戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 tinct subpopulations within the chick dorsal neural tube.
2 aling-dependent tissues such as the limb and neural tube.
3 t are initially located at the border of the neural tube.
4 l cell types are not specified in the mutant neural tube.
5 r excitatory neuronal lineages in the dorsal neural tube.
6 istinct progenitor domains in the developing neural tube.
7 ar behaviors underlying morphogenesis of the neural tube.
8  the level from which cells emerge along the neural tube.
9 closure, axial turning and patterning of the neural tube.
10 movements underlying the organization of the neural tube.
11 resolution during morphogenesis of the mouse neural tube.
12 for dorsoventral patterning of the overlying neural tube.
13 es, often manifested in the palate, heart or neural tube.
14 on that stem from the cranial portion of the neural tube.
15 icular zone and floor plate of the embryonic neural tube.
16 rom later-differentiating neurons toward the neural tube.
17 planin, which is expressed on the developing neural tube.
18 al folds, which meet and adhere to close the neural tube.
19 o complete the developmental transition to a neural tube.
20 chanics, pattern formation and growth in the neural tube.
21 s and phagocytose cellular debris around the neural tube.
22 senchymal cells at the dorsal midline of the neural tube.
23                            In the vertebrate neural tube, a morphogen-induced transcriptional network
24 Irf6 is also required for development of the neural tube and associated structures.
25 -migrating cells, originating from the trunk neural tube and associated with nerve fibres, differenti
26  results in severe patterning defects in the neural tube and defective Hedgehog signaling.
27 R-BI(-/-) embryos fail to close the anterior neural tube and develop exencephaly, a perinatal lethal
28 CEP120 morphants, cilia are shortened in the neural tube and disorganized in the pronephros.
29 defects leading to deformities of the limbs, neural tube and inner ear.
30 ), which is known to guide axons outside the neural tube and interneurons in the cortex, is expressed
31 sduction specifies ventral cell fates in the neural tube and is mediated by the Gli transcription fac
32 ng is antagonized by signals from the dorsal neural tube and loss of Hh leads to loss of ventral patt
33 he generation of motor neurons in both chick neural tube and mouse embryonic stem cells, suggesting t
34 way patterning the dorso-ventral axis of the neural tube and muscles, by controlling the degradation
35 nsion, resulting in compression of the axial neural tube and notochord; second, elongation of axial t
36 developing embryo and promote closing of the neural tube and other morphologic processes during devel
37 y symmetric interfaces between the zebrafish neural tube and paraxial mesoderm function as optimally
38  Ssdp2 (Ssdp1/2) are highly expressed in the neural tube and promote motor neuron differentiation in
39 ify the Shh gradient in the developing mouse neural tube and show that while the amplitude of the gra
40 11 are required for proper patterning of the neural tube and somites by regulating notochord formatio
41 trunk-like structures" (TLSs) comprising the neural tube and somites.
42 ate as a continuous mass of tissue along the neural tube and subsequently split into spatially distin
43  epithelial cells, as seen in the vertebrate neural tube and the Drosophila ventral furrow.
44 h temporal and spatial precision in both the neural tube and the embryo's enveloping layer epithelium
45  environmental barrier dorsal and lateral to neural tube and the somites that is normally formed by P
46 gical progression of MMC involves failure in neural tube and vertebral arch closure at early gestatio
47 ced the contribution of their progeny to the neural tube, and dramatically expanded the unsegmented m
48 asts differentiate in close contact with the neural tube, and they never loose contact with the neura
49  developing tissues in mice such as somites, neural tubes, and limb buds.
50 The Drosophila blastoderm and the vertebrate neural tube are archetypal examples of morphogen-pattern
51                          Using the zebrafish neural tube as a model, we uncover the in vivo mechanism
52 nic hedgehog (Shh) patterning of the ventral neural tube as an example, we show that the framework ca
53 red in the carapacial staging area above the neural tube at G16, and differentiated into pigment-form
54 etween the different posterior tissues (e.g. neural tube, axial and paraxial mesoderm, lateral plate,
55 and thoracic regions of the developing mouse neural tube between embryonic days 9.5-13.5.
