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1 ked the LD2 motif of the FAK binding partner paxillin.
2 ent to recruit the signaling adapter protein paxillin.
3 wnstream effectors focal adhesion kinase and paxillin.
4 ntegral focal adhesion proteins vinculin and paxillin.
5  expansion, involving positive regulation of Paxillin.
6 ctivation of focal adhesion kinase (FAK) and paxillin.
7 ed activation of the focal adhesion protein, paxillin.
8 egulatory proteins HSP20, VASP, cofilin, and paxillin.
9 nduced Akt- and MAPK-dependent activation of paxillin.
10 aling pathways mediated by Erk, Akt, FAK and paxillin.
11 illin, resulting in nuclear translocation of paxillin.
12 and phosphorylation of RLC, MYPT1, MBS85 and paxillin.
13 use it shares homology with the LD motifs of paxillin.
14  binding of focal adhesion kinase (FAK) with paxillin.
15 e it facilitates tyrosine phosphorylation of paxillin.
16 ed the preferred calpain proteolytic site in paxillin.
17 tion, which can be reversed by knocking down paxillin.
18 ylation of MYPT1 T853, MYPT1 T696, MBS85 and paxillin.
19 d the focal adhesion molecules FAK, Pyk2 and paxillin.
20 binant VHR directly dephosphorylated FAK and paxillin.
21 urs locally by two-channel imaging of RF and paxillin.
22 evertheless, the LD2-LD4 region of paxillin (paxillin(133-290)) binds to Pyk2-FAT as a 1:1 complex.
23                            Overexpression of paxillin, a cell adhesion protein downstream of NAD+ in
24                    Here, we demonstrate that paxillin, a known cytoplasmic adaptor protein, regulates
25 tly showed that the ability of Cat-1 to bind paxillin, a major constituent of focal complexes, is als
26 oline-rich tyrosine kinase 2 (Pyk2) modulate paxillin activation; however, their role in regulating I
27 mic NPLY(747) motif, to induce spreading and paxillin adapter recruitment to substrate- and talin-bou
28 late phosphorylation of endogenous CrkII and paxillin, adaptor proteins involved in activation of Rho
29                                      Nuclear paxillin also complexed with ERK and ELK1, mediating c-F
30 cal adhesion targeting (FAT) domain binds to paxillin, an adhesion molecule.
31 ins, expressed in CHO.B2 cells, co-flux with paxillin; an analogous cotransport was seen for alpha6be
32 sformation is coupled to its ability to bind paxillin and abrogate its actions as a negative regulato
33                CS induced phosphorylation of paxillin and activated p42/44-MAP kinase, Rho GTPase, an
34  decreased ILK levels and reduced binding to paxillin and alpha-parvin.
35  GIT1 led to enhanced protein degradation of paxillin and alpha5beta1 integrin via proteasome and lys
36  Pyk2 at Tyr(402) and of the Pyk2 substrates paxillin and ASAP1.
37 hesion and cell migration by phosphorylating paxillin and beta-catenin.
38                             Using mutants of paxillin and chimeric proteins between HIC-5 and paxilli
39 PT1 T696, myosin binding subunit 85 (MBS85), paxillin and CPI-17 (PKC-potentiated protein phosphatase
40 se inhibitor reveals a pathway that involves paxillin and CrkII, which ultimately elevates Rac-GTP le
41 aling partner of paxillin, and suggests that paxillin and FAK function cell-autonomously to control m
42 g that the physical molecular aggregation of paxillin and FAK regulates adhesion formation.
43  identify an important collaboration between paxillin and FAK signaling in the modulation of microtub
44               The ACh-induced recruitment of paxillin and FAK to the cell membrane was dependent on R
45 integrins and to intracellular proteins like paxillin and FAK, suggesting a dual role for IL-32 in in
46  co-transfected with either Myc-Hic-5 or Myc-paxillin and FLAG-tagged Smads 1, 5 or 8.
47  including normal phosphorylation of FAK and paxillin and formation of fibrillar adhesions.
