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1 hat Pkc53E regulates depolymerization of the actin microfilament.
2  a colocalization of the BCCV N protein with actin microfilaments.
3 everse transcription was dependent on intact actin microfilaments.
4 leocapsids are specifically localized on the actin microfilaments.
5 mmunolocalization of the junction-associated actin microfilaments.
6 a occludens 1 and of the junction-associated actin microfilaments.
7 , generate mechanical forces and couple with actin microfilaments.
8 like bodies (I-LBs) move in association with actin microfilaments.
9  and (5) an association of the receptor with actin microfilaments.
10  which contained fine fibers the diameter of actin microfilaments.
11 PCs) involve the assembly and disassembly of actin microfilaments.
12                Dys-ABD alone associated with actin microfilaments.
13 omplement factor C3 and that uptake requires actin microfilaments.
14 otubules was independent of the integrity of actin microfilaments.
15 uently associated with microtubules and with actin microfilaments.
16 on of spyA in HeLa cells resulted in loss of actin microfilaments.
17 uding the CH domain interacted directly with actin microfilaments.
18 ulating filaments had the same dimensions as actin microfilaments.
19 eletal proteins is implicated in stabilizing actin microfilaments.
20 ut not alphavbeta3 particle binding required actin microfilaments.
21 s are dependent upon cytoplasmic networks of actin microfilaments (6 nm), intermediate filaments (10
22  that axial strains caused by the sliding of actin microfilaments about the fixed integrin attachment
23 ntral surface and exhibits a localization of actin microfilaments along the free edges of the cells,
24             While disruption of the cellular actin microfilament and microtubule by cytochalasin D an
25                                  Coordinated actin microfilament and microtubule dynamics is required
26  is originated mostly from the remodeling of actin microfilaments and adhesion complexes, to less ext
27                          Junction-associated actin microfilaments and cell density were unchanged.
28  the peripheral cytoskeleton, disassembly of actin microfilaments and disaggregation of microtubules
29 stent and involved extensive organization of actin microfilaments and focal adhesions.
30                      Depolymerization of the actin microfilaments and inhibition of the Arp2/3 comple
31 li cell injury through disruptive effects on actin microfilaments and microtubule (MT) organization a
32  plants may employ unique KCHs to coordinate actin microfilaments and microtubules during cell growth
33 erted its regulatory effect by disorganizing actin microfilaments and microtubules in Sertoli cells s
34 res composed of an interconnected network of actin microfilaments and microtubules when mechanical st
35 t trajectories, and is dependent upon intact actin microfilaments and myosin motors, since treatment
36 nism that was dependent on polymerization of actin microfilaments and on a functional cytoskeleton, a
37 is effect does not require interactions with actin microfilaments, and it is possible that other acti
38 e, chromatin condensation, reorganization of actin microfilament architecture, and extensive detachme
39                                        While actin microfilaments are crucial for various cellular pr
40                    When LIMKs are inhibited, actin microfilaments are disorganized and microtubules a
41 ominant, but both intermediate filaments and actin microfilaments are involved in dynamic cross-linki
42 centriolar material (PCM) fails to assemble, actin microfilaments are not organized into furrows at t
43  major protein of muscle thin filaments, and actin microfilaments are the main component of the eukar
44                            Disruption of the actin microfilament array by cytochalasin D treatment of
45 me and nuclear envelope motility depended on actin microfilaments as well as tubulin.
46  and Arg colocalize with each other and with actin microfilaments at the apical surface of the develo
47      In summary, plastin 3 is a regulator of actin microfilament bundles at the ES in which it dictat
48                                        These actin microfilament bundles require rapid debundling to
49 increased interprocess spacing and haphazard actin microfilament bundles.
50 ndicating a requirement for rearrangement of actin microfilaments but less dependence on tyrosine kin
51 nd to be associated with transverse-cortical actin microfilaments, but never with axial actin cables
52 rms motile granules that are associated with actin microfilaments, but not with microtubules.
53 nges were the result of an alteration of the actin microfilaments, converting from their bundled to b
54 red in the absence of intact microtubule and actin microfilament cytoskeletal elements.
55 nd their structure is regulated primarily by actin microfilaments, cytoskeletal proteins present in h
56 reading is dependent on the integrity of the actin microfilament cytoskeleton, we sought to determine
57        The small G-protein Rho regulates the actin microfilament-dependent cytoskeleton.
58 ultinucleate cells, likely by inhibiting the actin microfilament-dependent step of cytokinesis.
59                       Finally, the effect of actin microfilament depolymerization on total release is
60 nsitive to treatment with cytochalasin D, an actin microfilament-depolymerizing drug.
61         In contrast, the depolymerization of actin microfilaments did not have any effect on virus bi
62 -dependent process, since treatment with the actin microfilament disrupter cytochalasin D prevented i
63 rane properties with cholesterol removal and actin microfilament disruption.
64  reversibly stabilized microtubules, blocked actin microfilament dynamics, inhibited cell motility in
65 t study was to evaluate the effect of BFT on actin microfilaments (F-actin) and cell volume.
66 ons requires the formation of filopodia from actin microfilaments (F-actin) and their engorgement wit
67  their ECM, the attached ECs rearrange their actin microfilaments first into peripheral stress fibers
68                                              Actin microfilaments form a three-dimensional cytoskelet
69                                Inhibition of actin microfilaments had the greatest effect on bulk com
70   Lifeact, a small peptide with affinity for actin microfilaments has become a gold standard in live
71          Our results support the notion that actin microfilaments impose a barrier for mobilization o
72 -permeability barrier, causing disruption of actin microfilaments in cell cytosol, perturbing the loc
73 dynamic interaction between microtubules and actin microfilaments in cotton fibers.
