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1 and exocytic membrane flow at the front of a migrating cell.
2 ransitions between blebs and lamellipodia in migrating cells.
3 otide exchange factor at the leading edge of migrating cells.
4 d for relocalization of DMIB to the front of migrating cells.
5 nitial fuzzy pattern into a compact group of migrating cells.
6 ll protrusions and retract trailing edges of migrating cells.
7 polarity, membrane dynamics, and the rate of migrating cells.
8 dients and to permit direct visualization of migrating cells.
9 ed tails and higher directional stability of migrating cells.
10 wn about the role of Lgl in cell polarity in migrating cells.
11 regulate polarization, speed, and turning of migrating cells.
12 he direction, efficiency, and persistence of migrating cells.
13  the extreme leading edge of lamellipodia of migrating cells.
14 o force-bearing sites at the leading edge of migrating cells.
15 s are transported toward cell protrusions in migrating cells.
16  paxillin and focal adhesion kinase (FAK) in migrating cells.
17 heir intended substrates at leading edges of migrating cells.
18 that governs protrusion-retraction cycles in migrating cells.
19 finding, PhdI located to the leading edge in migrating cells.
20 bling or sliding FAs at the trailing edge of migrating cells.
21 ws and dictates the initial direction of the migrating cells.
22 ocal adhesions mediates their disassembly in migrating cells.
23 2/3, and Myosin-I linker) family proteins in migrating cells.
24 nd overlaps with ARF6 at the leading edge of migrating cells.
25 h colocalize with FAK at the lamellipodia of migrating cells.
26 he direction of actin flow on the surface of migrating cells.
27 embly and disassembly in the lamellipodia of migrating cells.
28 atrix-degradative activity to the surface of migrating cells.
29 ation of lamellipodia at the leading edge of migrating cells.
30 e and are restricted to the basal surface in migrating cells.
31 bution, caspase 8 is recruited to lamella of migrating cells.
32 n complexes maintain front-rear asymmetry in migrating cells.
33 d in the formation of head-to-tail arrays of migrating cells.
34 e distinct distribution of these isoforms in migrating cells.
35 show isoform-specific front-back polarity in migrating cells.
36 al for the establishment of cell polarity in migrating cells.
37 eal activation of PKA at the leading edge of migrating cells.
38  to contribute to the protrusive activity of migrating cells.
39 ted its translocation to the leading edge of migrating cells.
40 gression, which may reduce the population of migrating cells.
41 etween the cytoskeleton and the substrate in migrating cells.
42 ve feedback signal necessary for polarity in migrating cells.
43  redistribution of the actin cytoskeleton in migrating cells.
44  filamentous actin bundles along the base of migrating cells.
45 ons and cell-matrix adhesions at the rear of migrating cells.
46 romote Rac activation at the leading edge of migrating cells.
47 TGalpha6 protein levels are increased in the migrating cells.
48 was found in cloche and scl(mo), possibly in migrating cells.
49 ator of F-actin functional specialization in migrating cells.
50 ation of a microtubule-associated protein in migrating cells.
51 matically relocalized to the leading edge of migrating cells.
52  actin polymerization at the leading edge of migrating cells.
53 is spatially and temporally regulated inside migrating cells.
54 ures for real-time observation of individual migrating cells.
55 icits mechanical behavior similar to that of migrating cells.
56 filament nucleation and cell shape change in migrating cells.
57 GM1, to stabilize MTs in the leading edge of migrating cells.
58 of the model for lamellipodial protrusion in migrating cells.
59 ellipodial protrusion at the leading edge of migrating cells.
60 ribution of mitochondria to the periphery of migrating cells.
61  cytoskeletal systems in the leading edge of migrating cells.
62 and the inactive, phosphorylated AC (pAC) in migrating cells.
63 thrin-coated pits and at the leading edge of migrating cells.
64 phrin signaling acting positively to pattern migrating cells.
65 nts that drive plasma membrane protrusion in migrating cells.
66  events at the leading edge of directionally migrating cells.
67 o macroscopic tracks created in scaffolds by migrating cells.
68 er alignment of contractile stress fibers in migrating cells.
69 n of Rab13 by DENND2B at the leading edge of migrating cells.
70 sive actin-based structures in spreading and migrating cells.
71 chemokine-dependent strategies used to guide migrating cells.
72  and dynamic cell-shape changes performed by migrating cells.
73 tiffness, but does not increase the speed of migrating cells.
74 re important for locomotion in many types of migrating cells.
75 ation and to provide directional guidance to migrating cells.
76 ments that protrude from the leading edge of migrating cells.