56 ed with a morphological change in the dorsal neural tube between stages mature G15 and G16.
57 and reduce the risk of folic acid-responsive neural tube birth defects (NTDs).
58 tify staple foods with folic acid to prevent neural tube birth defects.
59 ifferentiated peripheral sensory neurons and neural tube border cells with the cooperation of neural
60 d observed expression in the developing eye, neural tube, brain and kidney.
61 ially Sox2+ cells can contribute not only to neural tube but also to neural crest and epidermis.
62 er of neural crest cells arise from the head neural tube by epithelial-to-mesenchymal transition (EMT
63 DNA methylation in regulating the ability of neural tube cells to produce neural crest cells and the
64 terning process in the developing vertebrate neural tube (central nervous system, CNS), depends on So
65 eometry and packing that arise from the open neural tube characteristic of PCP mutants.
66 athway mediated by folate compromises normal neural tube closure (NTC) and ciliogenesis.
67 to regulate neural progenitor proliferation, neural tube closure and apical constriction.
68 K-AKT signaling and AJ biology, required for neural tube closure and CNCC delamination.
69 ts were embryonic lethal and showed impaired neural tube closure and CNCC delamination.
70 mmary, Myo10 is important for both prenatal (neural tube closure and digit formation) and postnatal d
71 croglia begin colonizing the forebrain after neural tube closure and during later stages of neurogene
72 evelopmental processes such as gastrulation, neural tube closure and hearing.
73                                       During neural tube closure and spinal cord development, many ce
74 he organization of the neural epithelium and neural tube closure are affected when actin dynamics are
75           However, the mechanisms of cranial neural tube closure are not well understood.
76 ocked, we examined the cellular basis of the neural tube closure defect in mouse mutants that lack th
77  of mutant embryos developed exencephalus, a neural tube closure defect.
78 n the organizer and along the axial midline, neural tube closure defects (NTDs) arose and dorsal exte
79                          Folic acid prevents neural tube closure defects (NTDs), but the causal metab
80                                              Neural tube closure defects are a major cause of infant
81 w that a decrease in ephrinB2 protein causes neural tube closure defects during Xenopus laevis embryo
82 n lead to human congenital disorders such as neural tube closure defects.
83 lly results in early embryonic lethality and neural tube closure defects.
84     Loss of XTRPM6 produced gastrulation and neural tube closure defects.
85 genital malformations caused by a failure of neural tube closure during early embryonic development.
86 fects (NTDs), which result from a failure of neural tube closure during embryogenesis.
87                                   Failure of neural tube closure during embryonic development can res
88  bifida (SB) is a complex disorder of failed neural tube closure during the first month of human gest
89                                              Neural tube closure has been studied for many decades, a
90 g tissue boundaries to control zippering and neural tube closure in the basal chordate, Ciona robusta
91 erior across the epidermis, is important for neural tube closure in the invertebrate chordate Ciona i
92                               The process of neural tube closure is complex and involves cellular eve
93                                              Neural tube closure is sensitive to environmental influe
94                                   Failure of neural tube closure results in severe birth defects and
95    Unidirectional zippering is a key step in neural tube closure that remains poorly understood.
96 1 in mouse embryos causes defects in cranial neural tube closure, accompanied by an increase in the p
97                                        After neural tube closure, amniotic fluid (AF) captured inside
98  lineage differentiation in embryos, delayed neural tube closure, and altered exon skipping.
99 in pure AF and nascent CSF, before and after neural tube closure, and to define how the AF and CSF pr
100 mplete key developmental processes including neural tube closure, axial turning and patterning of the
101 lar and biomechanical mechanisms involved in neural tube closure, based on studies of various vertebr
102  Apical F-actin is known to be important for neural tube closure, but the precise roles of actin dyna
103                       MARCKS is required for neural tube closure, but the regulation and of its biolo
104 nent thought absent in neuroepithelium after neural tube closure, OCLN isoform-specific expression ex
105 ine the mechanisms by which TRPM6 influences neural tube closure, we functionally characterized the r
106 ism underlying zippering during mouse spinal neural tube closure.
