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1 ets, did not reconstitute dynamic, elongated actin comets.
2 nsport carriers in association with PI5K and actin comets.
3 d the morphology and dynamics of Nck-induced actin comets.
4 on on membrane-bound vesicles to form motile actin comets.
5 ine whether Dyn2 is an integral component of actin comets.
6 from membrane-bound vesicles to form motile actin comets.
7 nformation on the structural organization of actin comets and in particular the spatial arrangement o
8 hermore, the dsbA mutant was able to produce actin comets and protrusions, indicating its capacity fo
10 a constant velocity and were reminiscent of actin comets associated with motile vesicles in cells ex
13 osphatidylinositol 5-kinase (PI5K) increased actin comet frequency in Madin-Darby canine kidney cells
14 teins of both dynamin 1 and 2, is present in actin comets generated by Listeria or by type I PIP kina
15 t PI(4,5)P(2) and PIP5K are both enriched at actin comets induced by Nck aggregates and that formatio
18 s suggest a previously unidentified role for actin comet-mediated propulsion in the biosynthetic deli
21 er a mechanism for Shigella flexneri-induced actin comet tail elongation that links Abl family kinase
22 ate an important role for CRMP-1 in Listeria actin comet tail formation and open the possibility that
27 tes N-WASP, a host cell protein required for actin comet tail formation, and mutation of the Abl phos
28 at the Abl kinases are required for Shigella actin comet tail formation, maximal intracellular motili
32 ost proteins to assemble an Arp2/3-dependent actin comet tail to power its movement through the host
33 e slowly, the actin filaments comprising the actin comet tail were significantly more stable, with an
34 surface of every vesicle associated with an actin comet tail, suggesting that vesicle movement resul
39 eleton, displaying prominent accumulation on actin "comet tails" that emanate from focal adhesions in
41 We find that motile vesicles associated with actin comet tails are significantly deformed due to an i
42 function we have simulated the structure of actin comet tails as well as the tracks adopted by bacul
43 otein Sla2p, patch motility was arrested and actin comet tails associated with endocytic patch comple
45 cs that distinguish vesicles associated with actin comet tails from other vesicles in the extract.
48 this mixture was insufficient to disassemble actin comet tails in the presence of physiological F-act
49 cting protein 1 is sufficient to disassemble actin comet tails in the presence of physiological G-act
50 itutively active TC10 (TC10/Q75L) can induce actin comet tails in Xenopus oocyte extracts in vitro an
51 the leading edge of motile cells and in the actin comet tails of intracellular pathogenic bacteria a
52 ma S and sodium orthovanadate stimulation of actin comet tails on GLUT4 intracellular compartments.
53 solved the three-dimensional architecture of actin comet tails propelling baculovirus, the smallest p
54 escence recovery after photobleaching of the actin comet tails revealed that endocytic complexes are
55 strate that insulin can induce GLUT4 vesicle actin comet tails that are necessary for the efficient t
58 filin can disassemble Listeria monocytogenes actin comet tails, it cannot efficiently disassemble com
59 tures, including podosomes, phagocytic cups, actin comet tails, subcortical ruffles, and stress fiber
60 ates the formation of Listeria monocytogenes actin comet tails, thereby implicating it in actin assem
61 n of Nck SH3 domains at the membrane induces actin comet tails--dynamic, elongated filamentous actin
67 uced by Nck aggregates and that formation of actin comets was strongly inhibited by coclustering with
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