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1  domain to recruit a moesin-NHE-1 complex to invadopodia.
2 A (ADF/cofilin) as an essential regulator of invadopodia.
3 n cell migration, invasion, and formation of invadopodia.
4 d cell migration, invasion, and formation of invadopodia.
5 cell protrusions, including lamellipodia and invadopodia.
6 d functional characteristics associated with invadopodia.
7 the invasive protrusion and the cessation of invadopodia.
8 crease in the number and stability of mature invadopodia.
9 vels, activated EGFR and ERK1, and activated invadopodia.
10 rane targeting of MT1-MMP and its associated invadopodia.
11 dation and invasion through the formation of invadopodia.
12 ion enhances cofilin phosphorylation outside invadopodia.
13 gulating cofilin's phosphorylation status at invadopodia.
14 y is spatially confined to areas surrounding invadopodia.
15  understand how substrate rigidity regulates invadopodia.
16 t is important for the stability of actin in invadopodia.
17 cTNs are structural or functional analogs of invadopodia.
18 letal mechanisms and functions for McTNs and invadopodia.
19 a PKC site, contributes to its regulation at invadopodia.
20 ve adhesions formed in cancer cells known as invadopodia.
21 rich membrane structures called podosomes or invadopodia.
22 g constitutively active c-Src failed to form invadopodia.
23 ofilin severing activity thereby stabilizing invadopodia.
24 rse collagen gels provided a weak barrier to invadopodia.
25 ly increases both the number and activity of invadopodia.
26 simulates ECM penetration and degradation by invadopodia.
27 matrix but not the formation of podosomes or invadopodia.
28 tive pathway and suppresses the formation of invadopodia.
29 shwork (TM) cells that resemble podosomes or invadopodia.
30 st cancer progression through its effects on invadopodia.
31 es associated with matrix degradation called invadopodia.
32  essential for the formation and function of invadopodia.
33 x by a mechanism independent of conventional invadopodia.
34 phosphorylation of cortactin tyrosine 421 at invadopodia.
35 e show that Vav2 promotes Rac3 activation at invadopodia.
36 icle formation but enhances the formation of invadopodia.
37 to subcellular degradative structures termed invadopodia.
38 mediated knockdown inhibits the formation of invadopodia.
39 that UNC-60A disassembles actin filaments at invadopodia.
40 brane traffic in the transport of MT1-MMP to invadopodia.
41 e more involved in cell-matrix adhesion than invadopodia [2-4].
42 shes the plasma membrane forward, whereas in invadopodia, actin polymerization couples with the extra
43                                              Invadopodia, actin-based protrusions of invasive carcino
44 e and tumor cell results in the formation of invadopodia, actin-rich matrix degrading protrusions, im
45 sed a possible role for RalB in formation of invadopodia, actin-rich membrane protrusions that contri
46 verexpression of Cas or FAK further enhances invadopodia activity in cells plated on rigid polyacryla
47 o correlated with a commensurate increase in invadopodia activity in metastatic cells compared with n
48 more, there is an optimal rigidity range for invadopodia activity that may be limited by BM rigidity.
49 rmal growth factor receptor (EGFR) modulates invadopodia activity through phosphorylation of the acti
50 matrix metalloproteinase (MT1-MMP)-dependent invadopodia activity.
51 s promotes the formation of matrix degrading invadopodia, adhesion structures linked to invasive migr
52                 Both Src and Arg localize to invadopodia and are required for EGF-induced actin polym
53 in resulted in a decrease in cytosolic pH at invadopodia and blocked cofilin-dependent actin polymeri
54 in pathway mediates functional maturation of invadopodia and breast cancer cell invasion.
55 lpain 2, PTP1B, and Src in the regulation of invadopodia and breast cancer invasion.
56  of invasive dynamics including formation of invadopodia and cell-membrane protrusions, and removal o
57 ell invasion by regulating actin dynamics at invadopodia and enhancing focalized extracellular matrix
58                                              Invadopodia and filopodia are dynamic, actin-based protr
59 otein fascin is known to play a role in both invadopodia and filopodia.
60 d was associated with decreased formation of invadopodia and gelatin degradation.
