ライフサイエンスコーパス: ectodermal

1 may provide a new path to understanding the ectodermal abnormalities associated with the APECED synd

2 Posterior ectodermal activation of Hox is initiated in the late la

3 pressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expres

4 is, cell polarity and the patterning of both ectodermal and endodermal derivatives along the primary

5 have been tested against many carcinomas of ectodermal and endodermal origin; however, sarcomas, ari

6 ltilineage mesodermal potential and possible ectodermal and endodermal potentials also, the ASC could

7 nsively and contribute to a diverse array of ectodermal and mesenchymal derivatives.

8 nimal pole, and partitioned into the nascent ectodermal and mesodermal cells during cleavage and earl

9 gastrulation, and Gata2 is required in both ectodermal and mesodermal cells to enable mesoderm to co

10 gmentation of the body axis encompasses both ectodermal and mesodermal derivatives.

11 rylation-mediated inhibition of p53-directed ectodermal and mesodermal gene expression.

12 he spontaneous specification and survival of ectodermal and mesodermal lineages during embryoid body

13 Because ectodermal and mesodermal mesenchyme can form in close p

14 nancies, including colon carcinoma, and with ectodermal and mesoendodermal morphogenesis.

15 BERKO EBs expressed higher levels of key ectodermal and neural progenitor markers and lower level

16 ing segmentation mechanisms that create both ectodermal and neural segments, as well as recent studie

17 the small RNAs specific to the interstitial, ectodermal, and endodermal lineages, we found that the t

18 factors with conserved roles in deuterostome ectodermal anteroposterior (AP) patterning in developing

19 benefits in animal models by stimulation of ectodermal appendage development with EDAR agonists.

20 EDA gene cause reduction or absence of many ectodermal appendages and have been identified as a caus

21 alatal rugae, which are a set of specialized ectodermal appendages serving as Shh signaling centers d

22 Ectodermal appendages such as feathers, hair, mammary gl

23 During development, Dlx3 is expressed in ectodermal appendages such as hair and teeth.

24 while also contributing to the formation of ectodermal appendages such as teeth, salivary glands and

25 stratified epithelia and aplasia of multiple ectodermal appendages, as well as orofacial clefting and

26 Development of ectodermal appendages, such as hair, teeth, sweat glands

27 EDA acts early during the development of ectodermal appendages-as early as the embryonic placode

28 se to structures including the epidermis and ectodermal associated appendages such as hair, eye, and

29 uced pluripotent stem cells of a self-formed ectodermal autonomous multi-zone (SEAM) of ocular cells.

30 e named this 2D colony a 'SEAM' (self-formed ectodermal autonomous multizone), and previously demonst

31 The fact that both endodermal and ectodermal beta-catenin knockout animals develop severe

32 yury-expressing region by a dorsal domain of ectodermal bmp2/4 expression.

33 atric central nervous system primitive neuro-ectodermal brain tumors (CNS-PNETs) are rare tumors with

34 le in chick and mouse in directly repressing ectodermal cadherin genes to contribute to the delaminat

35 fail to elongate, and endoderm organization, ectodermal cell polarity and patterning along the oral-a

36 from both mesoderm and the neural crest, an ectodermal cell population, via an epithelial to mesench

37 rait across this phylum is the cnidocyte, an ectodermal cell type with a variety of functions includi

38 systematic derivation of the entire range of ectodermal cell types.

39 The Hedgehog morphogen is secreted from ectodermal cells adjacent to the CNS midline and directs

40 tion of the nervous system is initiated when ectodermal cells adopt the neural fate.

41 ressed in chick, Wise causes delamination of ectodermal cells and attracts migrating neural crest cel

42 we analyzed the trajectories of hundreds of ectodermal cells and internalized mesodermal cells withi

43 hat these protrusions originate from surface ectodermal cells and that Rac1 is necessary for the form

44 The CBP/p300(-/-) ectodermal cells are viable and not prone to apoptosis.

45 Here we dissect the events that specify ectodermal cells as placode progenitors using newly iden

46 stula embryo in a small group of presumptive ectodermal cells as they become restricted to anterior n

47 dary is established before gastrulation, and ectodermal cells at the boundary are thought to provide

48 The SoxD factor, Sox5, is expressed in ectodermal cells at times and places where BMP signaling

49 Nv-NF-kappaB is expressed in a subset of ectodermal cells in juvenile and adult Nematostella anem

50 coding a growth factor known to recruit oral ectodermal cells into the pituitary.