77 rear Cdc42-GTP distribution in directionally migrating cells.
78 native ways of extending the leading edge of migrating cells.
79  of ATX, which redistributes to the front of migrating cells.
80 geometry to predict where blebs will form in migrating cells.
81 adients that provide directional signals for migrating cells.
82 ng cells with a morphology characteristic of migrating cells.
83 e adhesion protein and filopodia dynamics in migrating cells.
84  that extended into the collagen matrix with migrating cells.
85  activated both in the front and the rear of migrating cells.
86 and myosin II light chain/actin filaments in migrating cells.
87  and phagocytic cups and the leading edge of migrating cells.
88 d basic machinery, neurons differ from other migrating cells.
89 -bearing proteins present in lamellipodia of migrating cells.
90 ansport Ca-calmodulin to the leading edge of migrating cells.
91 ctin cytoskeleton and focal adhesion (FA) in migrating cells.
92 r, a region corresponding to the lamellum of migrating cells.
93 e formation of lamellipodia and filopodia in migrating cells.
94  measured by increased distance and speed of migrating cells.
95 nocytes was composed largely of pre-existing migrating cells (555.6 +/- 38.1/mm(2)) and to a lesser e
96 (EFs) are able to influence the direction of migrating cells, a process commonly referred to as elect
97                       In the leading edge of migrating cells, a subset of microtubules exhibits net g
98                                           In migrating cells actin remodeling is tightly regulated an
99                                           In migrating cells, actin polymerization promotes protrusio
100  MT1-MMP was directed to the leading edge of migrating cells along micropatterned fibronectin stripes
101 ike protrusions found at the leading edge of migrating cells and are believed to play a role in direc
102 orm protein complexes at the leading edge of migrating cells and balance patterns of Rac1 and Cdc42 s
103 een the nucleus and the leading edge in many migrating cells and contributes to directional migration
104 enriched in adhesions at the leading edge of migrating cells and depletion of beta2-adaptin by RNAi i
105 diates polarity in several systems including migrating cells and early embryos, which involve reorien
106 on of actin filaments in the lamellipodia of migrating cells and exerts significant forces on the sur
107 cells reactivate from dormancy more than non-migrating cells and exhibit differential migration-react
108 etworks within lamellipodia and filopodia of migrating cells and in actin comet tails.
109 oning and cell polarization were impaired in migrating cells and in cells plated on micropatterned su
110 ed in focal adhesions at the leading edge of migrating cells and inhibition or knockdown of Kir4.2 ca
111 p1 protein is present at the leading edge of migrating cells and interacts directly with cytoskeletal
112 ized distribution toward the leading edge in migrating cells and is clearly distinct from the Myo5a o
113 adients are generated at the leading edge of migrating cells and provide additional insight into the
114 contacts the leader TVC, then 'encases' both migrating cells and provides the inputs maintaining lead
115 n of 'sticky fingers' at the leading edge of migrating cells and show that an MIT complex drives thes
116 ccumulate at the leading edge of a number of migrating cells and that PI3Ks and PTEN associate with t
117 ositioning is an initial polarizing event in migrating cells and that the positions of the nucleus an
118 nces investigating the nature of polarity in migrating cells and the pathways that establish it.
119 egarding the localization of PCP proteins in migrating cells and their impact on the cell biology of
120 ctant stimulation and at the leading edge of migrating cells and this localization is dependent on PI
121 genous CIP4 localized to the leading edge of migrating cells and to invadopodia in cells invading gel
122      DdVASP localizes to the leading edge in migrating cells and to the tips of filopodia.
123 lized compartment-specific PKA activation in migrating cells and used it to reveal that adhesion-medi
124 iosynthetic exocytic pathway is polarized in migrating cells and whether polarized exocytosis promote
125  ZEB expression measurements in collectively migrating cells) and explains the lack of observed mesen
126 results show that motor neurons are actively migrating cells, and are normally trapped in a static po
127  three GTPases are activated at the front of migrating cells, and biochemical evidence suggests that
128 nonmuscle myosin IIA (NMIIA) to the front of migrating cells, and depletion of NMIIA by RNAi disrupts
129 a occurs specifically at the leading edge of migrating cells, and induces the interaction of adenomat
130  filopodia and regulate adhesion dynamics in migrating cells, and its expression is correlated with p
131 n of PKL and beta-PIX to the leading edge of migrating cells, and knockdown of Vav2 results in a decr
132 ically interact at the centrosomal region of migrating cells, and PKC-mediated phosphorylation on Thr
133 ration indirectly by exposing plasminogen to migrating cells, and second, fibrin selectively disrupts
134  possibility that in other contexts in which migrating cells appear to breach tissue barriers, they a
135  2D, or 3D environments, we hypothesize that migrating cells are also able to sense the dimension of
136 by which microtubules control FA turnover in migrating cells are beginning to emerge.
