ライフサイエンスコーパス: apicobasal

1 paper by Monier et al. (2015) identifies an apicobasal actomyosin cable that characterizes apoptotic

2 Thus, PAR proteins function in both apicobasal and anterior-posterior asymmetry during the f

3 asal bodies are mispositioned along both the apicobasal and planar polarity axes of mutant hair cells

4 in this process is independent of canonical apicobasal and planar polarity pathways.

5 or-posterior polarity, but showed defects in apicobasal asymmetries associated with gastrulation.

6 a, where orientation of the spindle into the apicobasal axis of polarised blastomeres generates inner

7 inct classes of dynamic protrusion along the apicobasal axis of the cell.

8 al array into a network positioned along the apicobasal axis of the cell.

9 lane of the epithelium, perpendicular to the apicobasal axis of the cell.

10 ct to both the AP axis of the embryo and the apicobasal axis of the notochord plate.

11 roliferation, their nuclei migrate along the apicobasal axis of the retina in phase with the cell cyc

12 lasts undergo asymmetric divisions along the apicobasal axis to produce two daughter cells of unequal

13 degrees change in alignment relative to the apicobasal axis, loss of centrosomal attachment, and api

14 be transition, cells are polarized along the apicobasal axis.

15 cell alignment, oriented cell division, and apicobasal cell elongation.

16 of aligned arrays of microtubules that drive apicobasal cell elongation.

17 Neural tube closure, for instance, involves apicobasal cell heightening, apical constriction at hing

18 Apicobasal cell polarity is crucial for morphogenesis of

19 deficient for Llgl1, a protein implicated in apicobasal cell polarity, asymmetric cell division, cell

20 is selectively involved in establishment of apicobasal cell polarity.

21 s, is bipolar migration directed towards the apicobasal centre of the retina.

22 n by microtubule- and actinomyosin-dependent apicobasal elongation, rather than by progressive epithe

23 uently, Notch signaling-dependent changes in apicobasal epithelial thickness drive elongation of thes

24 rols lost 24%, 33%, and 41% of peak systolic apicobasal force, respectively, whereas experimental hea

25 eins are provided maternally, distinguishing apicobasal from earlier anterior-posterior functions req

26 se or modify Rac activity, we demonstrate an apicobasal gradient of Rac activity that is required to

27 In controls, there was a left ventricular apicobasal gradient, with the shortest repolarization ti

28 Apicobasal gradients in repolarization time, with shorte

29 F-actin depolymerization disrupted both the apicobasal-like polarity and the diffusion barriers with

30 Large clones show defects in apicobasal membrane polarity, but small clones induced l

31 a PAR-1 regulates the density, stability and apicobasal organisation of microtubules.

32 inin1, and ectopic Laminin1 can redirect the apicobasal orientation of eye field cells.

33 s mutations, disrupted colon epithelial cell apicobasal polarity and adhesion to collagen I and lamin

34 , we show that presumptive eye cells acquire apicobasal polarity and adopt neuroepithelial character

35 nsition (EMT), whereby epithelial cells lose apicobasal polarity and cell-cell contacts, and gain mes

36 e maintenance of proper architecture through apicobasal polarity and cell-cell contacts.

37 Spheroids develop apicobasal polarity and complete lumens, and they are co

38 TEBs exhibit reduced apicobasal polarity and extensive proliferation.

39 ponents of basement membrane, HPPL developed apicobasal polarity and formed cysts, which had luminal

40 matrix, cholangiocytes developed epithelial/apicobasal polarity and formed functional cysts and bili

41 gest that MALS-3 plays a role in maintaining apicobasal polarity and is required for normal neurogene

42 alian epithelial cells and are important for apicobasal polarity and junction formation.

43 ECM protease degradability was required for apicobasal polarity and lumen formation.

44 hesive ligand density dramatically regulated apicobasal polarity and lumenogenesis independently of c

45 ells, modified to include the effects of the apicobasal polarity and natural curvature of epithelia.

46 -mediated DNA methylation in controlling RPE apicobasal polarity and neural retina differentiation.

47 sis-dependent pathways, resulting in loss of apicobasal polarity and relocation of abluminal CXCL12 t

48 gs provide a direct mechanistic link between apicobasal polarity and the cell cycle, which may explai

49 ex has been implicated in the development of apicobasal polarity and the formation of tight junctions

50 uishing feature of epithelial cells is their apicobasal polarity and the presence of apical junctions

51 gates the ability of VE-cadherin to regulate apicobasal polarity and vascular lumen formation.

52 tif at the C-terminus of VE-cadherin impairs apicobasal polarity and vascular lumen formation.

53 Interestingly, crb function in maintaining apicobasal polarity appears largely dispensable in prima

54 As stratification and loss of apicobasal polarity are early hallmarks of cancer, we ne

55 hogenesis involves sequential acquisition of apicobasal polarity by epithelial cells and development

56 ts with the Par6/Par3/aPKC and Scrib/Dlg/Lgl apicobasal polarity complexes.

57 regulation, as well as with epithelial cell apicobasal polarity establishment/maintenance.

