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 ingly however, Notch does not act through an apicobasal activity gradient as previously suggested, bu
2  paper by Monier et al. (2015) identifies an apicobasal actomyosin cable that characterizes apoptotic
3          Thus, PAR proteins function in both apicobasal and anterior-posterior asymmetry during the f
4 o transduce signals for the establishment of apicobasal and planar cell polarity during these process
5 asal bodies are mispositioned along both the apicobasal and planar polarity axes of mutant hair cells
6  in this process is independent of canonical apicobasal and planar polarity pathways.
7 or-posterior polarity, but showed defects in apicobasal asymmetries associated with gastrulation.
8 helia, cells can intercalate along their own apicobasal axes, adopting a shape named 'scutoid' that a
9 phed displacement of cells' nuclei along the apicobasal axis according to phases of their cell cycle.
10 nown to regulate RNA localization across the apicobasal axis of epithelial cells, establish LARP1 as
11 me-wide RNA spatial distributions across the apicobasal axis of human intestinal epithelial cells, we
12 a, where orientation of the spindle into the apicobasal axis of polarised blastomeres generates inner
13 inct classes of dynamic protrusion along the apicobasal axis of the cell.
14 al array into a network positioned along the apicobasal axis of the cell.
15 lane of the epithelium, perpendicular to the apicobasal axis of the cell.
16 ct to both the AP axis of the embryo and the apicobasal axis of the notochord plate.
17 roliferation, their nuclei migrate along the apicobasal axis of the retina in phase with the cell cyc
18 lasts undergo asymmetric divisions along the apicobasal axis to produce two daughter cells of unequal
19  degrees change in alignment relative to the apicobasal axis, loss of centrosomal attachment, and api
20 he polarization of myosin motors along their apicobasal axis.
21 be transition, cells are polarized along the apicobasal axis.
22  cell alignment, oriented cell division, and apicobasal cell elongation.
23 of aligned arrays of microtubules that drive apicobasal cell elongation.
24  Neural tube closure, for instance, involves apicobasal cell heightening, apical constriction at hing
25                                              Apicobasal cell polarity is crucial for morphogenesis of
26                                              Apicobasal cell polarity loss is a founding event in epi
27 deficient for Llgl1, a protein implicated in apicobasal cell polarity, asymmetric cell division, cell
28  is selectively involved in establishment of apicobasal cell polarity.
29 ., the partitioning-defective PARs) position apicobasal cellular membrane domains.
30 gated dorsal and ventral regions and layered apicobasal cellular organizations that mimic development
31 s, is bipolar migration directed towards the apicobasal centre of the retina.
32 them from undergoing apical constriction and apicobasal contraction.
33 of a pyramidally shaped soma with axonal and apicobasal dendritic processes.
34                                              Apicobasal differences in RT (human subjects) and repola
35 epithelia and how sorting confers long-range apicobasal directionality to vesicles is still unclear.
36  In addition, our data strongly suggest that apicobasal elongation of cells is not an emerging proper
37 n by microtubule- and actinomyosin-dependent apicobasal elongation, rather than by progressive epithe
38 uently, Notch signaling-dependent changes in apicobasal epithelial thickness drive elongation of thes
39 rols lost 24%, 33%, and 41% of peak systolic apicobasal force, respectively, whereas experimental hea
40 eins are provided maternally, distinguishing apicobasal from earlier anterior-posterior functions req
41 se or modify Rac activity, we demonstrate an apicobasal gradient of Rac activity that is required to
42    In controls, there was a left ventricular apicobasal gradient, with the shortest repolarization ti
43                                              Apicobasal gradients in repolarization time, with shorte
44 rophysiology by simultaneously adjusting the apicobasal gradients of the slow and rapid delayed recti
45  F-actin depolymerization disrupted both the apicobasal-like polarity and the diffusion barriers with
46 ning-defective PARs specify the positions of apicobasal membrane domains.
47 the growing epithelial membrane to partition apicobasal membrane domains.
48                 Large clones show defects in apicobasal membrane polarity, but small clones induced l
49 nterconnected network to a parallel array of apicobasal membrane tubules.
50 a PAR-1 regulates the density, stability and apicobasal organisation of microtubules.
51 , the membrane tubules do not assume a clear apicobasal orientation and appear to aggregate.
52 inin1, and ectopic Laminin1 can redirect the apicobasal orientation of eye field cells.
53  protein family, is essential for epithelial apicobasal polarity (ABP) in Drosophila However, a conse
54 f the LAP protein family, contributes to the apicobasal polarity (ABP) of epithelial cells.
55 s mutations, disrupted colon epithelial cell apicobasal polarity and adhesion to collagen I and lamin
56 , we show that presumptive eye cells acquire apicobasal polarity and adopt neuroepithelial character
57 nsition (EMT), whereby epithelial cells lose apicobasal polarity and cell-cell contacts, and gain mes
58 e maintenance of proper architecture through apicobasal polarity and cell-cell contacts.