137  actin filament array at the leading edge of migrating cells are interdependent and coupled, but the
138 in ciliary axonemes, neuronal processes, and migrating cells are marked by alpha-tubulin acetylation
139  a major reason for treatment failure: these migrating cells are not eliminated in surgical resection
140 rom the extracellular fluid by CCR2-positive migrating cells as they cross the BBB, resulting in decr
141 3 and the upregulation of MCT4 expression in migrating cells at the edge of the wound.
142 move by diffusion outside cells, attached to migrating cells, attached to carrier molecules, through
143                                              Migrating cells between the graft and the lesion express
144 , mammalian homolog of Diaphanous (mDia), in migrating cells, but factors responsible for localized s
145      MLCK is highly active in the lamella of migrating cells, but not at the retracting tail.
146  and migrating cells reacted to pgp 9.5, and migrating cells, but not the cell clusters, reacted to t
147 unction are regulated at the leading edge of migrating cells by a balance of kinase and phosphatase a
148 indicate that Lgl1 regulates the polarity of migrating cells by controlling the assembly state of NMI
149  by two-photon microscopy and by phenotyping migrating cells by flow cytometry.
150 el regulatory mechanism of NMII in polarized migrating cells by identifying a key molecular determina
151 ymmetric distribution of mitochondria within migrating cells by interfering with mitochondrial fusion
152  complex translocates to the leading edge of migrating cells by membrane trafficking that requires th
153     We found that the nucleus in an isolated migrating cell can move forward without any trailing-edg
154 reveal that the type of protrusion formed by migrating cells can be dynamically controlled independen
155                                              Migrating cells can sustain a relatively constant direct
156                                           In migrating cells, CARMIL2 is important for cell polarity,
157  suggest an "attractive path" model in which migrating cells closely follow a dynamic SDF1a source th
158 d that myosin IIA skewed toward the front of migrating cells, coincident with actin assembly at the l
159                          The leading edge of migrating cells contains rapidly translocating activated
160 :6HP formed in the photoreceptors, and these migrating cells could help modulate the inflammation.
161                                           In migrating cells, cytosolic Ca(2+) pool and Ca(2+) pulses
162                     Guidance of individually migrating cells depends critically on subcellularly loca
163 osome orientation toward the leading edge of migrating cells depends on dynein and microtubules (MTs)
164                                           In migrating cells, depletion of clathrin or Dab2 and ARH i
165 ycling compartment has specific functions in migrating cells discrete from early and recycling endoso
166 eveloping cerebellar white matter, where the migrating cells dispersed widely before entering the int
167                                        These migrating cells do not contribute to venous or lymphatic
168                                        These migrating cells do not replace the entire microglial poo
169 fected, although a decrease in the number of migrating cells does occur after CSF obstruction.
170 ctyostelium, TORC2 functions at the front of migrating cells downstream of the Ras protein RasC, cont
171  been suggested to be spatially regulated in migrating cells due to its ability to control signaling
172 d pseudopod extension at the leading edge of migrating cells during chemotaxis.
173                 Most studies have focused on migrating cells equipped with an existing polarity befor
174 turbations, which revealed that individually migrating cells exhibit diminished chemosensitivity.
175                                              Migrating cells exhibit distinct motility modes and can
176 , which extends from the leading edge of the migrating cell, exploring the cell's neighborhood.
177                                              Migrating cells extend protrusions, probing the surround
178                                           In migrating cells, external signals polarize the microtubu
179 actin also localized to the leading front of migrating cells, F-actin polymerization was unstable, an
180                                           In migrating cells, feedback loops can amplify stochastic f
181 MLC was redistributed to the leading edge of migrating cells following 6 hours of strain on collagen
182 1 (NHE1), which is necessary at the front of migrating cells for polarity and directional motility.
183 in cell transport and delivery that captures migrating cells from the circulating flow.
184 like actin protrusion at the leading edge of migrating cells, functions as a sensor of the local envi
185 osphere labeling with BrdU, we determined if migrating cells had gone through the S-phase of the cell
186 n, which is expressed along the route of the migrating cells, has an inhibitory role in guiding GnRH
187     This analysis revealed that non-radially migrating cells have a complex pattern of extending and
188                               In particular, migrating cells have been shown to sense substrate stiff
189 ominantly accumulates at the leading edge of migrating cells; however, the pathways that link the act
190  an extensive catalog of genes that act in a migrating cell, identify unique molecular functions invo
191 nalyze the co-flux of adhesion components in migrating cells imaged using total internal reflection f
192  the varying nanotopology experienced by the migrating cell in vivo.