51 y the effect of variant Kcnj2 on the Vmem of ectodermal cells of the developing face.

52 In Diptera, Malpighian tubules derive from ectodermal cells that evaginate from the primitive hindg

53 nal inactivation of both CBP and p300 in the ectodermal cells that give rise to the lens placode.

54 ic proteins (BMPs) are required to signal to ectodermal cells to generate secondary non-cell-autonomo

55 ctin (FN) fibrillogenesis and the ability of ectodermal cells to spread on a FN substrate.

56 However, BMP antagonism can only neuralize ectodermal cells when the BMP-inhibited cells form a con

57 In ectodermal cells, both Wnt5a and Lgl triggered morpholog

58 signal that activates only a narrow band of ectodermal cells, even though all ectoderm is competent

59 depends on N-cadherin that, when imposed in ectodermal cells, is sufficient to trigger their interna

60 stream activator, Endothelin1 (Edn1), within ectodermal cells.

61 with expression primarily being confined to ectodermal cells.

62 o an outer trophectoderm-like ring, an inner ectodermal circle and a ring of mesendoderm expressing p

63 le only Hau-Paxbeta1 rescued the symmetry of ectodermal cleavage.

64 EEC-iPSC from both patients showed early ectodermal commitment into K18(+) cells but failed to fu

65 neural columnar fates in increasingly dorsal ectodermal compartments.

66 Ctip2 is highly expressed in the ectodermal components of the developing tooth, including

67 arches, including both their mesenchymal and ectodermal components, as well as Rathke's pouch, were s

68 eage tracing of the neural crest (NC) versus ectodermal contribution to the developing nasal placode

69 neurulation, and the critical cells are the ectodermal cranial neural crest and placode lineages.

70 To discover novel ectodermal cues, we performed an unbiased RNA-Seq-based

71 a total of six individuals have had lifelong ectodermal defects.

72 ronic mucocutaneous candidiasis, and various ectodermal defects.

73 ies and adolescent onset of a broad range of ectodermal defects.

74 However, ectodermal deletion of Edn1 results in craniofacial defe

75 The unexpected finding that ectodermal deletion of Fgfr2 results in the most severe

76 oral clefts), and, less commonly, renal and ectodermal (dental and hair) anomalies.

77 cified, how they become different from other ectodermal derivatives and how they begin to diversify t

78 ial roles in morphogenesis and patterning of ectodermal derivatives as well as in controlling stem ce

79 it is well established that neural cells are ectodermal derivatives in bilaterian animals, here we re

80 ed scn1bb transcripts and protein in several ectodermal derivatives including neurons, glia, the late

81 y vesicle (brain), as well as other anterior ectodermal derivatives, including the palps and oral sip

82 congenital syndromes affecting a variety of ectodermal derivatives.

83 craniofacial development including regional ectodermal detachment associated with mesenchymal acellu

84 lling cell growth and differentiation during ectodermal development and regulating ESR1/ERalpha and o

85 The Ci-Dll-B gene is an early regulator of ectodermal development in the ascidian Ciona intestinali

86 -containing transcriptional repressor during ectodermal development.

87 ing role for FGF-mediated Smad inhibition in ectodermal development.

88 rate tailless genes function in neuronal and ectodermal developmental pathways.

89 Oct4 suppresses neural ectodermal differentiation and promotes mesendodermal di

90 hat ANG is expressed in neurons during neuro-ectodermal differentiation, and that it has both neurotr

91 hat ANG is expressed in neurons during neuro-ectodermal differentiation, and that it has both neurotr

92 g the role of TFAP2 transcription factors in ectodermal differentiation, revealing the importance of

93 During early ectodermal differentiation, sustained MYCN activity main

94 RY2 KD there was a tendency toward increased ectodermal differentiation.

95 dodermal differentiation and promotes neural ectodermal differentiation.

96 linked to the pathogenesis of p63-associated ectodermal disorders, the physiological role of the p63

97 patterning of nonskeletogenic mesodermal and ectodermal domains in early development of the cidaroid

98 transcripts are initially detected in broad ectodermal domains in future segments as well as in the

99 atial and temporal transcriptome of distinct ectodermal domains in the course of neurulation, during

100 is needed to define two molecularly distinct ectodermal domains, and for the formation of differentia

101 hat may serve roles in establishing distinct ectodermal domains.