48  molecular details of beta-parvin binding to paxillin and help define the requirements for beta-parvi
49                                              Paxillin and Hic-5 are homologous focal adhesion adaptor
50 orylation of focal adhesion proteins such as paxillin and Hic-5 are important for actin cytoskeleton
51 -parvin to focal adhesions requires both the paxillin and integrin-linked kinase binding sites and th
52 tion of the cytoskeletal scaffolding protein paxillin and other host regulatory proteins, as well as
53 angements, including F-actin redistribution, paxillin and PAK4 phosphorylation, and beta1-integrin ac
54 erin-11 co-localizes with beta1-integrin and paxillin and physically interacts with the fibronectin-b
55 ntly regulates Src/focal adhesion kinase and paxillin and prevents anoikis.
56 am signaling, such as the phosphorylation of paxillin and signal transducer and activator of transcri
57 ssociated with a decrease in focal proteins, paxillin and talin, and an impairment in actin depolymer
58 h CD44 and CD49d get access to src, FAK, and paxillin and via lck to the MAPK pathway, with the latte
59  phosphorylation that required expression of paxillin and was not supported by HIC5.
60 ocal adhesion proteins including ILK, PINCH, paxillin, and cdc42, as well as regulating the epithelia
61 osphorylated proteins focal adhesion kinase, paxillin, and cortactin were identified as substrates of
62 e 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intra
63 ma, protein kinase C, focal adhesion kinase, paxillin, and mitogen-activated protein kinases 1, 12, a
64 d increased tyrosine phosphorylation of Cas, paxillin, and Pyk2, which were previously also implicate
65 emingly through its capacity to control Cas, paxillin, and Pyk2.
66 dhesion kinase (FAK), a signaling partner of paxillin, and suggests that paxillin and FAK function ce
67 ppreciated relationship between Src kinases, paxillin, and survival of breast cancer patients.
68 e expression of focal adhesion kinase (FAK), paxillin, and the formation of FAK/Src/Paxillin complex,
69 e, we show that focal adhesion proteins FAK, paxillin, and vinculin but not the cytoskeletal protein
70      Mice with a neural-specific deletion of paxillin are also postnatal viable, but show evidence of
71 ctions between Cat-1 and its binding partner paxillin are necessary to ensure sufficient Akt activati
72  and the GIT1 ARF-GAP protein for binding to paxillin are required but not sufficient for transformat
73 icates that at least six distinct domains of paxillin are required for E6 transformation.
74                        Our results highlight paxillin as a core molecule in substrate modulus-control
75 vel role for calpain-mediated proteolysis of paxillin as a negative regulator of focal adhesion dynam
76                              This identified paxillin as a new Fhl-1 interacting partner, and consequ
77                  To summarize, we identified paxillin as a new regulator protein of PASMC growth.
78 lial cell line U2OS was transfected with GFP-paxillin as an FA marker and subjected to sustained unia
79  LD motif (LD1) of the FA-associated protein paxillin as the binding partner of the p130Cas CCHD (in
80 tion at the nanoscale and recruit a suite of paxillin-associated proteins implicated in invasion and
81 that the assembly of FAK-FAs occurs ahead of paxillin at cell front.
82  dynamics of focal adhesion kinase (FAK) and paxillin at FAs in the protrusion of living endothelial
83 difference between the assemblies of FAK and paxillin at nascent FAs, FAs containing both FAK and pax
84 n, we provide evidence of an accumulation of paxillin at the centrosome that is dependent on focal ad
85 , LD2, and LD4) from the scaffolding protein paxillin, at 2.8, 2.7, and 2.5 A resolution.
86 d Rho activity, indicating that the MLK3-JNK-paxillin axis limits Rho activity to promote focal adhes
87 d FAK (V744G), we find that calpain inhibits paxillin-based adhesion assembly through cleavage of tal
88 lamellipodia membrane and a strengthening of paxillin-based focal adhesion within the same lamellipod
89 sing endogenous wild-type ILK, implying that paxillin binding to ILK is required for its localization
90  self-association, Tyr(925) phosphorylation, paxillin binding, and FA targeting and turnover.