107 sensitive metabolic processes at the time of neural tube closure.
108 ng of the neural plate midline and defective neural tube closure.
109 multiple ectodermal lineages until or beyond neural tube closure.
110 but have distinct and essential roles during neural tube closure.
111 ation of septins governs ciliogenesis during neural tube closure.
112 s exhibiting exencephaly, a severe defect in neural tube closure.
113 bryonic vitamin E to the mouse embryo during neural tube closure.
114  in embryonic vitamin E uptake during murine neural tube closure.
115 ace ectoderm, are required for completion of neural tube closure.
116 ivator with ED-rich tail 2) is essential for neural tube closure.
117       FKBP8 is critical for proper mammalian neural tube closure.
118 activation of apical actomyosin required for neural tube closure.
119  sac, and embryo proper, as well as abnormal neural tube closure.
120 ion of de novo thymidylate synthesis impairs neural tube closure.
121 etal processes that govern cell shape during neural tube closure.
122 rainyhead-like2 (Grhl2), each prevent spinal neural tube closure.
123 ryonic days E8.5 and E10.5 (before and after neural tube closure; NTC) (Chau et al., 2018).
124 bation of the Fibronectin matrix rescues the neural tube convergence defect of cadherin 2 mutants.
125  namely an increase from two to four ectopic neural tubes, corresponding to the switch in NMP niche,
126 ms produced offspring at a rate of 11.3% for neural tube defect (NTD) formation, whereas no embryos i
127 nd B12, choline, betaine, and methionine and neural tube defect (NTD) outcomes among mothers meeting
128 aternal periconceptional NSD use between 334 neural tube defect cases and 7,619 nonmalformed controls
129        Caudal regression syndrome is a rare, neural tube defect characterized by an abnormal developm
130  assuming that a woman having a child with a neural tube defect incurs an extra DALY per year for the
131  become an obstacle to the wider adoption of neural tube defect prevention programs and have called f
132  without the potential for childbearing, and neural tube defect recurrence; and studies conducted in
133 rol this process is expected to reveal novel neural tube defect risk factors and increase our underst
134                                              Neural tube defect risk was associated with maternal per
135 ession of Irf6 caused exencephaly, a rostral neural tube defect, through suppression of Tfap2a and Gr
136 potential treatment for spina bifida (SB), a neural tube defect.
137                                              Neural tube defects (NTDs) are a group of severe congeni
138               Planar cell polarity (PCP) and neural tube defects (NTDs) are linked, with a subset of
139                                              Neural tube defects (NTDs) are the most severe congenita
140  Lin28a/b double knockout (dKO) mice display neural tube defects (NTDs) coupled with reduced prolifer
141          The Botswana Tsepamo study reported neural tube defects (NTDs) in 4 of 426 (0.94%) infants o
142 abetes mellitus in early pregnancy can cause neural tube defects (NTDs) in embryos by perturbing prot
143 rhl2 loss results in fully penetrant cranial neural tube defects (NTDs) in mice.
144  Gpr161 null and hypomorphic mutations cause neural tube defects (NTDs) in mouse models.
145 may be associated with an increased risk for neural tube defects (NTDs) in newborns if used by women
146  ART has been reported to be associated with neural tube defects (NTDs) in offspring.
147            Mouse models of folate-responsive neural tube defects (NTDs) indicate that impaired de nov
148                                  The risk of neural tube defects (NTDs) is influenced by nutritional
149                                              Neural tube defects (NTDs) represent a failure of the ne
150 ess is susceptible to disruption, leading to neural tube defects (NTDs), a common birth defect.
151 supplementation can reduce the prevalence of neural tube defects (NTDs), although just how folates be
152 he risk in infants of birth defects, such as neural tube defects (NTDs), known as diabetic embryopath
153 letion-induced autophagy deficiency leads to neural tube defects (NTDs), similar to those in diabetic
154 Folate supplementation prevents up to 70% of neural tube defects (NTDs), which result from a failure
155 ptions in neural tube (NT) closure result in neural tube defects (NTDs).