193 and high-dynamic-range time-lapse imaging of migrating cells in complex three-dimensional microenviro
194 rity pathway coordinates the polarity of non-migrating cells in epithelial sheets and is required for
195                              The majority of migrating cells in ischemic rats had a neuronal phenotyp
196 g process and nuclear translocation, and the migrating cells in the CC showed both modes.
197 t both attractive and repulsive responses in migrating cells in the central and peripheral nervous sy
198                                We also track migrating cells in the developing zebrafish embryo, demo
199 ly CCL4, significantly reduced the number of migrating cells in vitro, indicating their role in the i
200         Addition of DAN reduces the speed of migrating cells in vivo and in vitro, respectively.
201 nal information regarding the role of CaD in migrating cells in vivo.
202 , and phosphocofilin at the leading edges of migrating cells, in wound-healing assays.
203 adless Myo10 in regions of proliferating and migrating cells, including the embryonic ventricular zon
204 auses loss of vinculin in focal adhesions of migrating cells, increased cell adhesion and impeded rea
205 wth factor-independent and reorient randomly migrating cells inside the sheet when boundary cells beg
206                                           In migrating cells, integrin-based focal adhesions (FAs) as
207                                          The migrating cell is highly polarized with complex regulato
208                       Front-rear polarity of migrating cells is determined by local activation of a s
209       On rigid surfaces, the cytoskeleton of migrating cells is polarized, but tissue matrix is norma
210 nals from these chemokines are integrated by migrating cells is poorly understood.
211                                     Actin in migrating cells is regulated by Rho GTPases.
212 ly (adhesion turnover) in the protrusions of migrating cells is regulated by unclear mechanisms.
213 at MLC-dependent activation of myosin IIB in migrating cells is required to form an extended rear, wh
214                                           In migrating cells, it has been shown that the locations of
215 the disassembly of adhesive cell contacts at migrating cells' lagging ends, immunohistochemical analy
216  results in decreased expression of Cxcr4 in migrating cells, leading to a premature burst of granule
217                            We also show that migrating cells leave behind ACA-containing vesicles, li
218 GAP and actin motor protein, in collectively migrating cells led to altered organization of the actin
219 re dynamic constructs at the leading edge of migrating cells, linking them to the extracellular matri
220                                 Collectively migrating cells maintain group polarity and interpret ex
221 tribution in response to strain in confluent migrating cells may explain the matrix dependence of the
222                       The actin machinery in migrating cells may tune the number of filaments at the
223                                      In live migrating cells, membrane-associated PKA activity was hi
224 ha5beta1-fn adhesions located at the edge of migrating cell monolayers while also increasing alpha5be
225                                            A migrating cell must establish front-to-back polarity in
226  metazoan development and metastatic cancer, migrating cells must carry out a detailed, complex progr
227                                           In migrating cells, myosin contraction provides the driving
228                                              Migrating cells need to overcome physical constraints fr
229 a cells with significantly larger numbers of migrating cells observed in overexpressing clones compar
230                                              Migrating cells of Myxococcus xanthus (MX) in the early
231                                              Migrating cells often exhibit signal relay, a process in
232 al alterations that reduce the dependence of migrating cells on adhesion-contraction force coupling.
233 onditioned medium and reduced the numbers of migrating cells on injured explants.
234 volution of the strain energy exerted by the migrating cells on their substrate is quasi-periodic and
235 ify enhancing factors, measure the effect of migrating cells on underlying extracellular matrix (ECM)
236 r direct observation of H2O2 accumulation in migrating cells or protrusions.
237  with the lipophilic dye DiI shows that late-migrating cells, originating from the trunk neural tube
238                      In contrast to randomly migrating cells, PDGF-induced membrane protrusions have
239                                           In migrating cells, phosphorylated alpha4 accumulated along
240  study was to assess our hypothesis that the migrating cell population included chondrogenic progenit
241 he correlations observed experimentally in a migrating cell population.
242  retrieval of the distinct migrating and non-migrating cell populations for further analysis.
243                                              Migrating cells possess intracellular gradients of activ
244 zeta complex by Cdc42 at the leading edge of migrating cells promotes both the localized association
245 h caspase 8 is recruited to the lamella of a migrating cell, promoting cell migration independent of
246                       At the leading edge of migrating cells, protrusion of the lamellipodium is driv
247                            Cell clusters and migrating cells reacted to pgp 9.5, and migrating cells,
248                                              Migrating cells reorganize their actin and microtubule c
249 tail, but it has been unclear how individual migrating cells respond to Reelin.
