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1  phosphoinositides during endocytosis and at invadopodia.
2 tive pathway and suppresses the formation of invadopodia.
3 x by a mechanism independent of conventional invadopodia.
4 esion complexes involved in the formation of invadopodia.
5 phosphorylation of cortactin tyrosine 421 at invadopodia.
6 icle formation but enhances the formation of invadopodia.
7 to subcellular degradative structures termed invadopodia.
8 mediated knockdown inhibits the formation of invadopodia.
9 that UNC-60A disassembles actin filaments at invadopodia.
10 brane traffic in the transport of MT1-MMP to invadopodia.
11  domain to recruit a moesin-NHE-1 complex to invadopodia.
12 A (ADF/cofilin) as an essential regulator of invadopodia.
13 n cell migration, invasion, and formation of invadopodia.
14 d cell migration, invasion, and formation of invadopodia.
15 cell protrusions, including lamellipodia and invadopodia.
16 d functional characteristics associated with invadopodia.
17 the invasive protrusion and the cessation of invadopodia.
18 crease in the number and stability of mature invadopodia.
19 vels, activated EGFR and ERK1, and activated invadopodia.
20 dation and invasion through the formation of invadopodia.
21 ion enhances cofilin phosphorylation outside invadopodia.
22 gulating cofilin's phosphorylation status at invadopodia.
23 y is spatially confined to areas surrounding invadopodia.
24  understand how substrate rigidity regulates invadopodia.
25 t is important for the stability of actin in invadopodia.
26 cTNs are structural or functional analogs of invadopodia.
27 letal mechanisms and functions for McTNs and invadopodia.
28 a PKC site, contributes to its regulation at invadopodia.
29 containing scaffolds such as lamellipodin to invadopodia.
30 small actin-rich membrane protrusions called invadopodia.
31 protrusions, and increased AKT activation in invadopodia.
32 ed the mechanism by which PI3Kbeta regulates invadopodia.
33 e show that Vav2 promotes Rac3 activation at invadopodia.
34 rane targeting of MT1-MMP and its associated invadopodia.
35 nknown function for SHCA in the formation of invadopodia, a process that also required LPP.
36 shes the plasma membrane forward, whereas in invadopodia, actin polymerization couples with the extra
37                                              Invadopodia, actin-based protrusions of invasive carcino
38 e and tumor cell results in the formation of invadopodia, actin-rich matrix degrading protrusions, im
39 sed a possible role for RalB in formation of invadopodia, actin-rich membrane protrusions that contri
40  cells from the primary tumor is mediated by invadopodia, actin-rich protrusive organelles that secre
41 MT1-MMP recycling compartments, required for invadopodia activity and invasion in a 3D collagen matri
42 o correlated with a commensurate increase in invadopodia activity in metastatic cells compared with n
43 f matrix stiffness on the mechanical mode of invadopodia activity of cancer cells cultured in three-d
44 more, there is an optimal rigidity range for invadopodia activity that may be limited by BM rigidity.
45 rmal growth factor receptor (EGFR) modulates invadopodia activity through phosphorylation of the acti
46 matrix metalloproteinase (MT1-MMP)-dependent invadopodia activity.
47 s promotes the formation of matrix degrading invadopodia, adhesion structures linked to invasive migr
48 fness, cells form shorter and more transient invadopodia and are less likely to extend invadopodia ov
49                 Both Src and Arg localize to invadopodia and are required for EGF-induced actin polym
50 in resulted in a decrease in cytosolic pH at invadopodia and blocked cofilin-dependent actin polymeri
51 in pathway mediates functional maturation of invadopodia and breast cancer cell invasion.
52  of invasive dynamics including formation of invadopodia and cell-membrane protrusions, and removal o
53 ell invasion by regulating actin dynamics at invadopodia and enhancing focalized extracellular matrix
54                                              Invadopodia and filopodia are dynamic, actin-based protr
55 otein fascin is known to play a role in both invadopodia and filopodia.
56 d was associated with decreased formation of invadopodia and gelatin degradation.