156 ly pregnancy causes birth defects, including neural tube defects (NTDs).
157    High glucose in vivo and in vitro induces neural tube defects (NTDs).
158 suboptimal RBC folate for protection against neural tube defects (NTDs); among nonconsumers of folic
159 s have also been identified in patients with neural tube defects (NTDs); however, the relationship be
160 6, 0.43), and a 41% reduction in the odds of neural tube defects (OR: 0.59; 95% CI: 0.49, 0.70).
161 MP-SMX was associated with increased risk of neural tube defects (pooled OR 2.5, 95% CI 1.4-4.3), spo
162 tural pesticide use has been associated with neural tube defects and autism, but more subtle outcomes
163  similar to the testing/screening method for neural tube defects and common chromosomal anomalies dur
164 ulthood, heterotaxia, pre-axial polydactyly, neural tube defects and hydrocephalus.
165        Association of folate deficiency with neural tube defects and impact of fortification programs
166  an essential nutrient, increase the risk of neural tube defects and lead to low performance on cogni
167 tes to delineate the genetic architecture of neural tube defects and new therapeutic targets to preve
168  abnormalities with or without microcephaly, neural tube defects and other early brain malformations,
169 ously reported positive associations between neural tube defects and periconceptional exposure to NSD
170 lly lethal and recapitulates JBTS, including neural tube defects and polydactyly; however, the underl
171  during the periconception period to prevent neural tube defects and to ensure normal brain developme
172                                              Neural tube defects are among the most common congenital
173                                              Neural tube defects are among the most common major cong
174                 Few genetic risk factors for neural tube defects are known in humans, highlighting th
175 r Down syndrome, fetal alcohol syndrome, and neural tube defects combined.
176 from Hungary initiated in 1984, incidence of neural tube defects for folic acid supplementation compa
177 tudies such as Tsepamo are critically needed.Neural tube defects have been reported among infants bor
178 ance spread and a possible increased risk of neural tube defects in infants if used in women at the t
179 en of childbearing age for the prevention of neural tube defects in infants.
180 ant dam's drinking water on the incidence of neural tube defects in some genetic models.
181 sufficiency on the basis of elevated risk of neural tube defects in women 12-49 y old (e.g., RBC fola
182 dults to consider information on the risk of neural tube defects in women taking dolutegravir at time
183 fold fusion during neurulation leads to open neural tube defects including spina bifida.
184                                              Neural tube defects occur frequently, yet underlying gen
185 supplementation and birth defects other than neural tube defects remains unclear.
186 on folic acid supplementation for preventing neural tube defects to inform the US Preventive Services
187 ew of the severe congenital malformations - 'neural tube defects' - that result when closure fails.
188 ngl2 loss is embryonically lethal because of neural tube defects, and mutations in Vangl2 are associa
189 2, which had been previously associated with neural tube defects, and vitamin B-12 status, as well as
190                                              Neural tube defects, harms of treatment (twinning, respi
191      Some relate to birth defects other than neural tube defects, neurological functions or varied as
192  death, pneumonia, congenital heart disease, neural tube defects, preterm birth and low birth weight,
193 n in the periconceptional period can prevent neural tube defects.
194 sociation of folic acid supplementation with neural tube defects.
195  supplementation provided protection against neural tube defects.
196 in the prevention of many diseases including neural tube defects.
197 ood fortification are recommended to prevent neural tube defects.
198 s in lamin B1 are susceptibility factors for neural tube defects.
199 genetic basis underlying the pathogenesis of neural tube defects.
200  implications for a population-level risk of neural tube defects.
201 utations in Vangl2 are associated with human neural tube defects.
202 FR) 677C>T polymorphism is a risk factor for neural tube defects.
203 nesis in the neuroepithelium and ameliorated neural tube defects.
