ライフサイエンスコーパス: apicobasal polarity

1 hibited normal levels of growth and retained apicobasal polarity.

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

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

4 emonstrate is independent of Crb function in apicobasal polarity.

5 increases acinar size and modestly perturbs apicobasal polarity.

6 rchitecture, albeit without major changes in apicobasal polarity.

7 ulates cell energy metabolism and epithelial apicobasal polarity.

8 overns proliferation primarily by regulating apicobasal polarity.

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

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

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

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

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

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

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

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

17 TEBs exhibit reduced apicobasal polarity and extensive proliferation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 The apicobasal polarity of epithelial cells is critical for

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

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

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

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

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

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

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

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

68 Apicobasal polarity plays an important role in regulatin

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

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

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

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

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

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

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