ライフサイエンスコーパス: neural tube closure

1 etal processes that govern cell shape during neural tube closure.

2 development and suggest an important role in neural tube closure.

3 ously unsuspected role of Trpm6 in effecting neural tube closure.

4 nockdown disrupts cell behaviors integral to neural tube closure.

5 ufficient for radial glia formation prior to neural tube closure.

6 rainyhead-like2 (Grhl2), each prevent spinal neural tube closure.

7 Mena and VASP, in mice results in failure of neural tube closure.

8 tion of stereocilia, cochlear extension, and neural tube closure.

9 lation of DLHP formation during mouse spinal neural tube closure.

10 is are required in the midline to facilitate neural tube closure.

11 se, in convergent extension and the onset of neural tube closure.

12 tion is required at a critical threshold for neural tube closure.

13 xpressed in cellular populations involved in neural tube closure.

14 growth and in localized regions of disrupted neural tube closure.

15 MEKK4-deficient neuroepithelium at sites of neural tube closure.

16 aintained in a multipotent state until after neural tube closure.

17 required for neural convergent extension and neural tube closure.

18 euroepithelial sheet-bending, and failure of neural tube closure.

19 cannot achieve the apposition necessary for neural tube closure.

20 uired specifically in the midline for normal neural tube closure.

21 ying the processes occurring at the stage of neural tube closure.

22 is affected, owing to a failure to initiate neural tube closure.

23 defects in turning, cardiac development and neural tube closure.

24 heral nervous systems, first appearing after neural tube closure.

25 n that is established at or before stages of neural tube closure.

26 ism underlying zippering during mouse spinal neural tube closure.

27 sensitive metabolic processes at the time of neural tube closure.

28 n blastopore lip formation, gastrulation and neural tube closure.

29 h in the lateral edges of hindbrain prior to neural tube closure.

30 da, all of which can be attributed to failed neural tube closure.

31 ding lateral cells and midline cells, before neural tube closure.

32 exhibit exencephaly secondary to a defect in neural tube closure.

33 ch becomes the dorsoventral (D-V) axis after neural tube closure.

34 e and occurs at the 4-6 somite stage, before neural tube closure.

35 stages but is delayed anteriorly until after neural tube closure.

36 is that actin-based motility directs cranial neural tube closure.

37 tiating injury for autism around the time of neural tube closure.

38 ng of the neural plate midline and defective neural tube closure.

39 esults in defects of apical constriction and neural tube closure.

40 eraction of genetics and cell biology during neural tube closure.

41 had microcephaly with delayed and defective neural tube closure.

42 ion in the tissue plane and is essential for neural tube closure.

43 defects, including those arising from failed neural tube closure.

44 rmanent cell cycle arrest, occurs only after neural tube closure.

45 te cell biological mechanistic insights into neural tube closure.

46 e-level time-lapse microscopy during Xenopus neural tube closure.

47 aic mutations in shroom3, a key regulator or neural tube closure.

48 gh the enhanced supply of nucleotides during neural tube closure.

49 enes and reveals spatial signatures of mouse neural tube closure.

50 tional and required for embryo extension and neural tube closure.

51 multiple ectodermal lineages until or beyond neural tube closure.

52 but have distinct and essential roles during neural tube closure.

53 ation of septins governs ciliogenesis during neural tube closure.

54 s exhibiting exencephaly, a severe defect in neural tube closure.

55 bryonic vitamin E to the mouse embryo during neural tube closure.

56 in embryonic vitamin E uptake during murine neural tube closure.

57 ace ectoderm, are required for completion of neural tube closure.

58 ivator with ED-rich tail 2) is essential for neural tube closure.

59 activation of apical actomyosin required for neural tube closure.

60 FKBP8 is critical for proper mammalian neural tube closure.

61 sac, and embryo proper, as well as abnormal neural tube closure.

62 ion of de novo thymidylate synthesis impairs neural tube closure.

63 lling and undergo almost complete failure of neural tube closure.

64 mbryonic neuroepithelium and is required for neural tube closure.

65 crucial in posterior axis elongation and in neural tube closure.

66 ammals, in contrast to its essential role in neural tube closure.

67 ight genetic and epigenetic contributions to neural tube closure.

68 expansion as a result of uncompleted cranial neural tube closure.

69 ate metabolism, has the potential to support neural tube closure.

70 involved in wound healing and developmental neural tube closure.