91  Rac1 activity achieved by preventing alpha4/paxillin binding, confined migration requires myosin II-
92            Finally, FAK inhibited IL-32alpha/paxillin binding, whereas FAK also could interact with I
93 s increased when Rac1 is inhibited by alpha4/paxillin binding.
94  alpha-helix, suggesting an induced fit upon paxillin binding.
95 ctions, including recruitment to FAs through paxillin binding.
96                     On soft substrates, most paxillin binds to endocytic factors and facilitates vesi
97                           Phosphorylation of paxillin by Src family kinases, which regulates adhesion
98                                              Paxillin, by modulating microtubule acetylation through
99 egulated upon adhesion, including PYK2/FAK2, Paxillin, CASL and p130CAS consistent with focal adhesio
100    Finally, we show that endogenous CCM3 and paxillin co-localize in mouse cerebral pericytes.
101 ivation, paxillin Ser273 phosphorylation and paxillin complex assembly.
102 ever, our data suggest that the Pyk2-FAT and paxillin complex is dynamic and it appears to be a mixtu
103             Assembly of the Pak-GIT1-betaPIX-paxillin complex was necessary for cdc42 and neuronal Wi
104 FAK), paxillin, and the formation of FAK/Src/Paxillin complex, which are correlated with cell adhesio
105 ation, contractile actin bundles and dynamic paxillin-containing adhesions in the leading process and
106             These vimentin filaments link to paxillin-containing focal adhesions at the lamellipodial
107                 BDNF stimulation accelerates paxillin-containing point contact turnover and formation
108  the cellular focal adhesion adapter protein paxillin contributes to cell transformation and extends
109                             We found nuclear paxillin could then associate with androgen-stimulated a
110                                              Paxillin-deficient neurons have shorter leading processe
111            Multiphoton imaging revealed that paxillin-deficient neurons migrate approximately 30% slo
112  factors requires host serine proteases, and paxillin degradation specifically involves the serine pr
113 s similar in size to the alternative product paxillin delta.
114 d non-phosphorylatable paxillin Y118/31F and paxillin DeltaLD4 deletion mutants in SM tissues.
115 esion kinase (FAK), FAK(PY397), F actin, and paxillin-dependent protrusion formation localizing to th
116                                      Because paxillin depletion did not affect ILK localization to FA
117 h using the example of HeLa cells expressing paxillin-EGFP to visualize focal adhesions.
118 d phosphorylation of pathways involving MET, paxillin, EPHA2, and VEGFR.
119                   We show that knocking down paxillin expression in HeLa cells promotes their ability
120 ne intrapulmonary arteries revealed elevated paxillin expression in hypoxia-induced PH.
121                                 Silencing of paxillin expression led to decreased PASMC adhesion, pro
122 ic pulmonary arterial hypertension patients, paxillin expression was increased on mRNA and protein le
123 tein fibronectin was critically dependent on paxillin expression.
124                   We found that vinculin and paxillin FA area did not correlate with traction force m
125         The significantly higher FAK FI than paxillin FI at cell front indicates that the assembly of
126 illin in migrating cells, the normalized FAK/Paxillin fluorescence intensity (FI) ratio is > 1 ( appr
127  skeleton, and alters the number and size of paxillin focal adhesions.
128  to 0.58), respectively, whereas the average paxillin focal-adhesion-cluster (FAC, formed at poles) l
129 ttom of the cell through a pathway including paxillin, focal adhesion kinase (FAK) and vinculin.
130 e insight into the underlying selectivity of paxillin for Pyk2 and FAK that may influence the differi
131 on of KSHV-TK also induces a loss of FAK and paxillin from focal adhesions, resulting in activation o
132 esions, increase RhoA activity and sequester paxillin from the endocytic machinery, thereby delaying
133       This study proposes a novel concept of paxillin-GEF-H1-p42/44-MAPK module as a regulator of pat
134 sphorylation mutant decreased the CS-induced paxillin/GEF-H1 association (16.3 +/- 4.1%), GEF-H1 acti
135 ibition of p42/44-MAPK suppressed CS-induced paxillin/GEF-H1 interactions (15.9 +/- 7.9%), GEF-H1 act
136 activated p42/44-MAP kinase, Rho GTPase, and paxillin/GEF-H1/p42/44-MAPK association.