204                            The prevalence of neural-tube defects and major external structural defect
205                            The prevalence of neural-tube defects was higher in association with dolut
206              A preliminary safety signal for neural-tube defects was previously reported in associati
207                            The prevalence of neural-tube defects was slightly higher in association w
208 her was taking dolutegravir at conception, 5 neural-tube defects were found (0.30% of deliveries); th
209                            In comparison, 15 neural-tube defects were found among 14,792 deliveries (
210  examination that could be evaluated, and 98 neural-tube defects were identified (0.08% of deliveries
211 is an indicator of folate status and risk of neural-tube defects.
212 , each predetermined epigenetically prior to neural tube delamination.
213 e we show that the development of the dorsal neural tube-derived melanoblasts in turtle Trachemys scr
214 ulation of gene expression in the vertebrate neural tube determines the identity of neural progenitor
215 ensitivity to Hh ligand in vitro, and during neural tube development in vivo.
216 cluding probes annotated to SKI (involved in neural tube development), ZNF544 (previously implicated
217 irmed that the data accurately recapitulates neural tube development, allowing us to identify new mar
218 ll types that will support future studies of neural tube development, function and disease.
219 f Wnt3a and Nkx2.9 during the early stage of neural tube development, perhaps also contributing to ca
220 l chemical environments found in vivo during neural tube development.
221 ristic hyperpolarization of cells lining the neural tube; disruption of this spatial gradient of the
222  the paraxial mesoderm on either side of the neural tube, eventually differentiating into afferent ne
223 he time and distance to first division after neural tube exit were stochastic.
224  isolated from mouse embryonic day 9.5 trunk neural tube explants.
225 he development of many tissues including the neural tube, eye, intestines, and vasculature.
226 tor 1 (Folr1; also known as FRalpha) impairs neural tube formation and leads to NTDs.
227 ture of the NNE during the dynamic events of neural tube formation by both activating key epithelial
228 including gastrulation in many organisms and neural tube formation in vertebrates.
229 ient mouse embryos exhibit severe defects in neural tube formation, somitogenesis and cardiac develop
230  mechanisms involved in folate action during neural tube formation.
231 phogenetic events including gastrulation and neural tube formation.
232 ure, amniotic fluid (AF) captured inside the neural tube forms the nascent cerebrospinal fluid (CSF).
233            In the developing mouse and chick neural tube, hindbrain serotonergic neurons and spinal g
234  the embryonic ectoderm, delaminate from the neural tube in early vertebrate development and migrate
235 the context of the patterning of the ventral neural tube in response to a gradient of the morphogen S
236 in the p1 progenitor domain of the zebrafish neural tube in response to Sonic Hedgehog signaling.
237           This is the case in the vertebrate neural tube, in which neurons differentiate in a charact
238                The loss of Tsc1 in the mouse neural tube increases the number of the wild-type neuron
239 ces cranial crest emigration from the dorsal neural tube independent of Pax7.
240 otor and interneuron types in the vertebrate neural tube indicates conserved combinations, for exampl
241  and found that its expression in the caudal neural tube is dependent on retinoic acid and Pax6, and
242  a model, we show that, at the junction, the neural tube is elaborated by a unique developmental prog
243 Like many developing tissues, the vertebrate neural tube is patterned by antiparallel morphogen gradi
244  model revealed that the amphioxus incipient neural tube is unexpectedly complex, consisting of sever
245             Global transcriptome analyses on neural tubes isolated from E9.0 EpoR-null and littermate
246 lly establish NSC positional identity in the neural tube, it is unclear how such regional differences
247 ses affecting multiple organs, including the neural tube, kidney, and brain.
248   The initial rostrocaudal patterning of the neural tube leads to differential expression of Hox gene
249 etry-breaking events that ultimately lead to neural tube-like patterning along the dorsal-ventral (DV
250  deficiency did not prevent the formation of neural tube-like structures in teratomas.
251                                           In neural tube-like structures, endogenous NUAK2 colocalize
252  the normal development of the kidney, skin, neural tube, lung and limb, and many other organs and ti
253 n of neural crest cells to emigrate from the neural tube, miR-203 displays a reciprocal expression pa
254      Tbx6 knockout TLSs developed additional neural tubes mirroring the embryonic mutant phenotype, a
255     More recently, biomechanical inputs into neural tube morphogenesis have also been identified.
256       Whereas SR-BI(-/-) embryos with closed neural tubes (nSR-BI(-/-)) had high levels of reactive o
257                               Disruptions in neural tube (NT) closure result in neural tube defects (
258  essential role for Geminin during mammalian neural tube (NT) formation and patterning.