57 t time, how RhoC activation is controlled at invadopodia and how this activation regulates cofilin ph
58 ation of cofilin leads to destabilization of invadopodia and impairs cell invasion, although the acti
59 MITF-depleted cells display larger number of invadopodia and increased invasion.
60                         MTCBP-1 localizes to invadopodia and interacts with MT1-MMP.
61 s and triggered the appearance of individual invadopodia and invadopodial rosettes in CAFs.
62 formation but does cause decreases in mature invadopodia and matrix degradation, whereas SHIP2 overex
63 e role of c-Src activity on the formation of invadopodia and may provide insight into the mechanisms
64 ctin networks at protrusions associated with invadopodia and other leading edges.
65 ted actin polymerization drives extension of invadopodia and podosomes into the basement layer.
66 sembled that of similar structures (that is, invadopodia and podosomes) described in other cell types
67                                              Invadopodia and podosomes, collectively referred to as i
68 relies on invadosomes, a collective term for invadopodia and podosomes.
69 ranched radial F-actin fibers emanating from invadopodia and rosettes, which may facilitate rosette f
70 e that SHIP2 recruits Mena, but not VASP, to invadopodia and that disruption of SHIP2-Mena interactio
71 ity of KRAS mutant PDAC cell lines exhibited invadopodia and that expression of activated K-Ras is bo
72 show that fascin is an integral component of invadopodia and that it is important for the stability o
73 regulatory role in HNSCC where they suppress invadopodia and tumor invasion.
74  Vav2 SH2 domain disrupts its recruitment to invadopodia, and an SH2-domain mutant form of Vav2 canno
75 n of KIF5B, surface localization of MT1-MMP, invadopodia, and invasion in cancer cells.
76                      UNC-60A localizes to AC invadopodia, and its loss resulted in a dramatic slowing
77 ructures, including lamellipodia, filopodia, invadopodia, and membrane blebs, as well as on cell-cell
78 protein-lipid complexes, receptor complexes, invadopodia, and other cellular structures in the malign
79 nsitive structures, such as focal adhesions, invadopodia, and podosomes, that are directly implicated
80                                              Invadopodia are actin-based protrusions that mediate the
81                                              Invadopodia are actin-rich cell membrane projections use
82                                              Invadopodia are actin-rich protrusions that degrade the
83         Invasive membrane protrusions called invadopodia are believed to facilitate extracellular mat
84                                              Invadopodia are cell protrusions that mediate cancer cel
85                                              Invadopodia are dynamic protrusions that harbor matrix m
86                                              Invadopodia are invasive protrusions with proteolytic ac
87                                              Invadopodia are protrusive structures used by tumor cell
88                                              Invadopodia are protrusive, F-actin-driven membrane stru
89                                              Invadopodia are specialized membrane protrusions that su
90 ward the GTPase Cdc42, which is required for invadopodia assembly [4, 5].
91 y the Abl kinases as essential regulators of invadopodia assembly and function.
92                     Although early stages of invadopodia assembly have been elucidated, little is kno
93 oreover, Abl kinases are readily detected at invadopodia assembly sites and their inhibition prevents
94 TKS4, are key components of the mechanism of invadopodia assembly.
95 bundantly expressed metalloprotease, is also invadopodia associated.
96 We report podoplanin as a novel component of invadopodia-associated adhesion rings, where it clusters
97 MMP-positive endosomes, while LIMK2 controls invadopodia-associated cortactin.
98 that span kPa-GPa moduli, we found a peak of invadopodia-associated extracellular matrix degradation
99 uced calpain-mediated cleavage of the FA and invadopodia-associated proteins talin, focal adhesion ki
100 n is required for its proper localization in invadopodia at the leading edge of breast cancer cells d
101      HNSCC mediates invasion in part through invadopodia-based proteolysis of the extracellular matri
102 reas compliant matrices are not conducive to invadopodia biogenesis.
103 ollagen (HDFC) matrix is a potent inducer of invadopodia, both in carcinoma cell lines and in primary
104 work showed that beta1 integrin localizes to invadopodia, but its role in regulating invadopodial fun
105 were necessary for the efficient assembly of invadopodia by CAFs.
106  how RhoC activity is spatially regulated at invadopodia by p190RhoGEF and p190RhoGAP.