71 1 and couples non-canonical Wnt signaling to neural tube closure.

72 nd membrane dynamics required for vertebrate neural tube closure.

73 ression abolishes MHP formation and prevents neural tube closure.

74 This stage occurred shortly after neural tube closure (0.9 days, st 21) and followed the a

75 n of the mouse Spint2 gene led to defects in neural tube closure, abnormal placental labyrinth develo

76 1 in mouse embryos causes defects in cranial neural tube closure, accompanied by an increase in the p

77 After neural tube closure, amniotic fluid (AF) captured inside

78 to regulate neural progenitor proliferation, neural tube closure and apical constriction.

79 ose cells that will constrict during cranial neural tube closure and appears pivotal in regulating th

80 ZIP12 antisense morpholino knockdown impairs neural tube closure and arrests development during neuru

81 role in the convergent extension that drives neural tube closure and body axis elongation.

82 53 is the only required Pax3 function during neural tube closure and cardiac neural crest development

83 to function as a transcription factor during neural tube closure and cardiac neural crest development

84 en implicated in directing aspects of dorsal neural tube closure and cell fate specification.

85 K-AKT signaling and AJ biology, required for neural tube closure and CNCC delamination.

86 ts were embryonic lethal and showed impaired neural tube closure and CNCC delamination.

87 larized cellular movement that occurs during neural tube closure and cochlear extension.

88 mmary, Myo10 is important for both prenatal (neural tube closure and digit formation) and postnatal d

89 this function is critical to maintain proper neural tube closure and dorsal cell fate segregation.

90 croglia begin colonizing the forebrain after neural tube closure and during later stages of neurogene

91 eta-catenin signaling is required for caudal neural tube closure and elongation, acting through the t

92 ecting limb development, vascular integrity, neural tube closure and eyelid closure.

93 ving embryonic elongation that later support neural tube closure and formation of the central nervous

94 evelopmental processes such as gastrulation, neural tube closure and hearing.

95 his interaction may influence the process of neural tube closure and how these results may be relevan

96 for protease-activated receptor signaling in neural tube closure and identify a local protease networ

97 g late embryogenesis, and exhibit defects in neural tube closure and in the development of the tail b

98 the Lp mutant may be secondary to failure of neural tube closure and incomplete axial rotation.

99 ty of neural cells is plastic at the time of neural tube closure and is sensitive to positionally res

100 Here, we show that spinal neural tube closure and lateral migration of the caudal

101 l plate stages); expression of Sox-3 follows neural tube closure and lens specification.

102 1 and/or Fz2 mutations also cause defects in neural tube closure and misorientation of inner ear sens

103 velled (Xdsh) signaling is required for both neural tube closure and neural convergent extension, but

104 cleotides directed against ngd mRNA disrupts neural tube closure and neural crest migration; however,

105 tional lethality with defects in myogenesis, neural tube closure and neural crest-derived lineages in

106 Mechanisms underlying neural tube closure and NTDs may be informed by experime

107 e of canonical Wnt/beta-catenin signaling in neural tube closure and NTDs remains poorly understood.

108 uding Vangl2 and Dact1, results in defective neural tube closure and other developmental defects.

109 o form, and animals die at midgestation with neural tube closure and placental deficits.

110 s mutation exhibit severe defects in cranial neural tube closure and precocious neuron production in

111 solved map of gene expression during cranial neural tube closure and provide a resource for investiga

112 netic pathway required for the initiation of neural tube closure and provides an important new candid

113 d to adulthood, and exhibited delayed caudal neural tube closure and skeletal patterning defects that

114 scriptional regulators in pathways affecting neural tube closure and skeletal patterning, most likely

115 During neural tube closure and spinal cord development, many ce

116 tein with tyrosine kinase homology, disrupts neural tube closure and stereociliary bundle orientation

117 an unexpected role for protease signaling in neural tube closure and the formation of the central ner

118 lator of epithelial morphogenesis, including neural tube closure and the orientation of inner ear sen

119 report that Fz3 and Fz6 redundantly control neural tube closure and the planar orientation of hair b

120 een the oriented cell movements required for neural tube closure and tubulogenesis.

121 embryogenesis indicates a failure of cranial neural-tube closure and defects in cranial ganglia devel

122 lineage differentiation in embryos, delayed neural tube closure, and altered exon skipping.