59                            Spheroids develop apicobasal polarity and complete lumens, and they are co
60 ation, where a subset of cardiomyocytes lose apicobasal polarity and delaminate basally from the vent
61                         TEBs exhibit reduced apicobasal polarity and extensive proliferation.
62 ponents of basement membrane, HPPL developed apicobasal polarity and formed cysts, which had luminal
63  matrix, cholangiocytes developed epithelial/apicobasal polarity and formed functional cysts and bili
64 gest that MALS-3 plays a role in maintaining apicobasal polarity and is required for normal neurogene
65 alian epithelial cells and are important for apicobasal polarity and junction formation.
66  ECM protease degradability was required for apicobasal polarity and lumen formation.
67 hesive ligand density dramatically regulated apicobasal polarity and lumenogenesis independently of c
68 st type is characterized by reinforcement of apicobasal polarity and maintenance of the apical/lumina
69 ells, modified to include the effects of the apicobasal polarity and natural curvature of epithelia.
70 -mediated DNA methylation in controlling RPE apicobasal polarity and neural retina differentiation.
71 sis-dependent pathways, resulting in loss of apicobasal polarity and relocation of abluminal CXCL12 t
72 gs provide a direct mechanistic link between apicobasal polarity and the cell cycle, which may explai
73 ex has been implicated in the development of apicobasal polarity and the formation of tight junctions
74 evelopment, outside and inside cells rely on apicobasal polarity and the Hippo pathway to choose thei
75                             Establishment of apicobasal polarity and the organization of the cytoskel
76 uishing feature of epithelial cells is their apicobasal polarity and the presence of apical junctions
77 tif at the C-terminus of VE-cadherin impairs apicobasal polarity and vascular lumen formation.
78 gates the ability of VE-cadherin to regulate apicobasal polarity and vascular lumen formation.
79   Interestingly, crb function in maintaining apicobasal polarity appears largely dispensable in prima
80                As stratification and loss of apicobasal polarity are early hallmarks of cancer, we ne
81 en the two emergence types depends on tuning apicobasal polarity at the level of the HE.
82 hogenesis involves sequential acquisition of apicobasal polarity by epithelial cells and development
83 ts with the Par6/Par3/aPKC and Scrib/Dlg/Lgl apicobasal polarity complexes.
84 iven transgenic PREX1 expression resulted in apicobasal polarity defects and increased mammary epithe
85 activity, which is required to set up proper apicobasal polarity during sprout formation.
86 ing the two emergence types rely, or not, on apicobasal polarity establishment.
87  regulation, as well as with epithelial cell apicobasal polarity establishment/maintenance.
88                        Altered expression of apicobasal polarity factors is associated with cancer in
89                   PDE inherits and maintains apicobasal polarity from its epithelial precursor.
90                        Mutation of different apicobasal polarity genes activates c-Jun N-terminal kin
91 ts, we show that ICAM-1 regulates epithelial apicobasal polarity in a leukocyte adhesion-independent
92 te junctions and is required for maintaining apicobasal polarity in Drosophila epithelium.
93 ic interaction between aPKC and Lgl2 defines apicobasal polarity in early vertebrate development.
94 tardust mutants exhibit severe disruption in apicobasal polarity in embryonic epithelia, resulting in
95 umbs, Par, and Scribble complexes, establish apicobasal polarity in epithelial cells, and interferenc
96 tical to maintain oriented cell division and apicobasal polarity in normal mammary glands and to esta
97                            Thus, the role of apicobasal polarity in podocytes remains unclear.
98 ons, and functions as a major determinant of apicobasal polarity in retinal radial glia.
99 ilure to down-regulate Dystroglycan disrupts apicobasal polarity in the PFC, which includes mislocali
100                           Loss of epithelial apicobasal polarity is a key factor in the development o
101                                   Epithelial apicobasal polarity is controlled by many polarity genes
102 itical for sprout formation; in its absence, apicobasal polarity is entirely lost in vitro and in viv
103                                          How apicobasal polarity is established in the developing epi
104              However, it remains unclear how apicobasal polarity is regulated to meet the opposing ne
105  to obtain ciliated neuronal fate, inherited apicobasal polarity is required for generating ciliated
106 e, we show that N-Cad/ZO-1 complex-initiated apicobasal polarity is stabilized by the late-onsetting
107        By contrast, lineages with unrestored apicobasal polarity maintained SOX9 activity in sustaine
108 ibution of signaling complexes essential for apicobasal polarity may constitute a critical event in t
109 nascent pharyngeal lumen by reorientation of apicobasal polarity of anterior pharyngeal cells ("Reori
110 logy during evolution.SIGNIFICANCE STATEMENT Apicobasal polarity of epithelia is an important propert
111                                          The apicobasal polarity of epithelial cells is critical for
112 localization and function in controlling the apicobasal polarity of epithelial cells.
113 l localization of membrane proteins, and for apicobasal polarity of epithelial cells.
114 lantation failure associated with heightened apicobasal polarity of luminal epithelial cells during t
115  a poorly characterized reorientation of the apicobasal polarity of static epithelial cells into the
116 m patient biopsies displayed an inversion of apicobasal polarity of the epithelial cells that was nor
117 thout disrupting the fluid-tight barrier and apicobasal polarity of the epithelium.
