ライフサイエンスコーパス: foliation

1 cial function of BG in organizing cerebellar foliation.

2 e cell progenitors (GCP) regulate cerebellar foliation.

3 of lobules that arises during the process of foliation.

4 required in Bergmann glia during cerebellar foliation.

5 rved normal cerebellar anlage patterning and foliation.

6 tionally required to pattern anterior vermis foliation.

7 duced in size and exhibits defects in vermal foliation.

8 kness of the granule cell layer and abnormal foliation.

9 ebrinII/AldolaseC) independent of regulating foliation.

10 itical for patterning PC gene expression and foliation.

11 ting in smaller cerebella that are devoid of foliation.

12 signaling regulates the extent of cerebellar foliation.

13 escues GNP cell proliferation and cerebellar foliation.

14 edial posterior transverse migrations during foliation.

15 ion correlates spatially and temporally with foliation.

16 n in vivo, and tested whether they influence foliation.

17 displayed an abnormal pattern of cerebellar foliation.

18 in the cerebellum, which is small and lacks foliation.

19 ck cortical laminar structure and cerebellar foliation.

20 tical surface in vivo is impeded by its high foliation.

21 was associated with reduction in cerebellar foliation.

22 how the fracture would propagate relative to foliations.

23 or control (cerebellum) is small and lacking foliation, a characteristic not yet described for any ot

24 Yet, little is known about how foliation, a process involving large-scale and simultane

25 enes caused severe cerebellar hypoplasia and foliation abnormalities, primarily attributable to a fai

26 Unlike the foliation abnormalities, the M/L pattern disturbances we

27 Furthermore, En1/En2 continue to regulate foliation after embryonic day 14, at which time Fgf8 ist

28 n anterior region in which there is abnormal foliation, agranularity, and Purkinje cell (PC) ectopia.

29 entation of olivine crystals defining a weak foliation and a well-defined lattice-preferred orientati

30 aberrant proliferation and migration induce foliation and circuit defects.

31 bsequent disruptions in postnatal cerebellar foliation and lamination.

32 d the mouse model showed aberrant cerebellar foliation and severely impaired sensorimotor learning.

33 ndent mechanisms that use En1/2 must pattern foliation and spatial gene expression separately.

34 ans of alleviating these stresses are tectal foliation and the formation of pial holes.

35 o image the cerebellar cortex, including its foliations and lamination, in less than 20 minutes, reco

36 ormal neuronal migration, lack of cerebellar foliation, and chromatolytic changes of neurons in the b

37 granule neuron progenitors (GNPs), perturbs foliation, and leads to reduced cerebellar mass.

38 gmann glia-basement membrane adhesion during foliation, and provide new insights into the signaling p

39 uclei; produced defects in the patterning of foliation; and also affected litter size, body weight, a

40 Defects in cerebellar foliation are associated with a number of diseases.

41 of BG generation and its role in cerebellar foliation are less understood.

42 ll mice, which include attenuated cerebellar foliation as well as defective radial migration and incr

43 erebellum, Gli2 mutants have greatly reduced foliation at birth and a decrease in GCPs.

44 ome of which have a strong layering-parallel foliation, confirm a long-held belief that such rocks ar

45 General deficiency of CerS1 in mice caused a foliation defect, progressive shrinkage, and neuronal ap

46 nt, mutant cerebellar hemispheres had severe foliation defects and inferior lobe malformation, charac

47 ing Cxcr4 hyperactivation-show developmental foliation defects of the cerebellum correlating with sen

48 c4 in mice produces both cerebellar size and foliation defects similar to human DWM, confirming a req

49 ectural abnormalities, including hypoplasia, foliation defects, and Purkinje cell ectopia.

50 (Atoh1(S193A/lacZ)) exhibit mild cerebellar foliation defects, motor impairments, partial pontine nu

51 haracterised by cerebellar developmental and foliation defects.

52 s hypomorphs have CVH with medial fusion and foliation defects.

53 nts are viable with a smaller cerebellum and foliation defects.

54 xhibit granule cell ectopia concomitant with foliation defects.

55 ocampal abnormalities, absence of cerebellar foliation, disorganization of cortical neurons, and leth

56 cular mechanisms of neuronal positioning and foliation during cerebellar development.

57 in vitro, it is possible that Shh influences foliation during cerebellum development by regulating th

58 we show that listvenites with a penetrative foliation have abundant microstructures indicating that

59 h the En genes control cerebellar growth and foliation in distinct cell types.

60 ly restricted gene expression occur prior to foliation in mutants, and foliation is altered from the

61 c features such as compositional banding and foliation in rocks that are reacting or dissolving while

62 ive MEK1 rescues BG formation and cerebellar foliation in Shp2-deficient cerebella.

63 The cerebellum has evolved elaborate foliation in the amniote lineage as a consequence of ext

64 of cortical layers and absence of cerebellar foliation in these animals precisely mimic the phenotype

65 ion occur prior to foliation in mutants, and foliation is altered from the onset and is accompanied b

66 receptor smoothened, we found the extent of foliation is gradually reduced, and that this correlates

67 A crucial factor underlying foliation is the generation of granule cells (gcs), the

68 more, cerebellar cortical development (size, foliation, layering, cell number, and position), which p

69 arkably, in En1/2 mutants with almost normal foliation, ML molecular code patterning is severely disr

70 Foliation not only increases surface area, but may also

71 d in the disruption of the normal process of foliation of the cerebellar cortex and the alteration of

72 ositioning, lamination of the neocortex, and foliation of the cerebellum.

73 Foliation of the mouse cerebellum occurs primarily durin

74 nitors leads to strong defects in growth and foliation owing to its crucial role in the differentiati

75 m and spinal cord tracts; reduced cerebellar foliation, patchy loss of Purkinje cells, multifocal thi

76 normality, we found a profound change in the foliation pattern of the cerebellum.

77 s in cerebellar growth and the rostro-caudal foliation pattern reflect a reduced granule neuron popul

78 rmal domain does not grossly alter the basic foliation pattern, but does lead to prolonged proliferat

79 t, but primarily for defining the cerebellar foliation pattern.

80 al layers, and defects in the rostral-caudal foliation pattern.

81 istinct medial vermis and lateral hemisphere foliation patterns in mammalian cerebella.

82 ion direction and (010) perpendicular to the foliation plane define a B-type LPO.

83 stal directions parallel to the trace of the foliation plane in thin section.

84 In addition, cerebellar foliation reflects both absolute and relative cerebellar

85 reveal that the abnormal anterior cerebellar foliation results from local disruptions of the basement

86 - cerebellum revealed gross abnormalities in foliation; specifically, lobule VII in the anterior verm

87 hat are fundamental to patterning cerebellum foliation throughout the mediolateral axis and that act

88 The complexity of cerebellar foliation varies greatly between vertebrate species.

89 ernal granule layer thickness and defects in foliation were seen in embryonic and new-born LGI1 knock

90 e during late embryogenesis, at the onset of foliation, when ric-8a mutant Bergmann glia fail to main

91 sible for regional differences in cerebellum foliation, which interestingly are accompanied by region

92 tion, the rat model shows reduced cerebellar foliation, which is not observed in DS mouse models.

93 expansion, resulting in abnormal post-natal foliation, while deregulated transcriptional programs co