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1 ficient to induce restructuring of the focal adhesion plaque.
2 ween vesicles and also the total area of the adhesion plaques.
3 tant protein Y100F/Y1065F localized to focal adhesion plaques.
4 calizes to the actin stress fibers and focal adhesion plaques.
5 lasts, consistent with localization to focal adhesion plaques.
6 ed translocation of alpha-actinin from focal adhesion plaques.
7 its and is localized preferentially in focal adhesion plaques.
8 ta1 clustering and formation of mature focal adhesion plaques.
9 le cells attach to basement membrane through adhesion plaques.
10 ng edge, and/or facilitating the turnover of adhesion plaques.
11 lls by cleaving structural components of the adhesion plaques.
12 ecrease the formation of vinculin-associated adhesion plaques, actin-based stress fibers, and filopod
13 on of well-defined vinculin-containing focal adhesion plaques, although expression of each isoform ex
14 part of the supramolecular structure of the adhesion plaque and it modulates cell adhesion via a bet
15 on complexes in larvae and adults, including adhesion plaques and dense bodies (Z-disks) of striated
16 to a marked increase in the number of focal adhesion plaques and fibronectin production, and RhoA, R
18 s for a cytoskeletal protein, found in focal adhesion plaques and in cell-cell adherens junctions.
19 kinase and paxillin, which localize in focal adhesion plaques and may play important roles in the int
20 ion of PIPKIbeta blocks clathrin assembly at adhesion plaques and prevents complex formation between
21 ombospondin stimulates a rapid loss of focal adhesion plaques and reorganization of the actin cytoske
22 ated with the cytoskeleton, having a role in adhesion-plaque and actin-microfilament organization.
27 ndothelial cell (HUVEC) proliferation, focal adhesion plaque (FAP) organization, and integrin express
31 yrin directly underneath HA receptor (CD44s)-adhesion plaque-like structures in pl85(neu)-transfected
32 induces the HA receptor (i.e. CD44s) to form adhesion plaque-like structures, and causes an accumulat
33 s, demonstrating that cell-cell contacts and adhesion plaques may be targets of Jagged/Notch activity
34 AK activation induces the formation of focal adhesion plaques, multimolecular platforms for second-ph
35 ci at which the formation and dissolution of adhesion plaques occurs, consistent with hypotheses that
36 ion of its C-terminal domain, disrupts focal adhesion plaques, probably by local disruption of normal
37 of TRIP6 place it in the same family as the adhesion plaque protein, zyxin, and the lipoma preferred
38 n we observed between highly expressed focal adhesion plaque proteins and malignant transformation ac
40 AMF promoted marked rearrangement of focal adhesion plaque proteins in the AMF migration-responsive
43 as-inhibited cells displayed prominent focal adhesion plaque structures, enhanced adherence propertie
44 stress fibers and restructuring of the focal adhesion plaque that includes loss of vinculin and alpha
46 integrins was observed, especially at focal adhesion plaques; this indicates that these molecules ar
47 ions support the idea that vinculin can link adhesion plaques to the cytoskeleton by initiating the f
48 ted by Rac1 deletion, the number and size of adhesion plaques were significantly reduced, and the mol
49 han in neurons, and is concentrated at focal adhesion plaques, where phosphatidylinositol-4,5-bisphos
50 les move more quickly than the paxillin-rich adhesion plaques, which in turn move more quickly than t
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