123 h severely disturbed neurogenesis, including neural tube closure, and angiogenesis and caused embryon

124 l mice also exhibit defects in gastrulation, neural tube closure, and axial patterning, suggesting th

125 body causing stalled elongation, failure of neural tube closure, and axis rupture.

126 r the Tulp3 mutant allele exhibit failure of neural tube closure, and die by embryonic day 14.5.

127 ession is normal in AP-2alpha mutants during neural tube closure, and Grhl2;AP-2alpha trans-heterozyg

128 nd interacts with beta/delta-catenins during neural tube closure, and Irf6 is involved in defining ne

129 usion, ventricle shape, optic cup formation, neural tube closure, and layering of the cerebral cortex

130 s a cell shape change critical to vertebrate neural tube closure, and the contractile force required

131 re, notochord formation, somite development, neural tube closure, and the formation of cranial neural

132 rdiac morphogenesis, somite segmentation and neural tube closure, and there is functional redundancy

133 in pure AF and nascent CSF, before and after neural tube closure, and to define how the AF and CSF pr

134 he organization of the neural epithelium and neural tube closure are affected when actin dynamics are

135 Failures of neural tube closure are common and serious birth defects

136 of Pax3 required for cardiac development and neural tube closure are contained within the region 1.6

137 The mechanism(s) behind folate rescue of neural tube closure are not well understood.

138 However, the mechanisms of cranial neural tube closure are not well understood.

139 B2 protein as playing an instructive role in neural tube closure as members of a signaling complex we

140 regulates convergent extension movements and neural tube closure, as well as the orientation of stere

141 Initiation of neural tube closure at the forebrain-midbrain (FB-MB) bo

142 ral plate stage but becomes fixed just after neural tube closure, at stage 10-11.

143 mplete key developmental processes including neural tube closure, axial turning and patterning of the

144 lar and biomechanical mechanisms involved in neural tube closure, based on studies of various vertebr

145 The site at which cranial neural tube closure begins (so-called closure 2) is poly

146 nt overall growth retardation and defects in neural tube closure, blood vessel formation, and the for

147 Apical F-actin is known to be important for neural tube closure, but the precise roles of actin dyna

148 MARCKS is required for neural tube closure, but the regulation and of its biolo

149 in which folic acid can prevent a defect in neural tube closure by a mechanism other than the neutra

150 These results suggest that Pax-3 regulates neural tube closure by inhibiting p53-dependent apoptosi

151 morphic variations in the pattern of cranial neural tube closure can influence susceptibility to NTDs

152 CNS injuries occurring during or just after neural tube closure can lead to a selective loss of neur

153 t expression of Pax3 is sufficient to rescue neural tube closure, cardiac development and other neura

154 he nervous system, including neurulation and neural tube closure, cellular migration, and uniform ori

155 Failure of cranial neural tube closure coincided with increased neuroepithe

156 y, exposure to antimitotic agents just after neural tube closure could produce the observed pattern o

157 valproic acid (VPA) on day 11.5 (the day of neural tube closure), day 12, or day 12.5 gestation.

158 ocked, we examined the cellular basis of the neural tube closure defect in mouse mutants that lack th

159 of mutant embryos developed exencephalus, a neural tube closure defect.

160 s a corresponding human syndrome caused by a neural tube closure defect.

161 ffected embryos at embryonic day 10.5 have a neural-tube closure defect with ruffling of the neural f

162 n the organizer and along the axial midline, neural tube closure defects (NTDs) arose and dorsal exte

163 nvironmental and genetic aberrations lead to neural tube closure defects (NTDs) in 1 out of every 1,0

164 or LRP2 in humans are associated with severe neural tube closure defects (NTDs) such as anencephaly a

165 Folic acid prevents neural tube closure defects (NTDs), but the causal metab

166 s (JNK1 and -2) die during midgestation with neural tube closure defects and brain abnormalities.

167 frequent perinatal lethality associated with neural tube closure defects and cleft secondary palate.

168 ased apoptosis but do exhibit severe cranial neural tube closure defects and exencephaly.

