ライフサイエンスコーパス: neural fold

1 (Xcad-11) as they begin to emigrate from the neural fold.

2 -reaching, rapid separation of the elevating neural folds.

3 band of ectoderm contiguous to the midbrain neural folds.

4 lls to form one layer; and (4) fusion of the neural folds.

5 eural-crest cells migrating from the cranial neural folds.

6 g of AJ proteins was increased in the mutant neural folds.

7 tial during neurulation for elevation of the neural folds.

8 (JmjD2A/KDM4A), is expressed in the forming neural folds.

9 h the ligand PDGFD expressed in the midbrain neural folds.

10 t of neurulation through wide spacing of the neural folds.

11 hesion within the embryonic neural plate and neural folds.

12 dependent mechanical forces operating during neural folding.

13 y to reduce the distance between the nascent neural folds, allowing them to meet and fuse.

14 is derived from the nonneural ectoderm, the neural folds also contribute cells to the placode at lea

15 stage embryos, and blocking Smurf1 disturbs neural folding and neural, but not mesoderm differentiat

16 in regions of newly formed cranial and trunk neural folds and adjacent neural crest migratory pathway

17 rthermore, the mitotic index was elevated in neural folds and hindgut of treated embryos, consistent

18 rest cells (CNCCs) delaminate from embryonic neural folds and migrate to pharyngeal arches, which giv

19 r Pax7 by stage 4 + and later contributes to neural folds and migrating neural crest.

20 ls in the neural ectoderm shape and form the neural folds and neural tube.

21 ed PPP1R12A expression in the prosencephalic neural folds and protein localization in the lower urina

22 or Id2 is expressed in cranial but not trunk neural folds and subsequently in some migrating cranial

23 esoderm migration in elevation of the caudal neural folds and successful closure of the caudal neural

24 ain proper cell-cell interactions within the neural folds and suggest that NFPC and TAF1 participate

25 istinct SRF expression was seen later in the neural folds and the somites by HH stage 8.

26 but also for maintenance of integrity of the neural folds and tube, via correct formation of the apic

27 Noggin is expressed dorsally in the closing neural folds and ventrally in the notochord and somites.

28 is enriched in the anterior neural plate and neural folds, and depletion of MIM specifically inhibits

29 Subsequently, gtpbp2 is expressed in the neural folds, and in early tadpoles undergoing organogen

30 TDs), with the NTDs being caused by abnormal neural fold apposition and fusion.

31 e have focused on the final step wherein the neural folds approach one another and seal to form the c

32 ow that the NC cells induced at the anterior neural fold are able to migrate and differentiate as nor

33 emonstrate that: (i) progenitor cells in the neural folds are multipotent, having the ability to form

34 atterning and reshaping of the broad cranial neural folds are poorly understood.

35 erate neural crest cells when the endogenous neural folds are removed, probably via interaction of th

36 eventing the formation of NC in the anterior neural folds as loss-of-function experiments using a Dkk

37 crest formation, Shh or Noggin were added to neural folds at defined times in culture.

38 hat Cnot1 is expressed in the prosencephalic neural folds at gestational day 8.25 during the critical

39 lation of stem cells derived from the dorsal neural folds at the border between neural and non-neural

40 urulation is completed when the dorsolateral neural folds bend inwards, their tips make adhesive cont

41 and that the local release of Bmp2 inhibits neural fold bending.

42 be closure, and Irf6 is involved in defining neural fold borders by restricting AP2alpha expression.

43 Id2 is also expressed in Xenopus neural folds, branchial arches, cardiac outflow tract, i

44 This is compatible with apposition of the neural folds but not with progression of closure, unless

45 rm and in a restricted group of cells in the neural folds, but was largely absent from the neural pla

46 We suggest that the inherent movement of the neural folds can accomplish only a finite amount of medi

47 d that individual precursor cells within the neural folds can give rise to epidermal, neural crest, a

48 eis1 in several areas, including the lateral neural folds, caudal branchial arch, hindbrain, and opti

49 letion of MIM specifically inhibits anterior neural fold closure without affecting convergent extensi

50 retinoic acid (RA), starting at the time of neural fold closure, blocks expression of myocardial dif

51 nt extension movements, tissue separation or neural fold closure.

52 p antagonist noggin is expressed dorsally in neural folds containing DLHPs, noggin-null embryos show

53 In vivo chromatin immunoprecipitation of neural folds demonstrates that DNMT3A specifically assoc

54 isplays restricted expression to the lateral neural folds, developing lens, retina, limb, and CNS.

55 However, the neural folds do not fuse with one another, and the deep

56 nd SMC1A are expressed in the prosencephalic neural folds during primary neurulation in the mouse, co

57 te ribosomal RNA production in the prefusion neural folds during the early stages of embryogenesis.

58 ural crest cells are induced in chick as the neural folds elevate, recent data suggest that they are

59 presumptive cardiac crest at stage 7, as the neural folds elevate, results in reformation of migratin

60 rticularly, we find that MIM is required for neural fold elevation and apical constriction along with

61 Here we report that neural fold elevation during mouse spinal neurulation is

62 show that Xdsh signaling is not required for neural fold elevation, medial movement or fusion.