58 Altered expression of apicobasal polarity factors is associated with cancer in

59 Mutation of different apicobasal polarity genes activates c-Jun N-terminal kin

60 te junctions and is required for maintaining apicobasal polarity in Drosophila epithelium.

61 ic interaction between aPKC and Lgl2 defines apicobasal polarity in early vertebrate development.

62 tardust mutants exhibit severe disruption in apicobasal polarity in embryonic epithelia, resulting in

63 umbs, Par, and Scribble complexes, establish apicobasal polarity in epithelial cells, and interferenc

64 ons, and functions as a major determinant of apicobasal polarity in retinal radial glia.

65 ilure to down-regulate Dystroglycan disrupts apicobasal polarity in the PFC, which includes mislocali

66 However, it remains unclear how apicobasal polarity is regulated to meet the opposing ne

67 e, we show that N-Cad/ZO-1 complex-initiated apicobasal polarity is stabilized by the late-onsetting

68 ibution of signaling complexes essential for apicobasal polarity may constitute a critical event in t

69 nascent pharyngeal lumen by reorientation of apicobasal polarity of anterior pharyngeal cells ("Reori

70 The apicobasal polarity of epithelial cells is critical for

71 localization and function in controlling the apicobasal polarity of epithelial cells.

72 l localization of membrane proteins, and for apicobasal polarity of epithelial cells.

73 lantation failure associated with heightened apicobasal polarity of luminal epithelial cells during t

74 a poorly characterized reorientation of the apicobasal polarity of static epithelial cells into the

75 m patient biopsies displayed an inversion of apicobasal polarity of the epithelial cells that was nor

76 thout disrupting the fluid-tight barrier and apicobasal polarity of the epithelium.

77 ll-to-cell contacts and the establishment of apicobasal polarity of vascular endothelial cells.

78 Our data suggest that stepwise maturation of apicobasal polarity plays an essential role in vertebrat

79 Apicobasal polarity plays an important role in regulatin

80 develop excess layers of cells with altered apicobasal polarity reminiscent of dysplasia, suggesting

81 We demonstrate that during photoreceptor apicobasal polarity remodeling, Crb is required to exclu

82 We have built a computer model of apicobasal polarity that suggests that the combination o

83 y of apical transmembrane proteins regulates apicobasal polarity via protein interactions with a cons

84 different cell types, the epithelial cells (apicobasal polarity) and the oocyte (anteroposterior pol

85 role in the establishment and maintenance of apicobasal polarity, a cellular characteristic essential

86 with disruption of tight junction formation, apicobasal polarity, and contact-inhibited growth.

87 standing of the regulation of proliferation, apicobasal polarity, and epithelial motility during bran

88 cal domain, but does not result in a loss of apicobasal polarity, as would be predicted from current

89 epithelia deficient for Llgl1 retained overt apicobasal polarity, but had expanded apical domains.

90 omplex and is important in the definition of apicobasal polarity, but the localisation and function o

91 r, SMGs from Nfib (-/-) mice at E18.5 showed apicobasal polarity, but they were disorganized and lost

92 ficiency include abnormalities of enterocyte apicobasal polarity, increased apoptosis of intestinal c

93 n kinase C (aPKC), a protein associated with apicobasal polarity, is specifically enriched in PrE pre

94 e entire membrane resulted in a breakdown of apicobasal polarity, loss of adherens junctions, and a s

95 NA or its catalytically dead mutant disrupts apicobasal polarity, similar to HCV core.

96 ort that in addition to actively maintaining apicobasal polarity, the structures underwent rotational

97 d BicD mutant neuroblasts display defects in apicobasal polarity, which is consistent with apical Ins

98 ppaB pathway in addition to having a role in apicobasal polarity.

99 ot play identical roles in the generation of apicobasal polarity.

100 hibited normal levels of growth and retained apicobasal polarity.

101 n-Darby canine kidney (MDCK) cells, disrupts apicobasal polarity.

102 ts neural tube closure via the regulation of apicobasal polarity.

103 emonstrate is independent of Crb function in apicobasal polarity.

104 increases acinar size and modestly perturbs apicobasal polarity.

105 rchitecture, albeit without major changes in apicobasal polarity.

106 ulates cell energy metabolism and epithelial apicobasal polarity.

107 overns proliferation primarily by regulating apicobasal polarity.

108 erentiated, as indicated by a high degree of apicobasal polarization (i.e., presence of apical ZO-1 a

109 Correct apicobasal polarization and intercellular adhesions are

110 trally located cells; this apoptosis follows apicobasal polarization and precedes proliferative suppr

111 The process of apicobasal polarization in animal cells is controlled by

112 , but not oncogenic Ha-rasVal-12, blocks the apicobasal polarization of colon epithelial cells by pre

113 to date there has been little exploration of apicobasal polarization of its signaling.

114 ntation of peripheral MTs as well as for the apicobasal positioning of MTs.

115 about the contributions of transmural versus apicobasal repolarization gradients to the configuration

116 Importantly, such differential apicobasal signaling and VEGFR distribution were found i

117 e used to estimate the relative differential apicobasal tension in the epithelium.