74 al tight junctional ring and thickening of F-actin microfilaments in focal contacts at the basolatera
75 d cell death, highlighting the importance of actin microfilaments in rituximab/milatuzumab-mediated c
76 in roles in other cell types, is to assemble actin microfilaments in support of photoreceptor disk mo
77                                  The role of actin microfilaments in synaptic transmission was tested
78 th F-actin in vivo and that can cross-link F-actin microfilaments in vitro.
79 result of CRB3 KD-induced re-organization of actin microfilaments, in which actin microfilaments were
80 endocytosis via the accumulation of cortical actin microfilaments induced by the ROP2 effector protei
81      Cytochalasin D, an agent which disrupts actin microfilaments, inhibited BN- and TPA-induced tyro
82 crylamide, or colchicine was used to disrupt actin microfilaments, intermediate filaments, or microtu
83  an actin-dependent manner and to cross-link actin microfilaments into higher-order structures has be
84 ccur either through directed transport along actin microfilaments into one daughter cell or through c
85                   These results suggest that actin microfilaments may interact, either directly or in
86                                              Actin microfilaments mediated force transfer to the nucl
87 levation, apical recruitment of p150(Glued), actin microfilament meshwork organization, and ultrastru
88 ors embedded in membrane microdomains induce actin-microfilament meshwork formation, anchoring microt
89                                              Actin microfilament (MF) organization and remodelling is
90                         To determine whether actin microfilament (MF) organization is correlated with
91 l changes due to structural modifications in actin microfilaments (MFs) and microtubules (MTs).
92 s is structured by a scaffolding composed of actin microfilaments, microtubules, and intermediate fil
93 ed by the presence of an array of bundles of actin microfilaments near the Sertoli cell plasma membra
94  related to its known ability to disrupt the actin microfilament network and consequently to affect c
95 ized cell phenotype and the integrity of the actin microfilament network are important cellular deter
96            With a close examination of the F-actin microfilament network, these findings show that Pa
97  Unstretched HTM cells displayed a diffuse F-actin microfilament network, whereas stretched cells exh
98 otype is accompanied by modifications of the actin microfilament network, with shortened filaments, w
99  mechanism that utilizes the microtubule and actin microfilament network.
100 le of the polymeric form of actin, i.e., the actin microfilaments of the cytoskeletal framework, in t
101 M to the nucleus, endoplasmic reticulum, and actin microfilaments of the cytoskeleton in response to
102 domain of vitronectin resulted in changes in actin microfilament organization and the subcellular dis
103 o act by depolymerizing actin and disrupting actin microfilament organization.
104 eleton, having a role in adhesion-plaque and actin-microfilament organization.
105          These results strongly suggest that actin microfilaments play an important role in the repli
106  plants with cytochalasin E, an inhibitor of actin microfilament polymerisation.
107 reatment with cytochalasin D, which disrupts actin microfilaments, prevented the calcitonin-induced H
108                       In summary, CRB3 is an actin microfilament regulator, playing a pivotal role in
109        Interestingly, inhibitors that target actin microfilament remodeling do not affect cell sensit
110 sassemble actin microfilaments, we show that actin microfilament remodeling is part of fenestra bioge
111 milarly, wortmannin inhibited hep I-mediated actin microfilament reorganization and the hep I-induced
112 tes RIC4 to promote the assembly of cortical actin microfilaments required for localized outgrowth.
113 s concomitant to increased polymerization of actin microfilaments resulting in decreased G- to F-acti
114 ves the elongated oocyte microvilli, rich in actin microfilaments, since it can be blocked by the mic
115 titatively controlled conditions, to perturb actin microfilament structure and assembly in an attempt
116 of these channels requires interactions with actin microfilaments subjacent to the plasma membrane.
117 ngle-domain proteins which directly link the actin microfilament system to a variety of signalling pa
118 ulated by both phospholipase D (PLD) and the actin microfilament system.
119 n yeast, plant and animal cells that confers actin microfilaments their bundled configuration.
120  Sertoli cell cytosol, causing truncation of actin microfilament, thereby failing to support the Sert
121  the cytoskeletal protein vinculin, connects actin microfilaments to the intercalated disk and membra
122 , are large cytoskeletal proteins which link actin microfilaments to the plasma membrane.
123                 Here, our study reveals that actin microfilaments undergo remodeling and disassembly
124 (1) cell phenotype using antibodies to alpha-actin (microfilaments), vimentin and desmin (intermediat
125 eover, the association of the N protein with actin microfilaments was confirmed by coimmunoprecipitat
126 The localization of reverse transcription to actin microfilaments was mediated by the interaction of
127  use of agents that stabilize or disassemble actin microfilaments, we show that actin microfilament r
128 ganization of actin microfilaments, in which actin microfilaments were truncated, and extensively bra
129 termined by centrifugal cosedimentation with actin microfilaments, where bound protein is separated f
130                                              Actin microfilaments, which are prominent in pollen tube
131                                Disruption of actin microfilaments, which causes delocalization of Bif
132 ication, resulting in the re-organization of actin microfilaments, which rendered them similar to tho
133 n of microtubules with colchicine (Colch) or actin microfilaments with cytochalasin D (CD) dramatical
134  cone actin cytoskeleton, because disrupting actin microfilaments with cytochalasin D or stabilizing

 
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