259                                              Neural tube (NT) formation in the spinal region of the m
260 level morphogenetic movements that shape the neural tube (NT), the precursor of the brain and spinal
261                   When transplanted into the neural tube of developing chick embryos, iPSCMNs selecti
262 e' that remodels to the lateral edges of the neural tube-paraxial mesoderm interfaces where shear str
263 l morphogens can be maintained, resulting in neural tube patterning analogous to that observed in viv
264 2 protein expression is downregulated during neural tube patterning and adaptation continues when the
265 pment requires a tight orchestration between neural tube patterning and growth.
266 . (2016) tackle this issue in the context of neural tube patterning, discovering that differential se
267 in), similar to that operating in vertebrate neural tube patterning, functions to distinguish cell fa
268 ecies that differ in size during the time of neural tube patterning.
269  how the duration of Shh signaling regulates neural tube patterning.
270  three key ventral determinants in mammalian neural tube patterning: Nkx2.2, Nkx6.1 and Olig2.
271 r, Wnt1(Cre2SOR) mutants had an open cranial neural tube phenotype that was not evident in Wnt1(Cre)
272 l lethality and SHH-related abnormal ventral neural tube phenotypes.
273 s per multiciliated cell, and the numbers of neural tube primary cilia; it also led to abnormal devel
274 s a transcription factor essential in dorsal neural tube progenitors for specification of these inhib
275 echanisms that position motor neurons in the neural tube remain poorly understood.
276                  Formation of the vertebrate neural tube represents one of the premier examples of mo
277                         Failure to close the neural tube results in birth defects, with severity rang
278 eased Hedgehog signaling and completely open neural tubes showing co-expansion of all ventral neuropr
279                               In the ventral neural tube, sonic hedgehog (Shh) signaling, together wi
280 ly, PRDM13 also ensures a battery of ventral neural tube specification genes such as Olig1, Olig2 and
281 orsal midline Bmp signaling to drop at early neural tube stages.
282 es is the unique presence of a dorsal hollow neural tube that forms by internalization of the ectoder
283 ctional complexes.SIGNIFICANCE STATEMENT The neural tube, the CNS precursor, is shaped during neurula
284 ory along the anterior-posterior axis of the neural tube, the mechanisms establishing the cerebellar
285                            In the vertebrate neural tube, the morphogen Sonic Hedgehog (Shh) establis
286                         After closure of the neural tube, these cells undergo an epithelial-to-mesenc
287 ry showed strong expression of hFOXA2 in the neural tube, third ventricle, diencephalon and pancreas.
288  that Inpp5e attenuates Shh signaling in the neural tube through regulation of the relative timing of
289  of the vertebrate trunk but predisposes the neural tube to convergence defects that lead to spina bi
290 wo mechanisms are combined in the vertebrate neural tube to increase the range of cell types and deli
291 neural crest cells (crNCCs) migrate from the neural tube to the pharyngeal arches (PAs) of the develo
292 racellular matrix of Fibronectin adheres the neural tube to the two flanking columns of paraxial meso
293 rvous system migrate ventrally away from the neural tube toward and along the primitive gut.
294 l targets genome-wide in the embryonic mouse neural tube using ChIP-Seq and RNA-Seq.
295  of Sox2 or Pax7 alters the apportionment of neural tube versus neural crest fates.
296 e border, and subsequent emigration from the neural tube via canonical Wnt signaling.
297 on affect cell arrangement and growth of the neural tube, we used experimental measurements to develo
298  sonic hedgehog, and Notch) that pattern the neural tube were sequentially perturbed to identify an o
299 to anteriorize 5 Hoxa gene expression in the neural tube when inserted into a HoxA BAC reporter.
300 ronal lineages when they delaminate from the neural tube, whereas cranial neural crest cells acquire

 
Page Top