61 (OPN) displayed an increase in the number of invadopodia and gelatinolytic activity as compared with
62 t time, how RhoC activation is controlled at invadopodia and how this activation regulates cofilin ph
63 ation of cofilin leads to destabilization of invadopodia and impairs cell invasion, although the acti
64 l function for calpain 2 in the formation of invadopodia and in the invasive abilities of breast canc
65 MITF-depleted cells display larger number of invadopodia and increased invasion.
66 s and triggered the appearance of individual invadopodia and invadopodial rosettes in CAFs.
67 formation but does cause decreases in mature invadopodia and matrix degradation, whereas SHIP2 overex
68 e role of c-Src activity on the formation of invadopodia and may provide insight into the mechanisms
69 at MDA-MB-231 cells are capable of producing invadopodia and McTNs, both of which contain F-actin.
70 ctin networks at protrusions associated with invadopodia and other leading edges.
71 ted actin polymerization drives extension of invadopodia and podosomes into the basement layer.
72 sembled that of similar structures (that is, invadopodia and podosomes) described in other cell types
73                                              Invadopodia and podosomes, collectively referred to as i
74  domains and contributes to the formation of invadopodia and podosomes.
75 e that SHIP2 recruits Mena, but not VASP, to invadopodia and that disruption of SHIP2-Mena interactio
76 ity of KRAS mutant PDAC cell lines exhibited invadopodia and that expression of activated K-Ras is bo
77 show that fascin is an integral component of invadopodia and that it is important for the stability o
78 show that SV is a component of podosomes and invadopodia and that SV plays a role in invadopodial fun
79  ECM structure and modifications that affect invadopodia and tissue invasion by cells.
80 regulatory role in HNSCC where they suppress invadopodia and tumor invasion.
81  Vav2 SH2 domain disrupts its recruitment to invadopodia, and an SH2-domain mutant form of Vav2 canno
82 n of KIF5B, surface localization of MT1-MMP, invadopodia, and invasion in cancer cells.
83                      UNC-60A localizes to AC invadopodia, and its loss resulted in a dramatic slowing
84 ructures, including lamellipodia, filopodia, invadopodia, and membrane blebs, as well as on cell-cell
85 protein-lipid complexes, receptor complexes, invadopodia, and other cellular structures in the malign
86 nase (FAK) are present in actively degrading invadopodia, and the levels of phospho-Cas and phospho-F
87                                              Invadopodia are actin-based protrusions that mediate the
88                                              Invadopodia are actin-rich cell membrane projections use
89                                              Invadopodia are actin-rich membrane protrusions formed b
90                                              Invadopodia are actin-rich protrusions that degrade the
91                                Podosomes and invadopodia are actin-rich structures that have come und
92                                              Invadopodia are actin-rich subcellular protrusions with
93          The present study demonstrated that invadopodia are associated with invasion by degradation
94         Invasive membrane protrusions called invadopodia are believed to facilitate extracellular mat
95                                              Invadopodia are different from podosomes in the localiza
96 omparing ASAP1 and ASAP3, we also found that invadopodia are dispensable for the invasive behavior of
97                                              Invadopodia are invasive protrusions with proteolytic ac
98                                              Invadopodia are matrix-degrading membrane protrusions in
99                                              Invadopodia are protrusive structures used by tumor cell
100                                              Invadopodia are protrusive, F-actin-driven membrane stru
101 the levels of phospho-Cas and phospho-FAK in invadopodia are sensitive to myosin inhibitors.
102                                              Invadopodia are specialized membrane protrusions that su
103                                              Invadopodia are subcellular organelles thought to be cri
104 ward the GTPase Cdc42, which is required for invadopodia assembly [4, 5].
105 y the Abl kinases as essential regulators of invadopodia assembly and function.
106                     Although early stages of invadopodia assembly have been elucidated, little is kno
107 oreover, Abl kinases are readily detected at invadopodia assembly sites and their inhibition prevents
108 We report podoplanin as a novel component of invadopodia-associated adhesion rings, where it clusters
109 MMP-positive endosomes, while LIMK2 controls invadopodia-associated cortactin.
110 ht chain kinase, and Rho kinase all abrogate invadopodia-associated ECM degradation.