63 rgo synchronous apical constriction, driving neural fold elevation.

64 grating neural crest cells begin to exit the neural fold/epidermal ectoderm boundary, we examined the

65 Conversely, neural folds exposed to laminin alpha5 in vitro show a r

66 Cells from the juxtaposed neural folds extend long and short flexible extensions a

67 regeneration by NC precursors, we find that neural fold extirpation results in a loss of NC precurso

68 ibronectin-rich basement membrane, where the neural folds first contact each other.

69 A neural trough forms, and neural folds form and approach one another.

70 Although bilateral neural folds form, they are abnormally far apart and can

71 reduction in the number of somites, abnormal neural fold formation and a greatly increased degree of

72 arly intense expression at the apices of the neural folds from which the neural crest arises.

73 movements and prospective cell identities as neural folds fuse during neural tube formation in Xenopu

74 racterized GPCR-ligand pathway necessary for neural fold fusion and lens development, providing insig

75 n of medially directed cell migration during neural fold fusion and re-establishment of the neural tu

76 expressed far lateral to the medial site of neural fold fusion and that expression moves medially af

77 For example, failure of neural fold fusion during neurulation leads to open neur

78 After neural fold fusion, lateral deep neural cells move media

79 ression of these deep cell behaviors and for neural fold fusion.

80 tebrate neural crest cells, derived from the neural folds, generate a variety of tissues, such as car

81 tage 11.5 induces the endogenous eIF4AII and neural fold genes within 40 minutes.

82 we demonstrate that the Retina and anterior neural fold homeobox (Rax) gene plays a key role in esta

83 We observed that the retina and anterior neural fold homeobox transcription factor (Rax) is selec

84 ovel homeobox gene, rax (retina and anterior neural fold homeobox), whose expression pattern suggests

85 ing embryo were observed at the edges of the neural folds immediately prior to fusion, and also in th

86 expressed in the dorsal neural ectoderm and neural folds in the region where primary sensory neurons

87 use embryo, rax is expressed in the anterior neural fold, including areas that will give rise to the

88 ely large region of ectoderm adjacent to the neural folds, intermingled both with each other and with

89 k1-null mouse embryos transform the anterior neural fold into NC.

90 port the notion that posteriorization of the neural folds is an essential step in NC specification.

91 a concomitant increase of E-cadherin in the neural folds, likely leading to delayed and decreased ne

92 oper organization of the cells in the dorsal neural folds, manifested by a loss in the columnar epith

93 mation of border-like cells that express the neural fold markers MSX1 and BMP4 and the preplacodal re

94 ses loss of animal cell adhesion or delay in neural fold morphogenesis, respectively, without signifi

95 tion is designated shroom (shrm) because the neural folds "mushroom" outward and do not converge at t

96 on of cadherin6B and FoxD3 expression in the neural folds/neural tube, leading to premature neural cr

97 border (NPB), which is later elevated as the neural folds (NFs) form and fuse in the dorsal region of

98 cted as a dorsal stripe of expression in the neural folds of embryos at day 8.5 postcoitum (p.c.).

99 gene targeting of beta-catenin in the dorsal neural folds of mouse embryos represses the expression o

100 Here we unveil a new role for this gene in neural fold patterning.

101 Initially localized to the dorsal neural folds, premigratory neural crest cells undergo an

102 apical constriction in the lateral midbrain neural folds prior to closure.

103 l shape changes and diminished resistance to neural fold recoil upon ablation of the closure point.

104 neural crest cells for a limited time after neural fold removal.

105 ral-tube closure defect with ruffling of the neural fold ridges, a yolk sac erythropoietic failure, a

106 of this new closure initiation point causes neural fold separation, demonstrating its biomechanical

107 -actin or laser ablation of the cable causes neural fold separation.

108 we demonstrate that Gbx2 is upstream of the neural fold specifiers Pax3 and Msx1.

109 red-end dataset derived from alcohol-exposed neural fold-stage chick crania, wherein alcohol causes f

110 luding the notochord and is specified during neural fold stages in Xenopus laevis.

111 ons of Cnbp(-/-) embryos at gastrulation and neural-fold stages.

112 down the elongating spinal axis, uniting the neural fold tips in the dorsal midline.

113 cell protrusions emanating from the apposed neural fold tips, at the interface between the neuroepit

114 ch includes an actin cable running along the neural fold tips.

115 y contributes to an inability of the cranial neural folds to move toward the midline and results in N

116 , driving the zipper forward and drawing the neural folds together.

117 ural ectoderm cells on opposing sides of the neural folds undergo a dramatic change in shape to protr

118 Proliferation in cranial neural folds was reduced in homozygous Lrp6(-/-) mutants

119 from different axial levels to the anterior neural fold, we found that competence is initially broad

120 airs signaling, neural crest development and neural folding, whereas TRAF4 overexpression boosts sign

121 crest, including an "intermediate region" of neural folds which has never previously been tested for

122 in the levels of apoptosis in the prefusion neural folds, which are the site of the highest levels o

123 begins as the neural plate bends to form the neural folds, which meet and adhere to close the neural

124 ranial neural tissue that are independent of neural fold zipping.