102 anial sensory organs and ganglia), and other ectodermal domains.

103 Hypohidrotic ectodermal dysplasia (HED) results from mutation of the

104 mutations in Eda or Edar cause hypohidrotic ectodermal dysplasia (HED), a condition characterized by

105 intrastromal corneal ring segments (n = 2), ectodermal dysplasia (n = 1), and corneal choristoma (n

106 The X-linked hypohidrotic ectodermal dysplasia (XLHED), resulting from EDA deficie

107 atient, a female with mental retardation and ectodermal dysplasia and a balanced translocation, t(X;9

108 iciency, growth hormone deficiency, and mild ectodermal dysplasia as previously described.

109 ding sequence of the DLX3 gene results in an ectodermal dysplasia called Tricho-Dento-Osseous syndrom

110 tis-ichthyosis-deafness (KID) syndrome is an ectodermal dysplasia caused by dominant mutations of con

111 Hairless dog breeds show a form of ectodermal dysplasia characterised by a lack of hair and

112 the ability of recombinant Fc-EDA1 to rescue ectodermal dysplasia in Eda-deficient Tabby mice.

113 dages and have been identified as a cause of ectodermal dysplasia in humans, mice, dogs, and cattle.

114 Ectodermal dysplasia is a group of congenital syndromes

115 sseous (TDO) syndrome, an autosomal dominant ectodermal dysplasia linked to mutations in the DLX3 gen

116 alysis of patients with CID, anhidrosis, and ectodermal dysplasia of unknown etiology.

117 xplanation for the sensorineural deafness in ectodermal dysplasia patients with TRP63 mutations.

118 clinical findings of an autosomal-recessive ectodermal dysplasia syndrome provide insight into the r

119 nsistent with an unusual autosomal-recessive ectodermal dysplasia syndrome.

120 ypomorphic NEMO mutations result in X-linked ectodermal dysplasia with anhidrosis and immunodeficienc

121 y skin and intestinal disease in addition to ectodermal dysplasia with anhidrosis and immunodeficienc

122 n unrelated kindreds with CID, autoimmunity, ectodermal dysplasia with anhidrosis, and muscular dyspl

123 B cells of patients with X-linked anhidrotic ectodermal dysplasia with hyper-IgM syndrome (HED-ID) wh

124 Ectodermal dysplasia with immune deficiency (EDI) is an

125 Patients with ectodermal dysplasia with immunodeficiency (ED-ID) cause

126 mplicated in the genetic disorder anhydrotic ectodermal dysplasia with immunodeficiency (EDA-ID).

127 previously reported patients with anhidrotic ectodermal dysplasia with immunodeficiency caused by mut

128 he D406V mutation found in the NEMO ZF of an ectodermal dysplasia with immunodeficiency patients.

129 rosis, representing a new form of anhidrotic ectodermal dysplasia with immunodeficiency that is disti

130 O gene result in various forms of anhidrotic ectodermal dysplasia with immunodeficiency.

131 oreover, some affected individuals displayed ectodermal dysplasia, a congenital condition that can re

132 Among them, ectrodactyly, ectodermal dysplasia, and cleft lip/palate (EEC) syndrom

133 adult skin keratinocytes from ectrodactyly, ectodermal dysplasia, and cleft lip/palate (EEC) syndrom

134 hat are characterized by limb abnormalities, ectodermal dysplasia, and facial anomalies.

135 s with juvenile macular dystrophy (HJMD) and ectodermal dysplasia, ectrodactyly, macular dystrophy (E

136 EDA, the gene mutated in anhidrotic ectodermal dysplasia, encodes ectodysplasin, a TNF super

137 cause developmental disorders manifested in ectodermal dysplasia, limb defects, and orofacial clefti

138 an genetic disorders: monilethrix, hair-nail ectodermal dysplasia, pseudofolliculitis barbae and wool

139 fferentiation in TP63 mutant ankyloblepharon-ectodermal dysplasia-clefting (AEC) syndrome is unknown.

140 Mutations of p63 also cause the ectodermal dysplasia-ectrodactyly-cleft lip/palate (EEC)

141 ing wild type fetuses a marked and permanent ectodermal dysplasia.

142 cells, and Ig production, but did not cause ectodermal dysplasia.