111 that span kPa-GPa moduli, we found a peak of invadopodia-associated extracellular matrix degradation
112 uced calpain-mediated cleavage of the FA and invadopodia-associated proteins talin, focal adhesion ki
113 n is required for its proper localization in invadopodia at the leading edge of breast cancer cells d
114      HNSCC mediates invasion in part through invadopodia-based proteolysis of the extracellular matri
115                     Incorporation of dynamic invadopodia behavior into the model amplified the effect
116 reas compliant matrices are not conducive to invadopodia biogenesis.
117 ollagen (HDFC) matrix is a potent inducer of invadopodia, both in carcinoma cell lines and in primary
118 etion of FAK induces the formation of active invadopodia but impairs invasive cell migration.
119 work showed that beta1 integrin localizes to invadopodia, but its role in regulating invadopodial fun
120 were necessary for the efficient assembly of invadopodia by CAFs.
121  how RhoC activity is spatially regulated at invadopodia by p190RhoGEF and p190RhoGAP.
122 30 kPa, which also corresponded to a peak in invadopodia/cell.
123     Released HB-EGF induced the formation of invadopodia, cellular structures that aid cancer cell in
124 trix metalloproteinase (MT1-MMP), a critical invadopodia component required for matrix degradation.
125 ma, including up-regulated expression of the invadopodia component Tks5long, the embryonal proto-onco
126                      Many Src substrates are invadopodia components, including the novel Nox1 organiz
127  of PI4KIIbeta also induced the formation of invadopodia containing membrane type I matrix metallopro
128 /Arg(-/-) fibroblasts produced ECM degrading invadopodia containing pY421 cortactin, indicating that
129 he inhibitory effect of ECM cross-linking on invadopodia degradation and penetration.
130 n promotes visceral metastases via increased invadopodia-dependent invasion and anchorage-independent
131 bstantially more effective than conventional invadopodia, distinct in structural organization and reg
132 or SNARE-regulated trafficking of MT1-MMP to invadopodia during cellular invasion of ECM.
133  ezrin in regulating focal adhesion (FA) and invadopodia dynamics, two key processes required for eff
134 of Src to phosphorylate cortactin, promoting invadopodia ECM degradation activity and thus assigning
135 m HNSCC cells, where soluble HB-EGF enhanced invadopodia ECM degradation in HNSCC but not in MDA-MB-2
136 l/Arg to phosphorylate cortactin and promote invadopodia ECM degradation.
137 rylation, triggering actin polymerization in invadopodia, ECM degradation, and matrix proteolysis-dep
138 astasis, consistent with a direct link among invadopodia, ECM degradation, and metastasis.
139                                              Invadopodia enable polarized invasion of PC3 cells into
140 of actin-rich degradative protrusions called invadopodia, enabling tumor cells to degrade and break t
141 tivation, leading to actin polymerization in invadopodia, extracellular matrix degradation, and tumor
142                Invasive carcinoma cells form invadopodia, F-actin-rich matrix-degrading protrusions t
143 alloproteinases or actin regulators and lack invadopodia, F-actin-rich membrane protrusions that faci
144  and new therapeutic opportunities to target invadopodia for anti-metastasis treatment.
145 hese data suggest a potential mechanism, via invadopodia, for the reported correlation of tissue dens
146                                              Invadopodia formation accompanies the mesenchymal mode o
147 er, PTP1B activity is required for efficient invadopodia formation and breast cancer invasion, which
148 duced K19 expression in an autocrine manner, invadopodia formation and cell invasion.
149 ignaling leads to Rac1 activation to promote invadopodia formation and cell invasion.
150 lular Src (c-Src) as a negative regulator of invadopodia formation and dynamics in breast cancer cell
151 nphosphorylable mutants blocks SrcYF-induced invadopodia formation and ECM degradation, while the ove
152                                              Invadopodia formation and function are regulated by cyto
153 bl kinase signaling plays a critical role in invadopodia formation and function, and have far-reachin
154 actin cytoskeletal changes such as adhesion, invadopodia formation and invasion.
155  drives deposition of MT1-MMP at the site of invadopodia formation and is critical for metastasis in
156 Invasive 3D cancer cell migration as well as invadopodia formation and matrix degradation was impaire
157  cortactin to MT1-MMP-positive endosomes and invadopodia formation and matrix degradation.