137 eased activation of the cytoskeletal protein paxillin, growth factor-induced ischemic retinopathy in
138                                              Paxillin has five leucine-aspartate (LD) motifs (LD1-LD5
139 ed to bind to 14-3-3-zeta and associate with paxillin in a ternary complex that is regulated by serin
140 ependent co-fluxing of certain integrins and paxillin in adhesions in protrusions when they pause, an
141  sABs are capable of pulling down endogenous paxillin in complex with FAK and can visualize paxillin
142 ly, these data reveal a fundamental role for paxillin in coordinating MT acetylation-dependent cell p
143          These results highlight the role of paxillin in facilitating attachment-independent signal t
144 xillin in complex with FAK and can visualize paxillin in focal adhesions in cells.
145 our data implicates beta1 integrin, FAK, and paxillin in mediating the observed pro-adhesive effects
146          By tracking and quantifying FAK and paxillin in migrating cells, the normalized FAK/Paxillin
147 identified a cell-autonomous requirement for paxillin in migrating neurons.
148 nd its interactions with the Arf GTPases and paxillin in oncogenic transformation.
149                         Specific deletion of paxillin in postmitotic neurons using Nex-Cre-mediated r
150 opy (SMLM) to investigate integrin beta3 and paxillin in rat embryonic fibroblasts growing on two dif
151 role for the focal adhesion scaffold protein paxillin in regulating the posttranslational modificatio
152 on of ErbB2, ERK, focal adhesion kinase, and paxillin in response to NRG1, but fail to increase in si
153 AK assembles at the nascent FAs earlier than paxillin in the protrusions at cell front.
154 in soft agar, whereas ectopically expressing paxillin in these cells inhibits this transformed growth
155 horylation in attached cells did not require paxillin, in detached fibroblasts there was remaining FA
156              The phosphomimetic mutations on paxillin increase the size of the complex and the assemb
157 hesion remodeling and the phosphorylation of paxillin independently of upstream regulation by focal a
158                Actopaxin (alpha-parvin) is a paxillin, integrin-linked kinase, and F-actin binding fo
159  about the underlying mechanism by which Cat-paxillin interactions mediate this effect.
160 isruption of focal adhesion kinase (FAK) and paxillin interactions using the small molecule JP-153 in
161 ng "platforms" and are capable of inhibiting paxillin interactions, thereby useful as potential thera
162                                        Thus, paxillin is a liaison between extranuclear MAPK signalin
163 d protein kinase signaling cascades and that paxillin is also likely involved in the regulation of ad
164 cules to modulate the focal adhesion protein paxillin is an effective strategy for treating pathologi
165 ntegrin-linked kinase binding sites and that paxillin is important for early targeting of beta-parvin
166 e that MAPK-dependent targeting of GEF-H1 to paxillin is involved in the regulation of CS-induced Rho
167 lls from forming colonies in soft agar, when paxillin is knocked down together with Cat-1, the cells
168                                      Because paxillin is one of the key scaffold molecules in FAs, we
169 e the similarity between HIC-5 and paxillin, paxillin is required for E6 to transform mouse embryo fi
170 asp-2 with its binding partners vinculin and paxillin is significantly reduced in the presence of las
171 n vivo data show that the phosphorylation of paxillin is specific to adhesions and leads to localized
172                                              Paxillin is therefore a potential biomarker for prostate
173 that a critical difference between HIC-5 and paxillin is within the LIM domains of paxillin that do n
174 that an interaction with another CA protein, paxillin, is essential for correct localization of FAK i
175 thelial ICAM-1/JNK led to phosphorylation of paxillin, its association with VE-cadherin, and internal
176  in EC permeability, which was attenuated by paxillin knockdown.
177                     In the absence of FAK or paxillin, KSHV-TK has no effect on focal adhesion integr
178      The sABs are tools for investigation of paxillin LD binding "platforms" and are capable of inhib
179 by surface plasmon resonance that CCM3 binds paxillin LD motifs with affinities in the micromolar ran
180             The cleavage site is between the paxillin LD1 and LD2 motifs and generates a C-terminal f
181 ture of the p130Cas CCHD in complex with the paxillin LD1 motif by X-ray crystallography.