143 ly cause a syndrome of immune deficiency and ectodermal dysplasia.

144 Tabby) phenocopy human X-linked hypohidrotic ectodermal dysplasia.

145 , leading to the human disorder hypohidrotic ectodermal dysplasia.

146 g during development results in hypohidrotic ectodermal dysplasia.

147 7 patients to rule out the effects of other ectodermal dysplasias and other tooth-related genes and

148 The ectodermal dysplasias are a group of inherited autosomal

149 arber-Say syndrome (BSS) are rare congenital ectodermal dysplasias characterized by similar clinical

150 o date, the genetic defects underlying these ectodermal dysplasias have not been determined.

151 ions in the p63 pathway underlie a subset of ectodermal dysplasias, developmental syndromes in which

152 responsible for two rare diseases related to ectodermal dysplasias.

153 of the role of p63 in normal development and ectodermal dysplasias.

154 Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a monogenic autoimmune

155 Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is an autoimmune disorder

156 Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome is a complex immu

157 Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome, which is caused

158 th autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), a T cell-driven autoimmun

159 th autoimmune-polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED).

160 (autoimmune polyendocrinopathy, candidiasis, ectodermal dystrophy syndrome) or thymoma.

161 e, autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, a multiorgan autoimmune disorder r

162 th autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, directly impair IL-17 and IL-22 im

163 ed autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy.

164 st cells and neighboring cell populations of ectodermal, endodermal and mesodermal origin.

165 stereotyped spiral cleavage program in which ectodermal, endodermal, and mesodermal origins are known

166 o functional derivatives of each germ layer, ectodermal, endodermal, and mesodermal.

167 This result suggested that the ectodermal enhancer must cooperate with its neighboring

168 more severe than that reported when only the ectodermal enhancer was deleted.

169 reatic enhancers and a previously identified ectodermal enhancer, while a 450 bp sub-deletion (Pax6(P

170 xtension of the endodermal urethra within an ectodermal epithelial capsule.

171 the otic placode, a transient thickening of ectodermal epithelium adjacent to neural crest domains i

172 how that sensory and ganglion neurons in the ectodermal epithelium of the model organism hydra (a mem

173 nic sources: neural crest ectomesenchyme and ectodermal epithelium.

174 We also reinforce the evidence that ectodermal explants are naive, and that explants that la

175 In ectodermal explants from Xenopus embryos, inhibition of

176 results in the formation of neural tissue in ectodermal explants.

177 Ectopic Wnt ectodermal expression in Pbx mutants rescues the cleftin

178 Instead, we observe reductions in the ectodermal expression of Fibroblast growth factor 8a (Fg

179 Somatostatin controls ectodermal expression of nociceptin, and both peptides r

180 s neighboring sequences to regulate the Pax6 ectodermal expression.

181 meric embryos and preferentially adopting an ectodermal fate at the expense of the endoderm during em

182 zed by hypertrophic nail dystrophy and other ectodermal features.

183 complex urethral epithelium, whereas loss of ectodermal Fgfr2 results in severe hypospadias and absen

184 rest-derived signals were necessary for oral ectodermal gene expression.

185 as diverged more markedly than regulation of ectodermal genes.

186 We find that deletion of ectodermal Hdac1 and Hdac2 results in dramatic failure o

187 To directly test whether ectodermal Hh signaling was required for normal limb pat

188 ition zone between the endodermal midgut and ectodermal hindgut that shares molecular signatures of b

189 l tract, including the endodermal midgut and ectodermal hindgut/Malpighian tubules, maintain populati

190 st (NC), a transient cell population that is ectodermal in origin but undergoes a major transcription

191 nd the distal urethra forming from an apical ectodermal invagination, however this has never been tes

192 while they are still situated in the surface ectodermal layer.

193 s are often shared between cell types of the ectodermal lineage and that corneal epithelial super enh

194 s associated to genes that either define the ectodermal lineage or establish the stem cell and differ

195 Cs are capable of differentiation toward the ectodermal lineage, they do not exhibit pluripotency.

196 modular protocol for deriving the four main ectodermal lineages from hPSCs.

197 s maintain ability to contribute to multiple ectodermal lineages until or beyond neural tube closure.

198 etion of the p63 C-terminus in mice leads to ectodermal malformation and hypoplasia, accompanied by a

199 Ectodermal malformations, present in all patients, sugge

200 immunodeficiency (CID) without endocrine or ectodermal manifestations.

