戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ppaB pathway in addition to having a role in apicobasal polarity.
2 hibited normal levels of growth and retained apicobasal polarity.
3 n-Darby canine kidney (MDCK) cells, disrupts apicobasal polarity.
4 ts neural tube closure via the regulation of apicobasal polarity.
5 emonstrate is independent of Crb function in apicobasal polarity.
6  increases acinar size and modestly perturbs apicobasal polarity.
7 rchitecture, albeit without major changes in apicobasal polarity.
8 ulates cell energy metabolism and epithelial apicobasal polarity.
9 rized proteins and the achievement of proper apicobasal polarity.
10 overns proliferation primarily by regulating apicobasal polarity.
11 ot play identical roles in the generation of apicobasal polarity.
12 role in the establishment and maintenance of apicobasal polarity, a cellular characteristic essential
13  protein family, is essential for epithelial apicobasal polarity (ABP) in Drosophila However, a conse
14 f the LAP protein family, contributes to the apicobasal polarity (ABP) of epithelial cells.
15 s mutations, disrupted colon epithelial cell apicobasal polarity and adhesion to collagen I and lamin
16 , we show that presumptive eye cells acquire apicobasal polarity and adopt neuroepithelial character
17 nsition (EMT), whereby epithelial cells lose apicobasal polarity and cell-cell contacts, and gain mes
18 e maintenance of proper architecture through apicobasal polarity and cell-cell contacts.
19                            Spheroids develop apicobasal polarity and complete lumens, and they are co
20 ation, where a subset of cardiomyocytes lose apicobasal polarity and delaminate basally from the vent
21                         TEBs exhibit reduced apicobasal polarity and extensive proliferation.
22 ponents of basement membrane, HPPL developed apicobasal polarity and formed cysts, which had luminal
23  matrix, cholangiocytes developed epithelial/apicobasal polarity and formed functional cysts and bili
24 gest that MALS-3 plays a role in maintaining apicobasal polarity and is required for normal neurogene
25 alian epithelial cells and are important for apicobasal polarity and junction formation.
26  ECM protease degradability was required for apicobasal polarity and lumen formation.
27 hesive ligand density dramatically regulated apicobasal polarity and lumenogenesis independently of c
28 st type is characterized by reinforcement of apicobasal polarity and maintenance of the apical/lumina
29 ells, modified to include the effects of the apicobasal polarity and natural curvature of epithelia.
30 -mediated DNA methylation in controlling RPE apicobasal polarity and neural retina differentiation.
31 sis-dependent pathways, resulting in loss of apicobasal polarity and relocation of abluminal CXCL12 t
32 gs provide a direct mechanistic link between apicobasal polarity and the cell cycle, which may explai
33 ex has been implicated in the development of apicobasal polarity and the formation of tight junctions
34 evelopment, outside and inside cells rely on apicobasal polarity and the Hippo pathway to choose thei
35                             Establishment of apicobasal polarity and the organization of the cytoskel
36 uishing feature of epithelial cells is their apicobasal polarity and the presence of apical junctions
37 tif at the C-terminus of VE-cadherin impairs apicobasal polarity and vascular lumen formation.
38 gates the ability of VE-cadherin to regulate apicobasal polarity and vascular lumen formation.
39  different cell types, the epithelial cells (apicobasal polarity) and the oocyte (anteroposterior pol
40 with disruption of tight junction formation, apicobasal polarity, and contact-inhibited growth.
41 standing of the regulation of proliferation, apicobasal polarity, and epithelial motility during bran
42 s the formation of apical cell junctions and apicobasal polarity, and we investigated its role in ven
43   Interestingly, crb function in maintaining apicobasal polarity appears largely dispensable in prima
44                As stratification and loss of apicobasal polarity are early hallmarks of cancer, we ne
45 cal domain, but does not result in a loss of apicobasal polarity, as would be predicted from current
46 en the two emergence types depends on tuning apicobasal polarity at the level of the HE.
47 he maintenance of oriented cell division and apicobasal polarity, both of which are often deregulated
48 epithelia deficient for Llgl1 retained overt apicobasal polarity, but had expanded apical domains.
49 omplex and is important in the definition of apicobasal polarity, but the localisation and function o
50 r, SMGs from Nfib (-/-) mice at E18.5 showed apicobasal polarity, but they were disorganized and lost
51 hogenesis involves sequential acquisition of apicobasal polarity by epithelial cells and development
52 ts with the Par6/Par3/aPKC and Scrib/Dlg/Lgl apicobasal polarity complexes.