107                                     However, invadopodia can function mechanically, independent of th
108         However, the mechanisms by which the invadopodia can spatiotemporally reorganize their archit
109 30 kPa, which also corresponded to a peak in invadopodia/cell.
110     Released HB-EGF induced the formation of invadopodia, cellular structures that aid cancer cell in
111 trix metalloproteinase (MT1-MMP), a critical invadopodia component required for matrix degradation.
112 ma, including up-regulated expression of the invadopodia component Tks5long, the embryonal proto-onco
113  cells is associated with high expression of invadopodia components and an invasive phenotype.
114                                  In summary, invadopodia contain chemotaxis receptors that can respon
115  loss of function experiments, we determined invadopodia contain receptors involved in chemotaxis, na
116  of PI4KIIbeta also induced the formation of invadopodia containing membrane type I matrix metallopro
117 /Arg(-/-) fibroblasts produced ECM degrading invadopodia containing pY421 cortactin, indicating that
118 s indicate that increased stiffness promotes invadopodia degradation activity.
119 n promotes visceral metastases via increased invadopodia-dependent invasion and anchorage-independent
120 bstantially more effective than conventional invadopodia, distinct in structural organization and reg
121 or SNARE-regulated trafficking of MT1-MMP to invadopodia during cellular invasion of ECM.
122                                              Invadopodia dynamics and their coalescence into rosettes
123  ezrin in regulating focal adhesion (FA) and invadopodia dynamics, two key processes required for eff
124 of Src to phosphorylate cortactin, promoting invadopodia ECM degradation activity and thus assigning
125 m HNSCC cells, where soluble HB-EGF enhanced invadopodia ECM degradation in HNSCC but not in MDA-MB-2
126 l/Arg to phosphorylate cortactin and promote invadopodia ECM degradation.
127 rylation, triggering actin polymerization in invadopodia, ECM degradation, and matrix proteolysis-dep
128 astasis, consistent with a direct link among invadopodia, ECM degradation, and metastasis.
129 of actin-rich degradative protrusions called invadopodia, enabling tumor cells to degrade and break t
130 hat increased stiffness physically restricts invadopodia extension and cell migration in three-dimens
131 tivation, leading to actin polymerization in invadopodia, extracellular matrix degradation, and tumor
132                Invasive carcinoma cells form invadopodia, F-actin-rich matrix-degrading protrusions t
133 alloproteinases or actin regulators and lack invadopodia, F-actin-rich membrane protrusions that faci
134  and new therapeutic opportunities to target invadopodia for anti-metastasis treatment.
135 se actin-rich membrane protrusions, known as invadopodia, for efficient ECM degradation, which involv
136                                              Invadopodia formation accompanies the mesenchymal mode o
137 re both depletion or overexpression enhanced invadopodia formation and activity.
138 duced K19 expression in an autocrine manner, invadopodia formation and cell invasion.
139                                              Invadopodia formation and cell migration assays were per
140 nphosphorylable mutants blocks SrcYF-induced invadopodia formation and ECM degradation, while the ove
141 al Rac and Cdc42 activity, F-actin assembly, invadopodia formation and experimental metastasis.
142                                              Invadopodia formation and function are regulated by cyto
143 bl kinase signaling plays a critical role in invadopodia formation and function, and have far-reachin
144 LK, PTK7) or enhances (e.g., ABL2, AXL, CSK) invadopodia formation and function.
145 steps in the metastatic cascade by elevating invadopodia formation and in vivo extravasation.
146 actin cytoskeletal changes such as adhesion, invadopodia formation and invasion.
147  drives deposition of MT1-MMP at the site of invadopodia formation and is critical for metastasis in
148 Invasive 3D cancer cell migration as well as invadopodia formation and matrix degradation was impaire
149  cortactin to MT1-MMP-positive endosomes and invadopodia formation and matrix degradation.
150    Mechanistically, this is due to increased invadopodia formation and matrix metalloproteinase secre
151  comprising TKS5, FGD1, and CDC42, directing invadopodia formation and the polarization of MT1-MMP re
152 ugh which TKS proteins direct collagenolytic invadopodia formation are poorly defined.
