ライフサイエンスコーパス: reeler

1 several neuroanatomic defects reminiscent of reeler.

2 cribed that exhibit a phenotype identical to reeler.

3 al lamination that is indistinguishable from reeler.

4 scrambler cerebellum is identical to that of reeler.

5 te abnormally toward the central canal as in reeler.

6 (embryonic day [E]9.5-E12.5) was similar to reeler.

7 ogical abnormalities of migrating neurons in Reeler.

8 the location of SPN is identical to that of reeler.

9 tributing to the abnormal position of SPN in reeler.

10 normal SPN migration similar to that seen in reeler.

11 d behavioral abnormalities characteristic of reeler.

12 In reeler, 80% of SPN migrated dorsomedially to cluster aro

13 d-type SPNs were found laterally, whereas in reeler, 92% of these neurons were positioned medially.

14 nt SPN location that is identical to that of reeler and dab1-null mice.

15 the cdk5(-/-) phenotype to that reported in reeler and mdab-1(-/-) (scrambler/yotari) mutant brains,

16 tructures throughout the brain and ataxia in reeler and scrambler mice.

17 NADPH diaphorase were studied in E12.5-E17.5 reeler and wild-type embryos, and their final locations

18 ted HNSCs into the lateral ventricle of null reeler and wild-type mice.

19 At E13.5, both reeler and wild-type PPNs were found laterally, but by E

20 Initially reeler and wild-type SPNs were detected laterally near s

21 studies on neurological mutant mice, such as reeler, and human brain malformations.

22 However, in the reeler background, ectopic Reelin induced tyrosine phosp

23 idline raphe structure in both scrambler and reeler cerebellum that is not present in wild-type mice.

24 The reeler cortex has been described as a rough laminar inve

25 The reeler cortex is disrupted in a more complex fashion, wi

26 liest structural abnormalities detectable in reeler cortex, suggesting that this step is important fo

27 t is similar to that previously described in reeler cortex.

28 Application of Reelin protein to reeler cortices destabilized tangential neurites while s

29 In reeler cortices that lack the secreted glycoprotein Reel

30 of recombinant Reelin rescued the deficit in reeler cultures.

31 reelin (Reln), the gene responsible for the reeler defect.

32 The neurological mouse mutant strain reeler displays abnormal laminar organization of several

33 pixr, encoding a secreted gut protein with a Reeler domain.

34 In utero electroporation of L1-80 into reeler embryos normalised the migration of cortical neur

35 malised the migration of cortical neurons in reeler embryos.

36 es to the histoarchitectural division of the reeler entorhinal cortex into an external and an interna

37 Mutation of the reeler gene (Reln) disrupts neuronal migration in severa

38 s a mutation in the same gene pathway as the reeler gene (Relnrl) and is most likely downstream of Re

39 The reeler gene encodes a large protein, termed Reelin, that

40 e recent observation that the product of the reeler gene is an ECM-like protein that is expressed by

41 The product of the reeler gene, Reelin, is a secreted protein that has been

42 The neurological mutant mouse reeler has played a critical role in the evolution of ou

43 als displayed the major anatomic features of reeler including, cerebellar hypofoliation, failure of P

44 ells do not aggregate within the preplate in reeler; instead, preplate cells remain as an undivided s

45 large extracellular matrix protein absent in reeler, is found in wild-type neurons bordering both gro

46 From the earliest neuroanatomic studies of reeler, it was anticipated that the characterization of

47 s highly disorganized cortical lamination in reeler, led to spectacular compensatory remodeling of th

48 However, unlike reeler, levels of reelin in the C3G(gt)/(gt) spinal cord

49 d decreased levels of Reelin, resulting in a reeler-like cortical migration disorder.

50 ospinal neurons and, independent of Fezf2, a reeler-like inversion of layers.

51 Heterozygous reeler mice (HRM) haploinsufficient for reelin express a

52 ative study in the cerebella of heterozygous reeler mice (HRM), in which reelin expression is down-re

53 e disrupted cortical lamination phenotype in reeler mice and subsequent identification of the Reelin

54 Surprisingly, network activity in reeler mice displays similar characteristics and pharmac

55 te abnormalities are present in the brain of reeler mice lacking Reelin.

56 ding that the brains of developing and adult reeler mice of both sexes contained a markedly reduced n

57 isease phenotypes of the spastic and Orleans reeler mice respectively.

58 Heterozygous reeler mice that exhibit a 50% downregulation of reelin

59 In both normal and reeler mice the period of neurogenesis of SPN was simila

60 r initial migration, SPN in both control and reeler mice were closely apposed to radial glial fibers

61 ld be inverted in hem-ablated animals, as in reeler mice, deficient in reelin signaling.

62 In reeler mice, most of the injected HNSCs failed to migrat

63 yonic and postnatal layer 1 in wild-type and reeler mice, mutant in the production of reelin.

64 the extracellular matrix protein missing in reeler mice, plays an important role in neuronal migrati

65 In heterozygous reeler mice, reelin bound to DSPSD, and the expression o

66 reelin and GAD67 in both WT and heterozygous reeler mice, suggesting an epigenetic action through the

67 In reeler mice, the endogenous NSC population in the hippoc

68 rons migrated and differentiated normally in reeler mice, the migrations of both sympathetic (SPNs) a

69 This callosal phenotype is not detected in reeler mice, which also exhibit defects in cortical lami

70 rent from both wild-type mice and homozygous reeler mice.

71 ruption of cell positioning in the retina of reeler mice.

72 a developmental event that fails to occur in reeler mice.

73 lacement of neurons and associated ataxia in reeler mice.

74 ssed in normal mouse brain that is absent in reeler mice.

75 basal forebrain markers Dlx1/2 in normal and reeler mice.