158  participates in the control of podosome and invadopodia formation and suggest that intracellular sod
159 ition impairs matrix protein degradation and invadopodia formation associated with significantly fast
160 h the Ror2 receptor tyrosine kinase promotes invadopodia formation for tumor invasion.
161 paxillin phosphorylation, cell motility, and invadopodia formation in a manner dependent upon upstrea
162 role of Src and Abl kinases to regulate also invadopodia formation in cancer cells, our findings sugg
163 ates podosome formation in myeloid cells and invadopodia formation in cancer cells, we addressed whet
164 invasion through its effects on podosome and invadopodia formation in macrophages and melanoma cells.
165 f Tks5, a Src substrate that is required for invadopodia formation in mammalian cells blocked formati
166 lar matrix-coated coverslips showed enhanced invadopodia formation in response to VEGF that was HEF1-
167                                              Invadopodia formation involves membrane protrusions driv
168 odel stroma and BM, we expected to find more invadopodia formation on the stroma, and this was verifi
169  cell invasion yet does not appear to affect invadopodia formation or function.
170 nvolved in the redox-dependent regulation of invadopodia formation remain unclear.
171 -deficient breast cancer cells show impaired invadopodia formation that is rescued by expression of a
172  its activated state, is a potent inducer of invadopodia formation through Cdc42, even in the absence
173 ha and HIF2alpha drive melanoma invasion and invadopodia formation through PDGFRalpha and focal adhes
174 ty, matrix metalloproteinase expression, and invadopodia formation via the phosphatidylinositol 3-kin
175 ration, invasion, anchorage independence and invadopodia formation, and dystrophin inactivation was f
176 combinant reelin, suppressed cell migration, invadopodia formation, and invasiveness in vitro.
177                     CARMIL2 is necessary for invadopodia formation, as well as cell polarity, lamelli
178 s a critical mediator of TGF-beta-stimulated invadopodia formation, cell migration, and invasion.
179 domains (Tks5)/Fish is required for podosome/invadopodia formation, degradation of ECM, and cancer ce
180 ibits matrix metalloproteinase secretion and invadopodia formation.
181 other hand, overexpression of Exo70 promoted invadopodia formation.
182 ted Arp2/3-mediated actin polymerization and invadopodia formation.
183  to promote pro-invasive gene expression and invadopodia formation.
184 ired for, and, unexpectedly, sufficient for, invadopodia formation.
185 re, they identify Arg as a novel mediator of invadopodia function and a candidate therapeutic target
186                                  Analyses of invadopodia function from cells plated on cross-linked g
187 doplanin has a key role in the regulation of invadopodia function in SCC cells, controlling the initi
188  indicating that Abl/Arg are dispensable for invadopodia function in this system.
189 Furthermore, Rac1 activation is required for invadopodia function, while its inactivation promotes Rh
190 g cortactin pY421 and pS405/418 required for invadopodia function.
191 indicated that EGFR and Src are required for invadopodia function.
192 er physical or chemical ECM signals regulate invadopodia function.
193                              Here we examine invadopodia generation, turnover, and function in relati
194 n understanding of the mechanisms regulating invadopodia has been hindered by the difficulty of exami
195                                              Invadopodia have highly dynamic actin that is assembled
196  the formation of invasive structures called invadopodia; however, it is unclear how Stx4 function is
197                  We identify two pathways at invadopodia important for integrin activation and delive
198 e formation of mature, degradation-competent invadopodia in both two- and three-dimensional matrices
199 rn promotes the assembly of matrix-degrading invadopodia in CAFs and tumor cell invasion.
200 o the leading edge of migrating cells and to invadopodia in cells invading gelatin.
201 ental validation, using live-cell imaging of invadopodia in cells plated on cross-linked gelatin, was
202 f PI(3,4)P2, which correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated
203  necessary for the maintenance of functional invadopodia in human colon cancer cells.
204 -generated podosomes in COS-7 cells and with invadopodia in MDA-MB-231 cells.