153 ition impairs matrix protein degradation and invadopodia formation associated with significantly fast
154 ignaling pathways involved in collagenolytic invadopodia formation downstream of TKS4 or TKS5 in brea
155 ental cues and signaling factors that induce invadopodia formation during extravasation remain unclea
156 h the Ror2 receptor tyrosine kinase promotes invadopodia formation for tumor invasion.
157 paxillin phosphorylation, cell motility, and invadopodia formation in a manner dependent upon upstrea
158 role of Src and Abl kinases to regulate also invadopodia formation in cancer cells, our findings sugg
159 ates podosome formation in myeloid cells and invadopodia formation in cancer cells, we addressed whet
160 f Tks5, a Src substrate that is required for invadopodia formation in mammalian cells blocked formati
161 lar matrix-coated coverslips showed enhanced invadopodia formation in response to VEGF that was HEF1-
162 odel stroma and BM, we expected to find more invadopodia formation on the stroma, and this was verifi
163  cell invasion yet does not appear to affect invadopodia formation or function.
164 nvolved in the redox-dependent regulation of invadopodia formation remain unclear.
165  its activated state, is a potent inducer of invadopodia formation through Cdc42, even in the absence
166 ha and HIF2alpha drive melanoma invasion and invadopodia formation through PDGFRalpha and focal adhes
167 ty, matrix metalloproteinase expression, and invadopodia formation via the phosphatidylinositol 3-kin
168 ration, invasion, anchorage independence and invadopodia formation, and dystrophin inactivation was f
169 combinant reelin, suppressed cell migration, invadopodia formation, and invasiveness in vitro.
170                     CARMIL2 is necessary for invadopodia formation, as well as cell polarity, lamelli
171 s a critical mediator of TGF-beta-stimulated invadopodia formation, cell migration, and invasion.
172  binding protein 1 (MTCBP-1) with respect to invadopodia formation, matrix remodeling, and invasion b
173  to promote pro-invasive gene expression and invadopodia formation.
174 ired for, and, unexpectedly, sufficient for, invadopodia formation.
175 ibits matrix metalloproteinase secretion and invadopodia formation.
176 bition of Rac-dependent processes, including invadopodia formation.
177 nd haptotaxis as well as integrin-stimulated invadopodia formation.
178 ic invadopodia, which differ from dotty-like invadopodia forming on the gelatin substratum model.
179 s gelatin degradation and migration speed of invadopodia-forming A375 melanoma cells.
180 re, they identify Arg as a novel mediator of invadopodia function and a candidate therapeutic target
181 doplanin has a key role in the regulation of invadopodia function in SCC cells, controlling the initi
182  indicating that Abl/Arg are dispensable for invadopodia function in this system.
183 Furthermore, Rac1 activation is required for invadopodia function, while its inactivation promotes Rh
184 g cortactin pY421 and pS405/418 required for invadopodia function.
185 indicated that EGFR and Src are required for invadopodia function.
186 vate core invadopodia regulators and enhance invadopodia function.
187 n understanding of the mechanisms regulating invadopodia has been hindered by the difficulty of exami
188                                              Invadopodia have highly dynamic actin that is assembled
189  the formation of invasive structures called invadopodia; however, it is unclear how Stx4 function is
190                  We identify two pathways at invadopodia important for integrin activation and delive
191  Cancer cell invasion and metastasis rely on invadopodia, important extensions of the cytoskeleton th
192 vadopodia or migrate in the direction of the invadopodia in 2D environments.
193 e formation of mature, degradation-competent invadopodia in both two- and three-dimensional matrices
194 to the role of PI3Kbeta in the regulation of invadopodia in breast cancer cells.
195 rn promotes the assembly of matrix-degrading invadopodia in CAFs and tumor cell invasion.
196 f PI(3,4)P2, which correlated with increased invadopodia in epidermal growth factor (EGF)-stimulated
197  necessary for the maintenance of functional invadopodia in human colon cancer cells.
198 e of the tyrosine kinome in the formation of invadopodia in metastatic melanoma cells.