76 ese interneurons is not generally altered in reeler mice.

77 ially overlap with those of Reelin-deficient reeler mice.

78 elin, and radial glial fibers in control and reeler mice.

79 oth control (wild-type and heterozygous) and reeler mice.

80 and GAD67 mRNAs in both WT and heterozygous reeler mice.

81 transplanted HNSCs in wild-type, but not in reeler mice.

82 Reelin-deficient (Reeler) mice exhibited impaired respones to hypoxia comp

83 In contrast, the majority of SPN in reeler migrated in the same orientation as radial glial

84 did show a pattern of chain migration in the reeler mouse cortex.

85 own model for studying corticogenesis is the reeler mouse model.

86 LCH parallels the reeler mouse mutant (Reln(rl)), in which Reln mutations

87 features of abnormal patterning in the male reeler mouse not obvious with less specific markers or h

88 nalyzed the endogenous NSC population in the reeler mouse using bromodeoxyuridine injections.

89 the receptive field properties of neurons in reeler mouse visual cortex and the surprising conclusion

90 irst identified as the gene disrupted in the reeler mouse, a classic neurological mutant exhibiting a

91 tical malformation distinct from that of the reeler mouse, double cortex syndrome, and periventricula

92 se, which is phenotypically identical to the reeler mouse, is due to a mutation in the disabled-1 gen

93 t is indistinguishable from that seen in the reeler mouse.

94 ant phenotype is very similar to that of the reeler mouse.

95 cts of inside-out lamination, defects in the Reeler mutant and results of recent genetic and in utero

96 with Dab1 from brain extracts of normal and reeler mutant mice lacking Reelin, and from cell-free ex

97 signatures of connectivity are maintained in reeler mutant mice, in which neural positioning is scram

98 In reeler mutant mice, loss of Reelin protein is associated

99 In reeler mutant mice, Tbr2+ UBCs accumulated near the rhom

100 In reeler mutant mice, we show that GINs migrate normally i

101 In reeler mutant mice, which have a severe cerebellar malfo

102 cal axonal tracing in the same wild-type and reeler mutant mice.

103 ring embryonic development that is absent in reeler mutant mice.

104 We have analyzed this process in the reeler mutant mouse, in which cortical lamination is sev

105 neocortical development suggest that, in the reeler mutant mouse, the lack of the protein Reelin resu

106 logenetically older archicortex of the adult reeler mutant mouse, we studied the expression of 11 dif

107 its such as ataxic gait and trembling in the reeler mutant mouse.

108 ression of the cadherins is preserved in the reeler mutant mouse.

109 ish models for the cortical inversion in the reeler mutant mouse.

110 c neurons are known to migrate abnormally in reeler mutant spinal cord.

111 but not identical to those seen in the mouse reeler mutant, suggesting similar underlying development

112 In the archicortex of the reeler mutant, the cadherin-expressing cell layers are d

113 However, unlike the reeler mutant, where 5% of the Purkinje cells migrate su

114 (SPN) in the spinal cord is affected in the reeler mutant.

115 deep to the cerebellar cortex as seen in the reeler mutant.

116 ze the locomotor behavior of severely ataxic reeler mutants and compare and contrast it with that of

117 the receptor double knock-out mice resemble reeler mutants, we infer that Reln(CTRdel)/Apoer2(null)

118 homozygotes have phenotypes akin to those of reeler mutants, while Reln(CTRdel)/Vldlr(null) mice do n

119 mine whether their positions were altered in reeler mutants.

120 The reeler mutation in mice produces an especially well char

121 Adult mice heterozygous for the 'reeler' mutation (HR mice) have been found not to have a

122 Satb2 and Reeler mutations that shifted neuronal post-mitotic deve

123 For these reeler neurons, the tangential oriented primary neurites

124 s in cell position become apparent in either reeler or scrambler.

125 ived Reelin compensates some features of the reeler phenotype and is needed for the fine tuning of th

126 tion (HR mice) have been found not to have a reeler phenotype but to express a number of abnormal tra

127 , homozygous mutations in Reln result in the reeler phenotype, characterized by ataxia and disrupted

128 Tyr(200), Tyr(220), and Tyr(232)) exhibit a reeler phenotype, implying that tyrosine phosphorylation

129 SPN migration in crkl(-/-) showed a partial reeler phenotype, suggesting a partial loss of response

130 isolated and identified as the cause of the reeler phenotype.

131 neurons, and its absence causes the classic "Reeler" phenotype.

132 Lack of reelin causes the 'reeler' phenotype in mice and autosomal recessive lissen

133 ype PPNs were found laterally, but by E14.5, reeler PPNs were scattered across the intermediate spina

134 The gene mutated in reeler (reelin) encodes a protein secreted by neurons in

135 Reeler (rl/rl) and reeler/wild-type (+/rl) mice synthesi

136 s were not detectable in serum of homozygous reeler (rl/rl) mice.

137 he disease, the authors trained heterozygous reeler (+/rl) mice on a series of visual discriminations

138 The similar phenotypes of reeler, scrambler, yotari and mdab1 null mice indicate t

139 ar somatic motor neurons, but by E13.5, many reeler SPNs had mismigrated medially.

140 displays remarkably distinct phenotypes from reeler The mutant does not have an inverted cortex, but

141 In reeler, the major populations of displaced neurons conta

142 SPNs in reeler (which lacks reelin), and in mice deficient in co

143 In reeler, which lacks Reelin, SPN also undergo primary mig

144 Reeler (rl/rl) and reeler/wild-type (+/rl) mice synthesize Reln at subnorma

145 incipal neurons, requires Reelin, we crossed reeler with transgenic mice that contain Green Fluoresce