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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.
42 shes the plasma membrane forward, whereas in invadopodia, actin polymerization couples with the extra
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
51 s promotes the formation of matrix degrading invadopodia, adhesion structures linked to invasive migr
53 in resulted in a decrease in cytosolic pH at invadopodia and blocked cofilin-dependent actin polymeri
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
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
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.
72 sembled that of similar structures (that is, invadopodia and podosomes) described in other cell types
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
81 Vav2 SH2 domain disrupts its recruitment to invadopodia, and an SH2-domain mutant form of Vav2 canno
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
96 omparing ASAP1 and ASAP3, we also found that invadopodia are dispensable for the invasive behavior of
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
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
117 ollagen (HDFC) matrix is a potent inducer of invadopodia, both in carcinoma cell lines and in primary
119 work showed that beta1 integrin localizes to invadopodia, but its role in regulating invadopodial fun
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
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
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
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
137 rylation, triggering actin polymerization in invadopodia, ECM degradation, and matrix proteolysis-dep
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
143 alloproteinases or actin regulators and lack invadopodia, F-actin-rich membrane protrusions that faci
145 hese data suggest a potential mechanism, via invadopodia, for the reported correlation of tissue dens
147 er, PTP1B activity is required for efficient invadopodia formation and breast cancer invasion, which
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
153 bl kinase signaling plays a critical role in invadopodia formation and function, and have far-reachin
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
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
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-
168 odel stroma and BM, we expected to find more invadopodia formation on the stroma, and this was verifi
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
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
185 re, they identify Arg as a novel mediator of invadopodia function and a candidate therapeutic target
187 doplanin has a key role in the regulation of invadopodia function in SCC cells, controlling the initi
189 Furthermore, Rac1 activation is required for invadopodia function, while its inactivation promotes Rh
194 n understanding of the mechanisms regulating invadopodia has been hindered by the difficulty of exami
196 the formation of invasive structures called invadopodia; however, it is unclear how Stx4 function is
198 e formation of mature, degradation-competent invadopodia in both two- and three-dimensional matrices
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
206 eriments demonstrated that Tks5long promoted invadopodia in vitro and increased metastasis in transpl
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
213 whose recycling to form dynamic, functional invadopodia is dependent on localized F-actin disassembl
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
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
236 Surprisingly, we observed another peak in invadopodia numbers at 2 GPa as well as gene expression
238 l mechanisms for actin polymerization in the invadopodia of metastatic carcinoma cells and define fou
240 work was required for efficient induction of invadopodia on dense fibrillar collagen and for local de
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
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.
249 omotes actin polymerization at newly-forming invadopodia, promoting their maturation to matrix-degrad
251 ylated myosin light chain do not localize to invadopodia puncta, active phosphorylated forms of the m
258 doplanin downregulation in SCC cells impairs invadopodia stability, thereby reducing the efficiency o
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
265 uss several key components and regulators of invadopodia that have been uniquely implicated in tumor
268 -containing proteins from focal adhesions to invadopodia through the temporal and spatial regulation
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
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
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
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
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.
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