapitulated the Shh null phenotype, manipulation of SHH signaling in eit

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

275 campus raises a question about what role the Shh signaling pathway may play in these neurons.

276 es without an obvious biological link to the Shh pathway.

277 s the transcriptional program underlying the Shh-type medulloblastoma development.

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

279 nts the response of neuroepithelial cells to Shh, leading to the induction of higher expression level

280 The axon itself does not respond directly to Shh; instead, the Shh signal transduction originates fro

281 reduction in the transcriptional response to Shh pathway activation.

282 CTs form from blastema cells in response to Shh signals from regenerated spinal cords.

283 genes and cell proliferation in response to Shh stimulation in NIH3T3 and cerebellar granule neuron

284 f Gnaz dampen the axon-repulsive response to Shh, and Gnaz mutant intestines contain centrally projec

285 mechanisms permitting prolonged responses to Shh are not well understood.

286 s to decrease progenitor cell sensitivity to Shh signaling, thereby driving these cells towards diffe

287 re not required for this non-transcriptional Shh response.

288 s of transcriptional and non-transcriptional Shh signaling.

289 As ectopic tubular Shh and Ccl2 expression is seen after acute kidney injur

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

291 val, both during resting conditions and upon Shh pathway activation.

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

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

294 Shh overexpression, achieved in ovo using Shh-encoding retrovirus and in organ culture using recom

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

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

297 al tissue by asymmetric cell division, while Shh triggers cell rearrangement in this tissue to drive

298 reased significantly in neurons treated with Shh.

299 eral signalling pathways such as Notch, Wnt, Shh and RA are implicated in this process, yet how these

300 ied medulloblastoma into four subtypes: Wnt, Shh, Group 3 and Group 4.