182 re of beta-parvin CH2 domain in complex with paxillin LD1 motif to 2.9 A resolution and find that the
183 previously observed between alpha-parvin and paxillin LD1.
184 a indicate that a prokaryotic version of the paxillin LD2 domain targets the FAK signaling pathway, w
185    Here, we show that the second LD motif of paxillin, LD2, interacts with Pyk2-FAT, similar to the k
186 ealed a similar level of interaction between paxillin-LD2 and TarP-LD.
187 nt FAK tyrosine phosphorylation required the paxillin LIM domains and suggested that paxillin might f
188  and demonstrated essential functions of the paxillin LIM domains that are not found in HIC5 LIM doma
189 tion, and genetic approaches, we reveal that paxillin-linked endocytosis and adhesion are components
190                       Focal adhesion protein paxillin links integrin and growth factor signaling to a
191 tionship between traction force and vinculin-paxillin localization to single FAs in the context of su
192 hat the enhanced interaction of vinculin and paxillin may functionally destabilize focal adhesion com
193            Herein, we identify new roles for paxillin-mediated HDAC6 inhibition in regulating key asp
194                                              Paxillin mediates stretch-induced Rho signaling and endo
195 ced expression of adhesion complex molecules paxillin, metavincullin, and talin.
196  the paxillin LIM domains and suggested that paxillin might facilitate oncogenic transformation.
197 uced paxillin phosphorylation on Ser273; the paxillin mutant, paxillin S273A, inhibited paxillin Ser2
198                               Analysis using paxillin mutants dissociated domains of paxillin that ar
199 l kinase axis resulting in the activation of paxillin, NF-kappaB, and matrix metalloproteinase-2 (MMP
200 dues (ILK-VT/GG) could neither interact with paxillin nor localize to FA in cells expressing endogeno
201 osphorylation of the focal adhesion scaffold paxillin on Ser 178 and Tyr 118, which was blocked by si
202 eracting target 1 (GIT1), phosphorylation of paxillin on Ser273, and formation and distribution of ad
203 hosphorylates the adhesion junction protein, paxillin, on Ser273, which promotes the formation of a s
204                Our results indicate that the paxillin/p110gamma-PI3K/Cdc42/Rac1 axis is defective in
205 and endothelial permeability via assembly of paxillin-p42/44MAPK-GEF-H1 complex.
206 nsion to test the hypothesis that FA protein paxillin participates in CS-induced Rho activation by re
207  similarly as in the structures with natural paxillin partners.
208 stablish a requirement for the Lhx9-integrin-paxillin pathway in proepicardial organ positioning and
209 r loss of Lhx9 or disruption of the integrin-paxillin pathway results in mis-positioning of the proep
210          Nevertheless, the LD2-LD4 region of paxillin (paxillin(133-290)) binds to Pyk2-FAT as a 1:1
211     Despite the similarity between HIC-5 and paxillin, paxillin is required for E6 to transform mouse
212 dogenous Rgnef-FAK interaction and prevented paxillin phosphorylation and cell motility stimulated by
213                                  ACh induced paxillin phosphorylation and its association with the cd
214 rmore, initiation of downstream signaling by paxillin phosphorylation in residue Y118 was evident, ev
215  cascades, including MEK1/ERK activation and paxillin phosphorylation on S126, which in turn triggers
216                       Pak activation induced paxillin phosphorylation on Ser273; the paxillin mutant,
217 on of integrins and FAK but stronger FAK and paxillin phosphorylation upon attachment to fibronectin.
218  Akt, the formation of a spatial gradient in paxillin phosphorylation, and the activation of RhoA.
219 ouse lung metastases showed enhanced Ser 178 paxillin phosphorylation.