169 Utx-null embryos had reduced somite counts, neural tube closure defects and heart malformation that

170 nt embryos exhibit cranial neural tube closure defects and malformed somites and ar

171 lt in developmental imperfections, including neural tube closure defects and misaligned hair follicle

172 Neural tube closure defects are a major cause of infant

173 w that a decrease in ephrinB2 protein causes neural tube closure defects during Xenopus laevis embryo

174 Skeletal disorders and neural tube closure defects represent clinically signifi

175 Loss of PIP5KIgamma also results in neural tube closure defects that were associated with im

176 ation, exhibiting multiple defects including neural tube closure defects, abnormal dorsal/ventral pat

177 Abnormalities included neural tube closure defects, forebrain hypoplasia, delay

178 associated proteins have been shown to cause neural tube closure defects, neurodegeneration, and tumo

179 -B2(-/-) mutants die at birth as a result of neural tube closure defects.

180 n lead to human congenital disorders such as neural tube closure defects.

181 lly results in early embryonic lethality and neural tube closure defects.

182 Loss of XTRPM6 produced gastrulation and neural tube closure defects.

183 nhibits AC in hingepoint cells, resulting in neural tube closure defects.

184 urulation gene Vangl2 to facilitate midbrain neural tube closure, demonstrating roles for both cobl a

185 disparate developmental processes, including neural tube closure, digit septation, and placentation.

186 xial mesodermal cell migration during spinal neural tube closure, disruption of which may lead to spi

187 ate and axial and paraxial mesoderm prior to neural tube closure does not prevent elongation of ventr

188 e severe congenital defects caused by failed neural tube closure during early embryogenesis.

189 al malformations that result from failure of neural tube closure during early embryonic development,

190 genital malformations caused by a failure of neural tube closure during early embryonic development.

191 fects (NTDs), which result from a failure of neural tube closure during embryogenesis.

192 Failure of neural tube closure during embryonic development can res

193 erges its shape from the spinal cord follows neural tube closure during embryonic development.

194 imaging system by following the dynamics of neural tube closure during mouse embryogenesis and revea

195 bifida (SB) is a complex disorder of failed neural tube closure during the first month of human gest

196 in utero and exhibit exencephaly, defects in neural tube closure, enlarged craniofacial structures, a

197 The sequence of human neural tube closure events remains controversial, but st

198 ental defects, including failure of anterior neural tube closure (exencephaly), failure of digit sept

199 os display incompletely penetrant defects in neural tube closure, eye development, and gastrulation.

200 Neural tube closure fails in both mouse and Xenopus when

201 impaired folate and choline status to affect neural tube closure, fetal growth, and fertility in mice

202 Neural tube closure, for instance, involves apicobasal c

203 ion in these Par2-expressing cells disrupted neural tube closure, further implicating G protein-coupl

204 ) mutant mice, including skeletal, posterior neural tube closure, genitourinary tract and hindgut def

205 Neural tube closure has been studied for many decades, a

206 ny morphogenetic events including vertebrate neural tube closure, however, its spatial regulation is

207 ndidate genes either known to cause abnormal neural tube closure in animals or previously associated

208 nant of cell morphology that is required for neural tube closure in both mice and frogs.

209 at impeded anterior neural plate folding and neural tube closure in both model organisms.

210 Folates are important for normal neural tube closure in early gestation, and the efficacy

211 e show that peptide caspase inhibitors block neural tube closure in explanted chick embryos, suggesti

212 P) signalling is necessary for initiation of neural tube closure in higher vertebrates.

213 and highlight critical pathways required for neural tube closure in human embryogenesis.

214 nt as illustrated by its pivotal role during neural tube closure in human, mouse, Xenopus, and zebraf

215 how mesoderm migration influences posterior neural tube closure in mammals.

216 olizing enzyme that has been shown to affect neural tube closure in mice by directly inhibiting folat

217 Here, we have combined analysis of neural tube closure in mouse and in the African Clawed F

218 ired for dorsolateral bending, which ensures neural tube closure in the absence of sonic hedgehog sig

219 hat expression of Pax-3, a gene required for neural tube closure in the area of the midbrain and hind

220 g tissue boundaries to control zippering and neural tube closure in the basal chordate, Ciona robusta

221 ualize the dynamic cell behaviors comprising neural tube closure in the cultured mouse embryo.

222 etion of the MacMARCKS gene prevents cranial neural tube closure in the developing brain, resulting i

223 rnal dietary choline is important for normal neural tube closure in the fetus and, later in gestation

224 erior across the epidermis, is important for neural tube closure in the invertebrate chordate Ciona i

225 ression at six consecutive stages of cranial neural tube closure in the mouse embryo.

226 seudostratified epithelium, is essential for neural tube closure in the mouse spinal region.

227 transferase activity is required for cranial neural tube closure in the mouse.

