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1 ets, did not reconstitute dynamic, elongated actin comets.
2 nsport carriers in association with PI5K and actin comets.
3 on on membrane-bound vesicles to form motile actin comets.
4 ine whether Dyn2 is an integral component of actin comets.
5 d the morphology and dynamics of Nck-induced actin comets.
6  from membrane-bound vesicles to form motile actin comets.
7 decreased Rac1, shortened granule-associated actin comets and impaired exocytosis.
8 nformation on the structural organization of actin comets and in particular the spatial arrangement o
9 hermore, the dsbA mutant was able to produce actin comets and protrusions, indicating its capacity fo
10  lacking VAP accumulate high levels of PI4P, actin comets, and trans-Golgi proteins on endosomes.
11  a constant velocity and were reminiscent of actin comets associated with motile vesicles in cells ex
12                 Membrane internalization and actin comet formation are enriched in the anterior, and
13                                Modulation of actin comet formation by pharmacologic means, by overexp
14 osphatidylinositol 5-kinase (PI5K) increased actin comet frequency in Madin-Darby canine kidney cells
15 teins of both dynamin 1 and 2, is present in actin comets generated by Listeria or by type I PIP kina
16  where polystyrene beads are propelled by an actin comet in a microwell containing a limited amount o
17 t PI(4,5)P(2) and PIP5K are both enriched at actin comets induced by Nck aggregates and that formatio
18         Nck knockdown or knockout suppressed actin comets induced by phosphatidylinositol 5-kinase (P
19                                              Actin comets may provide a novel mechanism for raft-depe
20 s suggest a previously unidentified role for actin comet-mediated propulsion in the biosynthetic deli
21 r coat nucleate the majority of the numerous actin comets present in patient cells.
22             Utilizing a Listeria fluorescent actin comet tail assay to monitor actin disassembly rate
23 er a mechanism for Shigella flexneri-induced actin comet tail elongation that links Abl family kinase
24 ate an important role for CRMP-1 in Listeria actin comet tail formation and open the possibility that
25                                              Actin comet tail formation and steady-state bacterial mo
26 o scored as an important factor for Listeria actin comet tail formation in brain cytosol.
27                                              Actin comet tail formation in vivo was stimulated by the
28                                 In addition, actin comet tail formation is associated with polarizati
29 tes N-WASP, a host cell protein required for actin comet tail formation, and mutation of the Abl phos
30 at the Abl kinases are required for Shigella actin comet tail formation, maximal intracellular motili
31 tes intracellular motility and spreading via actin comet tail formation.
32 hing minus retarding) force generated by the actin comet tail is approximately 0.4-4 nN.
33 SP overexpression caused loss of the typical actin comet tail shape induced by Nck aggregation.
34 ost proteins to assemble an Arp2/3-dependent actin comet tail to power its movement through the host
35 e slowly, the actin filaments comprising the actin comet tail were significantly more stable, with an
36  surface of every vesicle associated with an actin comet tail, suggesting that vesicle movement resul
37 ll actin to form the typical F (filamentous)-actin comet tail.
38 C3, DFCP1, and p62 through a WHAMM-dependent actin-comet tail mechanism.
39 plex for autophagosome biogenesis through an actin-comet tail motility mechanism.
40 the bacterium to drive its movement using an actin comet-tail mechanism.
41  marked increase in actin polymerization and actin comet tailing on GLUT4 vesicles.
42 eleton, displaying prominent accumulation on actin "comet tails" that emanate from focal adhesions in
43                 N-WASP WH2 mutants assembled actin comet tails and initiated movement, but the comet
44 We find that motile vesicles associated with actin comet tails are significantly deformed due to an i
45  function we have simulated the structure of actin comet tails as well as the tracks adopted by bacul
46 otein Sla2p, patch motility was arrested and actin comet tails associated with endocytic patch comple
47 on, mimicking eukaryotic formins to assemble actin comet tails for Rickettsia motility.
48 cs that distinguish vesicles associated with actin comet tails from other vesicles in the extract.
49        Furthermore, vesicles associated with actin comet tails had the morphological features of mult
50          Several pathogens induce propulsive actin comet tails in cells they invade to disseminate th
51 this mixture was insufficient to disassemble actin comet tails in the presence of physiological F-act
52 cting protein 1 is sufficient to disassemble actin comet tails in the presence of physiological G-act
53 itutively active TC10 (TC10/Q75L) can induce actin comet tails in Xenopus oocyte extracts in vitro an
54  the leading edge of motile cells and in the actin comet tails of intracellular pathogenic bacteria a
55 ma S and sodium orthovanadate stimulation of actin comet tails on GLUT4 intracellular compartments.
56              In metaphase, this wave induces actin comet tails on mitochondria that propel these orga
57 solved the three-dimensional architecture of actin comet tails propelling baculovirus, the smallest p
58 escence recovery after photobleaching of the actin comet tails revealed that endocytic complexes are
59 strate that insulin can induce GLUT4 vesicle actin comet tails that are necessary for the efficient t
60        We used the speed and the size of the actin comet tails to evaluate the system's monomer consu
61      In addition, the insulin stimulation of actin comet tails was completely inhibited by Clostridum
62                                              Actin comet tails were often detected at the rear end of
63 filin can disassemble Listeria monocytogenes actin comet tails, it cannot efficiently disassemble com
64 tures, including podosomes, phagocytic cups, actin comet tails, subcortical ruffles, and stress fiber
65 ates the formation of Listeria monocytogenes actin comet tails, thereby implicating it in actin assem
66 n of Nck SH3 domains at the membrane induces actin comet tails--dynamic, elongated filamentous actin
67 otile, LC3-containing membranes that move on actin comet tails.
68 odia and filopodia of migrating cells and in actin comet tails.
69 a S) and sodium orthovanadate stimulation of actin comet tails.
70 ared with bacterially associated cytoplasmic actin comet tails.
71 e formation and maintenance of Nck-dependent actin comet tails.
72                 We show that the SNX9-driven actin comets that arise on human disease-associated ocul
73 uced by Nck aggregates and that formation of actin comets was strongly inhibited by coclustering with