118 ll-to-cell contacts and the establishment of apicobasal polarity of vascular endothelial cells.
119 Our data suggest that stepwise maturation of apicobasal polarity plays an essential role in vertebrat
120                                              Apicobasal polarity plays an important role in regulatin
121 porters determined the effects of disrupting apicobasal polarity proteins in Drosophila nephrocytes,
122 tion studies illuminated relationships among apicobasal polarity proteins.
123  develop excess layers of cells with altered apicobasal polarity reminiscent of dysplasia, suggesting
124     We demonstrate that during photoreceptor apicobasal polarity remodeling, Crb is required to exclu
125            We have built a computer model of apicobasal polarity that suggests that the combination o
126 y of apical transmembrane proteins regulates apicobasal polarity via protein interactions with a cons
127  different cell types, the epithelial cells (apicobasal polarity) and the oocyte (anteroposterior pol
128 role in the establishment and maintenance of apicobasal polarity, a cellular characteristic essential
129 with disruption of tight junction formation, apicobasal polarity, and contact-inhibited growth.
130 standing of the regulation of proliferation, apicobasal polarity, and epithelial motility during bran
131 s the formation of apical cell junctions and apicobasal polarity, and we investigated its role in ven
132 cal domain, but does not result in a loss of apicobasal polarity, as would be predicted from current
133 he maintenance of oriented cell division and apicobasal polarity, both of which are often deregulated
134 epithelia deficient for Llgl1 retained overt apicobasal polarity, but had expanded apical domains.
135 omplex and is important in the definition of apicobasal polarity, but the localisation and function o
136 r, SMGs from Nfib (-/-) mice at E18.5 showed apicobasal polarity, but they were disorganized and lost
137 ficiency include abnormalities of enterocyte apicobasal polarity, increased apoptosis of intestinal c
138 n kinase C (aPKC), a protein associated with apicobasal polarity, is specifically enriched in PrE pre
139 e entire membrane resulted in a breakdown of apicobasal polarity, loss of adherens junctions, and a s
140 NA or its catalytically dead mutant disrupts apicobasal polarity, similar to HCV core.
141 ort that in addition to actively maintaining apicobasal polarity, the structures underwent rotational
142                    We propose that inherited apicobasal polarity, together with apical cell-cell inte
143                            Podocytes exhibit apicobasal polarity, which can affect fundamental aspect
144 d BicD mutant neuroblasts display defects in apicobasal polarity, which is consistent with apical Ins
145 rized proteins and the achievement of proper apicobasal polarity.
146 overns proliferation primarily by regulating apicobasal polarity.
147 ot play identical roles in the generation of apicobasal polarity.
148 ppaB pathway in addition to having a role in apicobasal polarity.
149 hibited normal levels of growth and retained apicobasal polarity.
150 n-Darby canine kidney (MDCK) cells, disrupts apicobasal polarity.
151 ts neural tube closure via the regulation of apicobasal polarity.
152 emonstrate is independent of Crb function in apicobasal polarity.
153  increases acinar size and modestly perturbs apicobasal polarity.
154 rchitecture, albeit without major changes in apicobasal polarity.
155 ulates cell energy metabolism and epithelial apicobasal polarity.
156 erentiated, as indicated by a high degree of apicobasal polarization (i.e., presence of apical ZO-1 a
157                                      Correct apicobasal polarization and intercellular adhesions are
158 trally located cells; this apoptosis follows apicobasal polarization and precedes proliferative suppr
159                               The process of apicobasal polarization in animal cells is controlled by
160                This is due to defects in the apicobasal polarization in the context of the polarized
161 , but not oncogenic Ha-rasVal-12, blocks the apicobasal polarization of colon epithelial cells by pre
162 to date there has been little exploration of apicobasal polarization of its signaling.
163 ntation of peripheral MTs as well as for the apicobasal positioning of MTs.
164                                          The apicobasal repolarization gradient (ABRG) determines the
165                                          The apicobasal repolarization gradient (ABRG) plays an impor
166 about the contributions of transmural versus apicobasal repolarization gradients to the configuration
167 nstrates that the lateral ectoderm undergoes apicobasal shrinkage during gastrulation independently o
168 soderm and in-plane compression generated by apicobasal shrinkage of the surrounding ectoderm.
169               Importantly, such differential apicobasal signaling and VEGFR distribution were found i
170 trafficking becomes polarized independent of apicobasal target membrane domains.
171 e used to estimate the relative differential apicobasal tension in the epithelium.
172 -automatic region-of-interest selection, (3) apicobasal texture analysis, (4) glia segmentation, and
173 on three levels: (1) global image-level, (2) apicobasal texture, and (3) regional apicobasal vertical
174 ing the window of implantation, and impaired apicobasal transformation that prevents embryo implantat
175 el, (2) apicobasal texture, and (3) regional apicobasal vertical-to-horizontal alignment.

 
Page Top