201 ing BA1 patterning and morphogenesis through ectodermal-mesenchymal interaction and a novel genetic f

202 ation of the poliovirus receptor, Necl-5, in ectodermal/neuroectodermal cancers.

203 Mediator CDK8 kinase module can promote non-ectodermal neurogenesis and suggest that inhibiting CDK7

204 igin) with specific patterns of remodelling (ectodermal or endodermal origin).

205 diatric solid tumours arise from endodermal, ectodermal, or mesodermal lineages.

206 erivation from neuralized ectoderm, via meso-ectodermal, or neural-non-neural ectoderm interactions.

207 epithelium are an important initial step in ectodermal organ development.

208 of epidermal HDAC activity leads to improper ectodermal organ morphogenesis and disrupted hair follic

209 Using the mouse molar tooth as a model for ectodermal organ morphogenesis, we show here that vertic

210 anding of the cellular mechanisms underlying ectodermal organ morphogenesis.

211 stem cells-provides a model for the study of ectodermal organ renewal and regeneration.

212 this mechanism is conserved among different ectodermal organs and is, therefore, a novel and fundame

213 Interestingly, these ectodermal organs differ in their tissue homeostasis, wh

214 On the body surface, different ectodermal organs exhibit distinctive modes of regenerat

215 Ectodermal organs such as teeth, hair follicles, and mam

216 Animals lacking p63 fail to form many ectodermal organs, including the skin and hair follicles

217 cells adopt different fates and form diverse ectodermal organs, such as teeth, hair follicles, mammar

218 Ectodermal organs, which include teeth, hair follicles,

219 rmal condensation, an essential component of ectodermal organs.

220 s during the development and regeneration of ectodermal organs.

221 p that marks the developmental onset of many ectodermal organs.

222 Analysis of the ectodermal origin and distribution of these early postmi

223 crest cells (NCC) are multi-potent cells of ectodermal origin that colonize diverse organs, includin

224 support the hypothesis that oenocytes are of ectodermal origin.

225 rolateral (O fate) and dorsolateral (P fate) ectodermal pattern elements arises from a single founder

226 in Nematostella, wnt signaling mediates O-Ab ectodermal patterning across a surprisingly complex epit

227 e we show that Six1 and Eya2 are involved in ectodermal patterning and cooperate to induce preplacoda

228 , and homologous genetic mechanisms regulate ectodermal patterning in both animals.

229 During ectodermal patterning the neural crest and preplacodal e

230 ups to elucidate the evolutionary history of ectodermal patterning.

231 w, we also further consider the evolution of ectodermal patterning.

232 n the face and viscera, are composed of both ectodermal placode and neural crest cells.

233 First, a pseudostratified ectodermal placode forms at the oral pole of developing

234 sensory neurons have a dual origin from both ectodermal placodes and neural crest.

235 Cranial ectodermal placodes are thickenings in the ectoderm that

236 Vertebrate cranial ectodermal placodes are transient, paired thickenings of

237 region-specific factors transform thickened ectodermal placodes into complex sense organs containing

238 anglia are derived from the neural crest and ectodermal placodes, but the mechanisms that control the

239 ous system in the trunk of vertebrates, the "ectodermal placodes," together with neural crest, form t

240 have a dual origin from the neural crest and ectodermal placodes.

241 ated moved slowly for 45 y until an assay of ectodermal pocks of the chorioallantoic membrane of chic

242 ols the transition of a proliferative neural ectodermal population to a committed neural plate popula

243 are derived from the Pax6-expressing surface ectodermal precursors, also failed to differentiate.

244 ied Pax6 promoter that is active in the lens ectodermal precursors.

245 retain-->In C. teleta, the ectodermal primary somatoblast, 2d, is the key cell resp

246 s commitment of cells arising from the major ectodermal progenitor (AB blastomere) several cell divis

247 Notch signaling in the molecular control of ectodermal progenitor cell specification to the epiderma

248 ts that specify epidermal keratinocytes from ectodermal progenitor cells are not well understood.

249 l and hair follicle development from surface ectodermal progenitor cells requires coordinated changes

250 d transcriptional changes to specify surface ectodermal progenitor cells to the keratinocyte lineage.

251 echanisms that direct keratinocyte fate from ectodermal progenitor cells.

