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1 vated contractility by increasing junctional afadin.
2 AJ reannealing mediated by the Rap1 effector afadin.
3 ynapses through the scaffolding protein AF-6/afadin.
4 y associates with the nectin-binding protein afadin.
5 d with the cytoplasmic actin-binding protein afadin.
6 h protein harbors a cryptic binding site for afadin.
9 that lumen formation and elongation require afadin, a nectin adaptor protein implicated in adherens
10 Infectious-center growth is facilitated by afadin, a protein connecting the adherens junction and t
13 neuroblasts), the scaffolding protein Canoe (Afadin/Af-6 in mammals) regulates spindle orientation, b
16 through their cytoplasm-associated proteins, afadin and catenins, it is not fully understood how nect
17 we show that the adherens junction proteins afadin and CDH2 are critical for the control of cell pro
18 ll-cell adhesion sites after both the nectin-afadin and E-cadherin-catenin systems had been assembled
19 nin-binding protein that connects the nectin-afadin and E-cadherin-catenin systems through alpha-acti
22 tion facilitates formation of a complex with Afadin and PDZ-GEF2 that activates Rap1A, which regulate
23 ted with the PDZ domain-containing molecules Afadin and PDZ-guanine nucleotide exchange factor (GEF)
26 lial permeability via association with ZO-2, afadin, and PDZ-GEF1 to activate Rap2c and control contr
27 physical interactions between MAGI-1, AFD-1/afadin, and SAX-7/L1CAM, which are part of a functional
28 iates directly with ZO-2 and indirectly with afadin, and this complex, along with PDZ-GEF1, activates
31 e Rap1 and the actin-junctional linker Canoe/afadin are essential for polarity establishment, as both
32 the synaptic localization of nectin-1 and l-afadin are F-actin-dependent and that the shedding of ne
34 data demonstrate that activation of the Rap1-afadin axis is a physiological mechanism driving restora
38 upts the synaptically localized nectin-1 and afadin cluster at an early stage and elicits nectin-1 ec
42 elial cells, MV spread requires the nectin-4/afadin complex and is based on cytoplasm transfer betwee
43 its role in promoting cadherin recruitment, afadin deletion resulted in 70% fewer and less intense N
44 ether, these results support a model whereby afadin determines lumen placement by directing apical-ba
46 We show that loss of the scaffolding protein Afadin disrupts de novo lumenogenesis and lumen continui
47 age and roles of the linkage regulator Canoe/afadin during Drosophila germband extension (GBE), a con
48 we studied the distribution of nectin-1 and afadin during hippocampal synapse formation using cultur
49 between nectin-1 and the cytoplasmic protein afadin for HSV entry and spread as well as the effects o
51 oncomitant shuttling of the scaffold protein afadin from the cytosol to the nucleus and synapses.
61 ently found that the F-actin-binding protein afadin is required for lumen continuity in developing re
66 acts with the putative actin regulator AFD-1/afadin; knocking down magi-1 or afd-1 function in a hypo
68 that LMO7 localized at cell-cell AJs, where afadin localized, in epithelial cells of rat gallbladder
69 sing an in vitro 3D cyst model, we find that afadin localizes to the cell cortex adjacent to the spin
70 ether with the intracellular binding partner afadin, mediate adhesion and signaling at a variety of i
71 role in mediating synaptogenesis, we deleted afadin (mllt1), using a conditional allele, in postmitot
72 The alpha-catenin fragment 385-651 binds afadin more strongly than the full-length protein, sugge
78 equired for the colocalization of the nectin/afadin/ponsin adhesion system to adherens junctions, and
79 pletion of the actomyosin regulator RhoA and Afadin results in defects in the central lumens and arre
81 motes neuronal Cdh2 function via nectin3 and afadin, thus directing the broadly expressed homophilic
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