228 c movements, such as mesoderm elongation and neural tube closure in vertebrate embryos.

229 luding gastrulation in diverse organisms and neural tube closure in vertebrates.

230 his tissue during the final stages of spinal neural tube closure in wild type embryos.

231 localization at apical junctions and delays neural tube closure in Xenopus embryos.

232 number of genes are known to be required for neural tube closure, in only a very few cases has the af

233 All embryos lacking Mthfd1l exhibit aberrant neural tube closure including craniorachischisis and exe

234 Neural tube closure is a critical morphogenetic event th

235 Neural tube closure is a fundamental embryonic event who

236 ate that variation in the pattern of cranial neural tube closure is a genetically determined factor i

237 Vertebrate neural tube closure is associated with complex changes i

238 The process of neural tube closure is complex and involves cellular eve

239 nding of common human birth defects in which neural tube closure is compromised.

240 Finally, we show that the effect of MIM on neural tube closure is not due to modulation of Hedgehog

241 Neural tube closure is sensitive to environmental influe

242 Shortly after neural tube closure, lunatic fringe is expressed in most

243 acid deficiency, such as defects in anterior neural tube closure, microcephaly with small eye formati

244 l1 and observed neither increased failure of neural tube closure nor detectable proliferation defects

245 athway mediated by folate compromises normal neural tube closure (NTC) and ciliogenesis.

246 Neural tube closure (NTC) is a complex process of embryo

247 Neural tube closure (NTC) is a conserved morphogenetic p

248 ion between NTDs and tissue stiffness during neural tube closure (NTC), we imaged an NTD murine model

249 ryonic days E8.5 and E10.5 (before and after neural tube closure; NTC) (Chau et al., 2018).

250 dies and apoptosis associated with embryonic neural tube closure occur in the absence of AIF, indicat

251 nent thought absent in neuroepithelium after neural tube closure, OCLN isoform-specific expression ex

252 l defect characterized by primary failure of neural tube closure of the spinal column during the embr

253 Three mutant lines display defects in neural tube closure: one is caused by an allele of the o

254 mpletely rescued defects in digit septation, neural tube closure, placental labyrinth morphology, lun

255 during cranial/anterior and spinal/posterior neural tube closure, provides mechanistic insight into t

256 sis of Shroom function and how it influences neural tube closure remain to be elucidated.

257 The function of MIM during neural tube closure requires both its membrane-remodelin

258 For example, neural tube closure requires the actin binding protein S

259 Reduction of Shh signaling after neural tube closure resulted in a transient decrease in

260 Failure of neural tube closure results in severe birth defects and

261 Removal of this population after neural tube closure results in severe septation defects

262 The timing of neural tube closure seemed to be temporally uncoupled wi

263 genes encoding its subunits have defects in neural-tube closure similar to those in human spina bifi

264 During neural tube closure, specialized regions called hinge po

265 ssively elevated apoptosis before and during neural tube closure, suggesting an antiapoptotic role fo

266 Genetically, Tmem132a regulates neural tube closure synergistically with another PCP reg

267 Unidirectional zippering is a key step in neural tube closure that remains poorly understood.

268 c events, such as vertebrate gastrulation or neural tube closure, that place embryonic tissues in the

269 r the non-canonical Wnt signaling pathway in neural tube closure, the underlying mechanism remains po

270 After neural tube closure, these cells undergo an epithelial-m

271 detected only in neurons from late stages of neural tube closure through premetamorphic stages.

272 provide evidence that BMP modulation directs neural tube closure via the regulation of apicobasal pol

273 egional specificity of cell behaviors during neural tube closure, we analyzed the dynamic localizatio

274 ine the mechanisms by which TRPM6 influences neural tube closure, we functionally characterized the r

275 Since Sox-3 is activated following neural tube closure, we tested its dependence on the lat

276 diate BMP-dependent phase around the time of neural tube closure, when BMP-4 is expressed in the dors

277 lens ectoderm of wild-type embryos prior to neural tube closure, when lens induction is under way.

278 n of specific genetic interactions affecting neural tube closure will facilitate our understanding of

279 We achieved neural tube closure with an alternative model combining

280 reated chicken embryos during the process of neural tube closure with sufficient homocysteine thiolac

281 of mesodermal and neural tissues, as well as neural tube closure, without direct effects on tissue di

282 kinase (JNK), are implicated in facilitating neural tube closure, yet upstream regulators remain to b