252 naling is activated before p63 expression in ectodermal progenitor cells.

253 ivisions of mesodermal proteloblast DM'' and ectodermal proteloblast DNOPQ'''.

254 at about stage 16 within Sof-pax3/7-negative ectodermal regions before they are covered by the defini

255 cluded, though universally expressed and pan-ectodermal regulatory genes are in general not.

256 th factor 8 (Fgf8) is produced by the apical ectodermal ridge (AER) at the distal tip of the limb bud

257 Half a century ago, the apical ectodermal ridge (AER) at the distal tip of the tetrapod

258 The apical ectodermal ridge (AER) in the vertebrate limb is require

259 The apical ectodermal ridge (AER) is a transient embryonic structur

260 rodactyly is linked to defects of the apical ectodermal ridge (AER) of the developing limb buds.

261 air follicle placode, but also at the apical ectodermal ridge (AER) of the limb bud.

262 h contrasts with the situation in the apical ectodermal ridge (AER) of the limb.

263 of polarizing activity (ZPA) and the apical ectodermal ridge (AER), are known to cause limb malforma

264 trol posterior fin development via an apical ectodermal ridge (AER), whereas an alternative Homeobox

265 of the Hh signaling pathway, from the apical ectodermal ridge (AER).

266 8 (FGF8) produced by the newly formed apical ectodermal ridge (AER).

267 extrinsic signals from the trunk and apical ectodermal ridge specify the stylopod and zeugopod/autop

268 ndent on a posterior extension of the apical ectodermal ridge, and this also allows the additional di

269 nd to a specialized region of it, the apical ectodermal ridge, controls the distribution of cell beha

270 signaling pathway, emanating from the apical ectodermal ridge, does not regulate cell orientation in

271 ed response to FGF signaling from the apical ectodermal ridge, which disrupts the feedback loop betwe

272 sx1 and a decrease in Fgf4 within the apical ectodermal ridge.

273 ers and the duration of the overlying apical ectodermal ridge.

274 es of bone, which are overlain by keratinous ectodermal scutes.

275 s, the NC-specific Wnt1Cre mouse line and an ectodermal-specific Crect mouse line.

276 BMP2/4, previously shown to be activators of ectodermal specification and the secondary embryonic axi

277 developmental GRNs directing mesodermal and ectodermal specification have undergone marked alteratio

278 for Notch signaling in p63 expression during ectodermal specification in hESCs or mouse embryos, resp

279 During embryogenesis, ectodermal stem cells adopt different fates and form div

280 ein destabilizes the nuclear protein Bowl in ectodermal structures.

281 ervical somites, and conditional ablation of ectodermal Tbx3 expression eliminated all normally posit

282 By gastrulation the ectodermal territories of the sea urchin embryo have dev

283 that specify future mesodermal, neural, and ectodermal territories.

284 instead contributes to the patterning of an ectodermal territory, which then, in turn, provides cues

285 rates, the neurogenic placodes are transient ectodermal thickenings that give rise to sensory neurons

286 l nervous system of the head is derived from ectodermal thickenings, called placodes, that delaminate

287 as allele (Lox-Stop-Lox (LSL)-Kras(G12D)) in ectodermal tissue using two different Cre transgenic lin

288 RAC channel-deficient patients and mice with ectodermal tissue-specific deletion of Orai1 (Orai1K14Cr

289 at expand and cover Sof-pax3/7-negative head ectodermal tissues.

290 sarcomas, but is rarely expressed in normal ectodermal tissues.

291 -1 and pgl family of genes in intestinal and ectodermal tissues.

292 uring the development of both mesodermal and ectodermal tissues.

293 stratification, phenocopying loss of the key ectodermal transcription factor p63.

294 and nonpineal supratentorial primitive neuro-ectodermal tumors when treated with multiple different s

295 ion translocators, we show that a change in ectodermal voltage, not tied to a specific protein or io

296 s controlled by signals from the frontonasal ectodermal zone (FEZ), and the divergent morphologies th

297 ial ectoderm, which we named the frontonasal ectodermal zone (FEZ), regulates proximo-distal extensio

298 tical for facial patterning, the frontonasal ectodermal zone (FEZ).

299 tes are induced from a Spalt major/Engrailed ectodermal zone by MAPK signaling.

300 that cells isolated from the ocular surface ectodermal zone of the SEAM can be sorted and expanded e