199                          Instead, actin-rich invadopodia in the pioneer axon are necessary and suffic
200 eriments demonstrated that Tks5long promoted invadopodia in vitro and increased metastasis in transpl
201 EGF via assembly, stability, and turnover of invadopodia in vivo.
202 ntly enhanced McTN formation, but suppressed invadopodia, including the appearance of F-actin cores a
203 r Hic-5 in orchestrating the organization of invadopodia into higher-order rosettes, which may promot
204 cidated, little is known about maturation of invadopodia into structures competent for ECM proteolysi
205 of phosphatidylinositol(3,4)-bisphosphate at invadopodia is a key determinant for invadopodia maturat
206              Early podoplanin recruitment to invadopodia is dependent on lipid rafts, whereas ezrin/m
207  whose recycling to form dynamic, functional invadopodia is dependent on localized F-actin disassembl
208                    Trafficking of MT1-MMP to invadopodia is required for the function of these struct
209 e phosphorylation-dephosphorylation cycle at invadopodia is unknown.
210            Rac3 activity, at and surrounding invadopodia, is controlled by Vav2 and betaPIX.
211 d for the development of focal adhesions and invadopodia, key machineries for cell migration and inva
212 nd cofilin-dependent barbed-end formation at invadopodia, leading to a significant decrease in the nu
213 ECM degradation associated with formation of invadopodia-like feature, suggesting that TIMP2 is a neg
214                       ROS generators induced invadopodia-like protrusions and invasion in heterozygou
215 ssed, noncancerous cells developed prominent invadopodia-like protrusions and showed increased matrix
216          Activation of Src-signaling induced invadopodia-like protrusions in wild type epithelial cel
217 mediated by enhanced PI3K-Akt activation and invadopodia-like protrusions.
218 ever, at higher stress values, cells utilize invadopodia-like structures to mediate protease-dependen
219 trusions within the epithelium that resemble invadopodia, matrix-degrading protrusions present in inv
220  regulation and the roles of this pathway in invadopodia maturation and cell invasion are not fully u
221 w that the ER protein Protrudin orchestrates invadopodia maturation and function.
222 trate that this occurs through inhibition of invadopodia maturation and shedding of membrane-derived
223 ly, we demonstrate that podoplanin regulates invadopodia maturation by acting upstream of the ROCK-LI
224                                     Complete invadopodia maturation depends on protrusion outgrowth a
225 rtactin phosphorylation is a key step during invadopodia maturation, regulating Nck1 binding and cofi
226 hate at invadopodia is a key determinant for invadopodia maturation.
227                                   Tumor cell invadopodia mediate degradation of matrix barriers.
228 fold function of SHIP2 as a prerequisite for invadopodia-mediated ECM degradation.
229  a high Tks5long to Tks5short ratio promotes invadopodia-mediated invasion and metastasis.
230 cell carcinomas (SCCs), in the regulation of invadopodia-mediated matrix degradation.
231 eed for combined therapy in order to prevent invadopodia-mediated metastasis in melanoma.
232    Surprisingly, we observed another peak in invadopodia numbers at 2 GPa as well as gene expression
233           Pyk2 colocalizes with cortactin to invadopodia of invasive breast cancer cells, where it me
234                                              Invadopodia of tumor cells are actin-rich proteolytic pr
235 work was required for efficient induction of invadopodia on dense fibrillar collagen and for local de
236 ctivity, and cells do not form fully matured invadopodia or migrate in the direction of the invadopod
237 t phenotypes and the degradative activity of invadopodia, our findings show that increased stiffness
238 osomes to the plasma membrane, enabling both invadopodia outgrowth and MT1-MMP exocytosis.
239 nt invadopodia and are less likely to extend invadopodia overall, contrasting with results from 2D st
240 CC cells treated with inhibitors of the EGFR-invadopodia pathway indicated that EGFR and Src are requ
241 nase c-Src is necessary for the formation of invadopodia, phosphotyrosine-rich structures which degra
242 dings present the first direct evidence that invadopodia play a role in tissue cell invasion in vivo.