205                  To find out the presence of invadopodia in PC3 cells, we performed a few comparative
206 eriments demonstrated that Tks5long promoted invadopodia in vitro and increased metastasis in transpl
207                      Molecular components of invadopodia include branched actin-assembly proteins, me
208 ntly enhanced McTN formation, but suppressed invadopodia, including the appearance of F-actin cores a
209 cidated, little is known about maturation of invadopodia into structures competent for ECM proteolysi
210 t that actin polymerization and formation of invadopodia involve the WASP-Arp2/3 complex pathway.
211 of phosphatidylinositol(3,4)-bisphosphate at invadopodia is a key determinant for invadopodia maturat
212              Early podoplanin recruitment to invadopodia is dependent on lipid rafts, whereas ezrin/m
213  whose recycling to form dynamic, functional invadopodia is dependent on localized F-actin disassembl
214                    Trafficking of MT1-MMP to invadopodia is required for the function of these struct
215 e phosphorylation-dephosphorylation cycle at invadopodia is unknown.
216            Rac3 activity, at and surrounding invadopodia, is controlled by Vav2 and betaPIX.
217 d for the development of focal adhesions and invadopodia, key machineries for cell migration and inva
218 nd cofilin-dependent barbed-end formation at invadopodia, leading to a significant decrease in the nu
219 ECM degradation associated with formation of invadopodia-like feature, suggesting that TIMP2 is a neg
220                       ROS generators induced invadopodia-like protrusions and invasion in heterozygou
221          Activation of Src-signaling induced invadopodia-like protrusions in wild type epithelial cel
222 mediated by enhanced PI3K-Akt activation and invadopodia-like protrusions.
223 ermine whether TM cells exhibit podosome- or invadopodia-like structures (PILS) and whether they prod
224 ever, at higher stress values, cells utilize invadopodia-like structures to mediate protease-dependen
225 4 colocalized with cortactin in podosome- or invadopodia-like structures, but ADAMTS-1 and -5 did not
226 trusions within the epithelium that resemble invadopodia, matrix-degrading protrusions present in inv
227  regulation and the roles of this pathway in invadopodia maturation and cell invasion are not fully u
228 trate that this occurs through inhibition of invadopodia maturation and shedding of membrane-derived
229 ly, we demonstrate that podoplanin regulates invadopodia maturation by acting upstream of the ROCK-LI
230 rtactin phosphorylation is a key step during invadopodia maturation, regulating Nck1 binding and cofi
231 hate at invadopodia is a key determinant for invadopodia maturation.
232                                   Tumor cell invadopodia mediate degradation of matrix barriers.
233 fold function of SHIP2 as a prerequisite for invadopodia-mediated ECM degradation.
234  a high Tks5long to Tks5short ratio promotes invadopodia-mediated invasion and metastasis.
235 cell carcinomas (SCCs), in the regulation of invadopodia-mediated matrix degradation.
236    Surprisingly, we observed another peak in invadopodia numbers at 2 GPa as well as gene expression
237           Pyk2 colocalizes with cortactin to invadopodia of invasive breast cancer cells, where it me
238 l mechanisms for actin polymerization in the invadopodia of metastatic carcinoma cells and define fou
239                                              Invadopodia of tumor cells are actin-rich proteolytic pr
240 work was required for efficient induction of invadopodia on dense fibrillar collagen and for local de
241 ferent than ASAP1, ASAP3 did not localize to invadopodia or podosomes.
242 CC cells treated with inhibitors of the EGFR-invadopodia pathway indicated that EGFR and Src are requ
243 ement membranes, is an effective obstacle to invadopodia penetration and degradation, particularly wh
244 and macrofibrils, little or no inhibition of invadopodia penetration was observed in simulations of s
245  large enough so as to have little impact on invadopodia penetration/degradation.
246 nase c-Src is necessary for the formation of invadopodia, phosphotyrosine-rich structures which degra
247 dings present the first direct evidence that invadopodia play a role in tissue cell invasion in vivo.
248                                The number of invadopodia positively correlated with degradation, whil
249 omotes actin polymerization at newly-forming invadopodia, promoting their maturation to matrix-degrad
250                                              Invadopodia provide an elegant way for tumor cells to pr
251 ylated myosin light chain do not localize to invadopodia puncta, active phosphorylated forms of the m
252 responsible for cortactin phosphorylation in invadopodia remain unknown.