250  electron microscopy (TEM) demonstrated that migrating cells retain neuronal structures for signal tr
251                                 Profiling of migrating cells revealed a possible SCF/c-Kit paracrine
252                                  In randomly migrating cells, RhoA activity is concentrated in a shar
253 d by an overall increase in the speed of the migrating cell sheet.
254                    Our results indicate that migrating cells show patterns of local matrix deformatio
255 lipodia, which, in contrast to nonexpressing migrating cells, stained for pAC.
256 s controlled by the small GTPase Rho in fast migrating cells such as leukocytes.
257     The integrin alpha9beta1 is expressed on migrating cells, such as leukocytes, and binds to multip
258  directional persistence and polarization in migrating cells, suggesting a coordination between PKL/V
259  assume distinct subcellular distribution in migrating cells suggests that discrete spatiotemporal re
260                                           In migrating cells, syntaxin clusters polarize to the leadi
261 flects formation of clusters of coordinately migrating cells that are generated further away from the
262 increasingly larger clusters of coordinately migrating cells that move faster with enhanced alignment
263                                           In migrating cells, the actin filament nucleation activity
264 rane protein, present at the leading edge of migrating cells, the expression of which in normal tissu
265  and adaptation of leading-edge machinery in migrating cells, the invasion of one cell into another d
266                                           In migrating cells, the majority of PhdB was found at the l
267 ion of focal contacts at the leading edge of migrating cells, the mechanisms and signaling pathways r
268 tracking and quantifying FAK and paxillin in migrating cells, the normalized FAK/Paxillin fluorescenc
269                                           In migrating cells, the relative importance of myosin II co
270  this invasive migration, acting both in the migrating cells themselves and in the non-migratory pola
271 the same region, and is not expressed in the migrating cells themselves.
272 tegrin transcytosis from the leading edge of migrating cells thereby inhibiting adequate turnover of
273 ocalize p130Cas to nascent adhesive sites in migrating cells thereby leading to the activation of Rac
274 also regulates actin at the leading edges of migrating cells, therefore coordinating cytoskeleton and
275 fic information that precedes the arrival of migrating cells, thus priming the node for a more effect
276 ocytes into inflammatory tissue requires the migrating cell to overcome mechanical forces produced by
277 pithelial migration describes the ability of migrating cells to cross epithelial tissues and occurs d
278 erse polarities, from front-back polarity in migrating cells to dendritic spine morphology in neurons
279           Thus, PGI2 may act as a "brake" on migrating cells to facilitate cell-cell contact and fusi
280 d adherens junction proteins at the front of migrating cells to locally activate Rac1 in response to
281 hosphorylated Rabaptin-5 toward the front of migrating cells to promote delivery of alphavbeta3 to th
282     One month later, OECs formed an apparent migrating cell tract continuously extending from the inj
283 are interdependent and suggest that distinct migrating cell types can coordinately influence each oth
284                                              Migrating cells typically form filopodia that extend fro
285 tin turnover in lamellipodia and lamellae of migrating cells, using quantitative Fluorescent Speckle
286                              We propose that migrating cells utilize dscam to remodel the developing
287 es to cellular polarization in directionally migrating cells via effects on Rho GTPase activity.
288                             In spreading and migrating cells we find local periodic contractions of l
289 tanding of actomyosin function in individual migrating cells, we know little about the mechanisms by
290 nitor cytoskeletal and signaling dynamics in migrating cells, we show that peripheral F-actin bundles
291  serially imaged by confocal microscopy, and migrating cells were evaluated for chondrogenic progenit
292                                              Migrating cells were highly clonogenic and multipotent a
293 orylated CaD is found at the leading edge of migrating cells where dynamic actin filament remodeling
294 se and tensin homolog (Pten) accumulation in migrating cells, whereas Pten overexpression slows ENS p
295 ntains a repulsive activity for tangentially migrating cells, whereas the cerebral cortex contains an
296  in distinct clusters at the leading edge of migrating cells, whereas unphosphorylated alpha4 and pax
297 olocalizes with actin at the leading edge of migrating cells, wherein active actin polymerization and
298  induced mislocalized activation of Cdc42 in migrating cells, which coincided with a displacement of
299 ndito et al.(2006) reveals that tangentially migrating cells within the ventral telencephalon are ess
300 D44 functions to provide directional cues to migrating cells without affecting the motility apparatus

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