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 ells of all lineages sort to the interior of ectodermal aggregates, including single ectodermal cells

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

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

6 ular features and behaviors that distinguish ectodermal and endodermal lineages to drive sorting have

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

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

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

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

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

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

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

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

15 Because ectodermal and mesodermal mesenchyme can form in close p

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

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

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

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

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

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

22 he homeostasis and repair of a fast-turnover ectodermal appendage.

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

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

25 Ectodermal appendages such as feathers, hair, mammary gl

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

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

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

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

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

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

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

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

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

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

36 Ectodermal cell collectives adopt their position at the

37 ion during mesoderm invagination, and native ectodermal cell divisions with ectopic activation of api

38 Therefore, PRDM1 plays multiple roles during ectodermal cell fate allocation.

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

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

41 ons of extracellular signals induce distinct ectodermal cell populations, such as the neural crest an

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

43 reas a 30-min Erk pulse specifies a distinct ectodermal cell type, intermediate neuroblasts.

44 is a prerequisite for proper segregation of ectodermal cell types.

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

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

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

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

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

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

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

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

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

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

55 e methylation and accessibility landscape of ectodermal cells is already established in the early epi

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

57 Ectodermal cells segregated from endodermal and extraemb

58 These ectodermal cells subsequently produce various keratinize

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

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

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

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

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

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

65 with expression primarily being confined to ectodermal cells.

66 r of ectodermal aggregates, including single ectodermal cells.

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

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

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

70 up to analyze their elusive function in the ectodermal compartment, using the mouse limb bud as a mo

71 neural columnar fates in increasingly dorsal ectodermal compartments.

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

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

74 In addition to known ectodermal contributions, we use lineage tracing and tim

75 ry ADH-like structure in the near absence of ectodermal contributions.

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

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

78 features included skeletal abnormalities and ectodermal defects of variable severity in five individu

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

80 ronic mucocutaneous candidiasis, and various ectodermal defects.

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

82 However, ectodermal deletion of Edn1 results in craniofacial defe

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

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

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

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

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

88 congenital syndromes affecting a variety of ectodermal derivatives.

89 craniofacial development including regional ectodermal detachment associated with mesenchymal acellu

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

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

92 -containing transcriptional repressor during ectodermal development.

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

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

95 Oct4 suppresses neural ectodermal differentiation and promotes mesendodermal di

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

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

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

99 During early ectodermal differentiation, sustained MYCN activity main

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

101 dodermal differentiation and promotes neural ectodermal differentiation.

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

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

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

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

106 hat may serve roles in establishing distinct ectodermal domains.

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

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

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

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

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

112 f Hoxc13, which is the causative gene of the ectodermal dysplasia 9 (ECTD9) in human patients.

113 We identified in an adult with ectodermal dysplasia and immunodeficiency a germline, ga

114 LRP6 mutation in patients with hypohidrotic ectodermal dysplasia and reveal the dynamic expression p

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

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

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

118 ral human genetic syndromes featuring CP and ectodermal dysplasia have been linked to mutations in ge

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

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

121 Ectodermal dysplasia is a group of congenital syndromes

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

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

124 c.2292G>A; p.W764*) presented a hypohidrotic ectodermal dysplasia phenotype.

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

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

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

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

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

130 Ectodermal dysplasia with immune deficiency (EDI) is an

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

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

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

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

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

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

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

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

139 gene result in immunodeficiency, anhidrotic ectodermal dysplasia, and enamel defects.

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

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

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

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

144 , leading to the human disorder hypohidrotic ectodermal dysplasia.

145 g during development results in hypohidrotic ectodermal dysplasia.

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

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

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

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

150 7 patients to rule out the effects of other ectodermal dysplasias and other tooth-related genes and

151 The ectodermal dysplasias are a group of inherited autosomal

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

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

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

155 of genetic causes of rare diseases, such as ectodermal dysplasias, orofacial clefts, and other crani

156 responsible for two rare diseases related to ectodermal dysplasias.

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

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

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

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

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

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

163 nd autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED).

164 th autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy show diverse endocrine and nonendoc

165 th autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy suffer from early-onset cutaneous i

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

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

168 th autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy-like kinase-dead Ikkalpha knockin m

169 th autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy.

170 ed autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy.

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

172 lly in pluripotent cells and subsequently in ectodermal, endodermal, and mesodermal derivatives.

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

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

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

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

177 We further identified two mammalian-specific ectodermal enhancers located upstream of the HoxC gene c

178 reveals similar competency of endodermal and ectodermal epithelia to generate all endocrine cell type

179 yDs) that localize at the apical membrane of ectodermal epithelial cells and are planar polarized per

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

181 re adherent passengers for engulfment by the ectodermal epithelium.

182 nic sources: neural crest ectomesenchyme and ectodermal epithelium.

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

184 Ectopic Wnt ectodermal expression in Pbx mutants rescues the cleftin

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

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

187 s neighboring sequences to regulate the Pax6 ectodermal expression.

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

189 ithelial cells with anterior neuroectodermal/ectodermal fates, including retinal cell fate.

190 zed by hypertrophic nail dystrophy and other ectodermal features.

191 sing Fgf10 expression in the emu LPM induces ectodermal Fgf8 expression and a limb bud.

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

193 as diverged more markedly than regulation of ectodermal genes.

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

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

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

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

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

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

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

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

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

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

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

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

206 Ectodermal malformations, present in all patients, sugge

207 immunodeficiency (CID) without endocrine or ectodermal manifestations.

208 ing of the developing mouse face to identify ectodermal, mesenchymal and endothelial populations asso

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

210 The orthogonally oriented endodermal and ectodermal muscle fibers are jointly activated during lo

211 al tube that forms by internalization of the ectodermal neural plate specified via inhibition of BMP

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

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

214 crest cells, cranial placodes are considered ectodermal novelties that drove evolution of the vertebr

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

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

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

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

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

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

221 anding of the cellular mechanisms underlying ectodermal organ morphogenesis.

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

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

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

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

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

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

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

229 Ectodermal organs, which include teeth, hair follicles,

230 rmal condensation, an essential component of ectodermal organs.

231 s during the development and regeneration of ectodermal organs.

232 te Hoxc gene expression in the hair and nail ectodermal organs.

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

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

235 cell RNA sequencing of 51,199 mouse cells of ectodermal origin, gene regulatory network (GRN) screens

236 support the hypothesis that oenocytes are of ectodermal origin.

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

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

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

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

241 e are currently no systems in which to study ectodermal patterning in humans.

242 Ectodermal patterning is required for the establishment

243 During ectodermal patterning the neural crest and preplacodal e

244 Here, we develop an in vitro model of human ectodermal patterning, in which human embryonic stem cel

245 ups to elucidate the evolutionary history of ectodermal patterning.

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

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

248 Cranial ectodermal placodes are thickenings in the ectoderm that

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

250 ealth of embryonic and adult tissues such as ectodermal placodes, the trachea, the ureter, the gut an

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

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

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

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

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

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

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

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

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

260 echanisms that direct keratinocyte fate from ectodermal progenitor cells.

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

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

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

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

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

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

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

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

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

270 differentiation and do not develop an apical ectodermal ridge (AER).

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

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

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

274 me, including focused analyses of the apical ectodermal ridge, limb mesenchyme and skeletal muscle.

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

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

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

278 d epithelial structure similar to the apical ectodermal ridge.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

293 -1 and pgl family of genes in intestinal and ectodermal tissues.

294 pecification in differentiating epiblast and ectodermal tissues.

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

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

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

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