253         RhoC activation in areas surrounding invadopodia restricts cofilin activity to within the inv
254 CM cross-linking led to higher rates of both invadopodia retraction and formation.
255                        Molecular analysis of invadopodia revealed that their composition resembled th
256              Conversely, Tks5short decreased invadopodia stability and proteolysis, acting as a natur
257                                   Control of invadopodia stability is critical for efficient degradat
258 doplanin downregulation in SCC cells impairs invadopodia stability, thereby reducing the efficiency o
259 sembly of actin and cortactin into organized invadopodia structures.
260  involved in the formation and maturation of invadopodia, such as integrin beta1, cortactin, neuronal
261 pecializations of the plasma membrane termed invadopodia that act both to sequester and release matri
262  binding is regulated by local pH changes at invadopodia that are mediated by the sodium-hydrogen exc
263 ls display enhanced assembly and dynamics of invadopodia that are rescued by expression of wild-type
264 rhabditis elegans, we identify F-actin-based invadopodia that breach basement membrane.
265 uss several key components and regulators of invadopodia that have been uniquely implicated in tumor
266                        In marked contrast to invadopodia, this degradation does not require the actio
267 ment, which indicates that calpain modulates invadopodia through PTP1B.
268 -containing proteins from focal adhesions to invadopodia through the temporal and spatial regulation
269                  p190RhoGEF localizes around invadopodia to activate RhoC, whereas p190RhoGAP localiz
270                     Invasive cells use small invadopodia to breach basement membrane (BM), a dense ma
271 te RhoC, whereas p190RhoGAP localizes inside invadopodia to deactivate the GTPase within the structur
272 e specialized, actin-rich protrusions called invadopodia to degrade and invade through the extracellu
273 tin polymerization-driven protrusions called invadopodia to degrade and possibly invade through the e
274 umor cells use actin-rich protrusions called invadopodia to degrade extracellular matrix (ECM) and in
275  switch between the use of microvesicles and invadopodia to facilitate invasion through the extracell
276  use invasive finger-like protrusions termed invadopodia to invade into and degrade extracellular mat
277 ized actin-based membrane protrusions termed invadopodia to perform matrix degradation.
278 ites lack the punctate shape of conventional invadopodia to spread along the cell base and are reticu
279 ver actin filaments to create barbed ends at invadopodia to support Arp2/3-dependent actin polymeriza
280  is critical for integrating the adhesion of invadopodia to the extracellular matrix (ECM) with their
281 sive breast cancer cells impairs both FA and invadopodia turnover.
282 of proteolytic cellular protrusions known as invadopodia, undergoes an isoform switch during metastat
283 ling, as demonstrated by a rapid decrease in invadopodia upon inhibition of autocrine HBEGF/EGFR sign
284 podium assembly and maturation and show that invadopodia use cortactin phosphorylation as a master sw
285 noma cells, HDFC matrix induced formation of invadopodia via a specific integrin signaling pathway th
286 hosignaling mechanism regulates cell surface invadopodia via kindlin2 for local proteolytic remodelin
287 ad to increased matrix-degrading activity at invadopodia, via a myosin II-FAK/Cas pathway.
288                Although a role for N-WASP in invadopodia was known, we now show how N-WASP regulates
289 ar invadosomes." Interestingly, podosomes or invadopodia were replaced by linear invadosomes upon con
290  matrix degradation and the number of mature invadopodia were significantly decreased with APOE knock
291 ent of suspended cells in vitro, even though invadopodia were strongly suppressed.
292 e an inherent capacity to generate extensive invadopodia when embedded in a blood clot.
293 e identified L-plastin as a new component of invadopodia, where it contributes to degradation and inv
294 ed protrusions of the plasma membrane called invadopodia, where the trans-membrane type 1 matrix meta
295 Rac3 knockdown reduces matrix degradation by invadopodia, whereas a constitutively active Rac3 can re
296 adative protrusions (invasive pseudopods and invadopodia), which allows their efficient dispersal dur
297 can partially rescue actin polymerization in invadopodia while Src overexpression cannot compensate f
298 invasiveness of cancer cells, and we compare invadopodia with invasive filopod-like structures in 3D.
299 calization revealed that HEF1 colocalized to invadopodia with MT1-MMP.
300  Tks5 in Src-transformed fibroblasts blocked invadopodia without affecting McTNs.

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