243 ruitment of the metalloproteinase MT1-MMP to invadopodia plays a critical role in this invasive proce
244                                The number of invadopodia positively correlated with degradation, whil
245 omotes actin polymerization at newly-forming invadopodia, promoting their maturation to matrix-degrad
246                                 Cells extend invadopodia protrusions to create channels in the nanopo
247                                              Invadopodia provide an elegant way for tumor cells to pr
248  a unique interplay between AXL and ERBB3 in invadopodia regulation that points to the need for combi
249 naling pathway, which can also activate core invadopodia regulators and enhance invadopodia function.
250 responsible for cortactin phosphorylation in invadopodia remain unknown.
251  are mediated in part by PAK1 which controls invadopodia responsiveness to ligands such as GABA and E
252         RhoC activation in areas surrounding invadopodia restricts cofilin activity to within the inv
253                        Molecular analysis of invadopodia revealed that their composition resembled th
254 nisms and suggest that targeting of multiple invadopodia signaling networks may serve as a potential
255              Conversely, Tks5short decreased invadopodia stability and proteolysis, acting as a natur
256                                   Control of invadopodia stability is critical for efficient degradat
257 doplanin downregulation in SCC cells impairs invadopodia stability, thereby reducing the efficiency o
258 extracellular matrix as a result of impaired invadopodia stability.
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 rhabditis elegans, we identify F-actin-based invadopodia that breach basement membrane.
264 ed by the proto-oncogene Src form individual invadopodia that can spontaneously self-organize into la
265 uss several key components and regulators of invadopodia that have been uniquely implicated in tumor
266 of stiffness, we find that cells form mature invadopodia that often precede migration in the directio
267 that this interaction displaces MT1-MMP from invadopodia, thereby attenuating their number and functi
268                        In marked contrast to invadopodia, this degradation does not require the actio
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  switch between the use of microvesicles and invadopodia to facilitate invasion through the extracell
275  use invasive finger-like protrusions termed invadopodia to invade into and degrade extracellular mat
276 ized actin-based membrane protrusions termed invadopodia to perform matrix degradation.
277 ites lack the punctate shape of conventional invadopodia to spread along the cell base and are reticu
278  is critical for integrating the adhesion of invadopodia to the extracellular matrix (ECM) with their
279 sive breast cancer cells impairs both FA and invadopodia turnover.
280  the formation and function of adhesions and invadopodia, two key cellular structures required for br
281 of proteolytic cellular protrusions known as invadopodia, undergoes an isoform switch during metastat
282 ling, as demonstrated by a rapid decrease in invadopodia upon inhibition of autocrine HBEGF/EGFR sign
283 noma cells, HDFC matrix induced formation of invadopodia via a specific integrin signaling pathway th
284 hosignaling mechanism regulates cell surface invadopodia via kindlin2 for local proteolytic remodelin
285                Although a role for N-WASP in invadopodia was known, we now show how N-WASP regulates
286 ar invadosomes." Interestingly, podosomes or invadopodia were replaced by linear invadosomes upon con
287  matrix degradation and the number of mature invadopodia were significantly decreased with APOE knock
288 ent of suspended cells in vitro, even though invadopodia were strongly suppressed.
289 rotrudin or Synaptotagmin VII, respectively, invadopodia were unable to expand and elongate.
290 e an inherent capacity to generate extensive invadopodia when embedded in a blood clot.
291 e identified L-plastin as a new component of invadopodia, where it contributes to degradation and inv
292 ed protrusions of the plasma membrane called invadopodia, where the trans-membrane type 1 matrix meta
293 Rac3 knockdown reduces matrix degradation by invadopodia, whereas a constitutively active Rac3 can re
294 adative protrusions (invasive pseudopods and invadopodia), which allows their efficient dispersal dur
295 s accompanied by the formation of actin-rich invadopodia, which adhere to the extracellular matrix an
296 ollagen fibers form elongated collagenolytic invadopodia, which differ from dotty-like invadopodia fo
297 can partially rescue actin polymerization in invadopodia while Src overexpression cannot compensate f
298 calization revealed that HEF1 colocalized to invadopodia with MT1-MMP.
299  Tks5 in Src-transformed fibroblasts blocked invadopodia without affecting McTNs.
300 to the capacity of AXL to directly stimulate invadopodia, yet its suppression upregulates the ERBB3 s

 
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