ライフサイエンスコーパス: neural tube closure

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

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

3 ation of septins governs ciliogenesis during neural tube closure.

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

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

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

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

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

9 xpressed in cellular populations involved in neural tube closure.

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

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

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

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

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

15 required for neural convergent extension and neural tube closure.

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

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

18 cannot achieve the apposition necessary for neural tube closure.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

37 activation of apical actomyosin required for neural tube closure.

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

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

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

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

42 mbryonic neuroepithelium and is required for neural tube closure.

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

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

45 ight genetic and epigenetic contributions to neural tube closure.

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

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

48 involved in wound healing and developmental neural tube closure.

49 1 and couples non-canonical Wnt signaling to neural tube closure.

50 nd membrane dynamics required for vertebrate neural tube closure.

51 ression abolishes MHP formation and prevents neural tube closure.

52 multiple ectodermal lineages until or beyond neural tube closure.

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

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

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

56 nockdown disrupts cell behaviors integral to neural tube closure.

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

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

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

60 1 in mouse embryos causes defects in cranial neural tube closure, accompanied by an increase in the p

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

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

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

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

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

66 53 is the only required Pax3 function during neural tube closure and cardiac neural crest development

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 1 and/or Fz2 mutations also cause defects in neural tube closure and misorientation of inner ear sens

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 Failure of cranial neural tube closure coincided with increased neuroepithe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 Skeletal disorders and neural tube closure defects represent clinically signifi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 Neural tube closure fails in both mouse and Xenopus when

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

161 Neural tube closure, for instance, involves apicobasal c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 Neural tube closure is a critical morphogenetic event th

184 Neural tube closure is a fundamental embryonic event who

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

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

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

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

189 Neural tube closure is sensitive to environmental influe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 During neural tube closure, specialized regions called hinge po

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

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

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

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

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

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

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

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

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

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

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

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

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

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