53 iven transgenic PREX1 expression resulted in apicobasal polarity defects and increased mammary epithe
54 activity, which is required to set up proper apicobasal polarity during sprout formation.
55 ing the two emergence types rely, or not, on apicobasal polarity establishment.
56  regulation, as well as with epithelial cell apicobasal polarity establishment/maintenance.
57                        Altered expression of apicobasal polarity factors is associated with cancer in
58                   PDE inherits and maintains apicobasal polarity from its epithelial precursor.
59                        Mutation of different apicobasal polarity genes activates c-Jun N-terminal kin
60 ts, we show that ICAM-1 regulates epithelial apicobasal polarity in a leukocyte adhesion-independent
61 te junctions and is required for maintaining apicobasal polarity in Drosophila epithelium.
62 ic interaction between aPKC and Lgl2 defines apicobasal polarity in early vertebrate development.
63 tardust mutants exhibit severe disruption in apicobasal polarity in embryonic epithelia, resulting in
64 umbs, Par, and Scribble complexes, establish apicobasal polarity in epithelial cells, and interferenc
65 tical to maintain oriented cell division and apicobasal polarity in normal mammary glands and to esta
66                            Thus, the role of apicobasal polarity in podocytes remains unclear.
67 ons, and functions as a major determinant of apicobasal polarity in retinal radial glia.
68 ilure to down-regulate Dystroglycan disrupts apicobasal polarity in the PFC, which includes mislocali
69 ficiency include abnormalities of enterocyte apicobasal polarity, increased apoptosis of intestinal c
70                           Loss of epithelial apicobasal polarity is a key factor in the development o
71                                   Epithelial apicobasal polarity is controlled by many polarity genes
72 itical for sprout formation; in its absence, apicobasal polarity is entirely lost in vitro and in viv
73                                          How apicobasal polarity is established in the developing epi
74              However, it remains unclear how apicobasal polarity is regulated to meet the opposing ne
75  to obtain ciliated neuronal fate, inherited apicobasal polarity is required for generating ciliated
76 e, we show that N-Cad/ZO-1 complex-initiated apicobasal polarity is stabilized by the late-onsetting
77 n kinase C (aPKC), a protein associated with apicobasal polarity, is specifically enriched in PrE pre
78 e entire membrane resulted in a breakdown of apicobasal polarity, loss of adherens junctions, and a s
79        By contrast, lineages with unrestored apicobasal polarity maintained SOX9 activity in sustaine
80 ibution of signaling complexes essential for apicobasal polarity may constitute a critical event in t
81 nascent pharyngeal lumen by reorientation of apicobasal polarity of anterior pharyngeal cells ("Reori
82 logy during evolution.SIGNIFICANCE STATEMENT Apicobasal polarity of epithelia is an important propert
83                                          The apicobasal polarity of epithelial cells is critical for
84 localization and function in controlling the apicobasal polarity of epithelial cells.
85 l localization of membrane proteins, and for apicobasal polarity of epithelial cells.
86 lantation failure associated with heightened apicobasal polarity of luminal epithelial cells during t
87  a poorly characterized reorientation of the apicobasal polarity of static epithelial cells into the
88 m patient biopsies displayed an inversion of apicobasal polarity of the epithelial cells that was nor
89 thout disrupting the fluid-tight barrier and apicobasal polarity of the epithelium.
90 ll-to-cell contacts and the establishment of apicobasal polarity of vascular endothelial cells.
91 Our data suggest that stepwise maturation of apicobasal polarity plays an essential role in vertebrat
92                                              Apicobasal polarity plays an important role in regulatin
93 porters determined the effects of disrupting apicobasal polarity proteins in Drosophila nephrocytes,
94 tion studies illuminated relationships among apicobasal polarity proteins.
95  develop excess layers of cells with altered apicobasal polarity reminiscent of dysplasia, suggesting
96     We demonstrate that during photoreceptor apicobasal polarity remodeling, Crb is required to exclu
97 NA or its catalytically dead mutant disrupts apicobasal polarity, similar to HCV core.
98            We have built a computer model of apicobasal polarity that suggests that the combination o
99 ort that in addition to actively maintaining apicobasal polarity, the structures underwent rotational
100                    We propose that inherited apicobasal polarity, together with apical cell-cell inte
101 y of apical transmembrane proteins regulates apicobasal polarity via protein interactions with a cons
102                            Podocytes exhibit apicobasal polarity, which can affect fundamental aspect
103 d BicD mutant neuroblasts display defects in apicobasal polarity, which is consistent with apical Ins

 
Page Top