220 etween the p130Cas CCHD and the LD1 motif of paxillin plays an important role in p130Cas FA targeting
221 D phosphomimetic mutant localized to motile, paxillin-positive cytoplasmic complexes, whereas the pho
222 ncrease in the size of focal-adhesion-kinase/paxillin-positive peripheral adhesions and reduced migra
223        To determine whether calpain-mediated paxillin proteolysis regulates focal adhesion dynamics a
224                     Moreover, the density of paxillin puncta is significantly lower in hippocampal gr
225 dent phosphorylation blocks Cdc15 binding to paxillin Pxl1 and C2 domain protein Fic1 and enhances Cd
226 Amphiphysin-Rvs167 (F-BAR) protein Cdc15 and paxillin Pxl1.
227 te cell attachment and cell migration called paxillin (PXN) and HIC-5 (also known as HIC5, ARA55, HIC
228 sphorylation of the focal adhesion component paxillin (PXN) in a VEGF/VEGFR2-independent but NRP1-dep
229 in and the focal adhesion-associated protein paxillin (Pxn) in downstream signaling and functional ac
230 ase (FAK) and the downstream adaptor protein paxillin (PXN), resulting in enhanced cell migration and
231 ampened activation of focal adhesion kinase, paxillin, Rac1, and Erk1/2 during cell adhesion.
232 ion of integrin alpha6, integrin beta4, Fak, paxillin, Rac1/2/3, and ROCK1 in vitro.
233                                              Paxillin recruitment and residence time at FAs, however,
234 assembled at FA first, which was followed by paxillin recruitment to the FA.
235 dependent regulation of the MT cytoskeleton, paxillin regulates both Golgi organelle integrity and po
236 estingly, we find that the scaffold molecule paxillin regulates both processes, making it a critical
237                                 In contrast, paxillin residence time at FAs was independent of local
238 orylation of focal adhesion kinase (FAK) and paxillin resulting in FA disassembly.
239 F promoted MAPK-dependent phosphorylation of paxillin, resulting in nuclear translocation of paxillin
240 ctomyosin bundles move more quickly than the paxillin-rich adhesion plaques, which in turn move more
241 of MLK3, inhibition of JNK, or expression of paxillin S178A all led to enhanced Rho activity, indicat
242 sphorylation on Ser273; the paxillin mutant, paxillin S273A, inhibited paxillin Ser273 phosphorylatio
243  lamin B1, nonmuscle myosin heavy chain IIB, paxillin, Sec61 beta, tight junction protein ZO1, and To
244 e paxillin mutant, paxillin S273A, inhibited paxillin Ser273 phosphorylation and inhibited actin poly
245 f Pak to adhesion junctions, Pak activation, paxillin Ser273 phosphorylation and paxillin complex ass
246 ociated cells showed that Pak activation and paxillin Ser273 phosphorylation triggered the formation
247 issue post-SBI, Robo4 remained unchanged and Paxillin showed a decreasing trend.
248                                      Most of paxillin signaling activity is regulated via leucine-ric
249 we found that Lhx9 acts upstream of integrin-paxillin signaling and consistently demonstrate that eit
250 ther, our findings suggest that the MLK3-JNK-paxillin signaling axis may represent a potential therap
251 hat VEGF-dependent activation of the Src/FAK/paxillin signalsome is required for human retinal endoth
252 ac1 activity which was reversed by Robo4 and Paxillin siRNA.
253 y to alpha-parvin, beta-parvin does not bind paxillin, suggesting distinct interactions and cellular
254 e a mixture of two distinct conformations of paxillin that almost equally compete for Pyk2-FAT bindin
255 sing paxillin mutants dissociated domains of paxillin that are required for regulation of cell migrat
256 , relaying signals from cell-ECM adhesion to paxillin that control cell migration and proliferation.
257 -5 and paxillin is within the LIM domains of paxillin that do not directly interact with E6.
258 an adhesion junction signalling complex with paxillin that included G-protein-coupled receptor kinase
259 Lamina ancestor (LAMA), the scaffold protein Paxillin, the endocytotic regulator Shibire (Dynamin), a
260 h the interaction of lasp-2 with vinculin or paxillin, this effect is greatly diminished in the prese
261     We observe recruitment of phosphorylated paxillin to activated EGFR at these patterned features,
262  the first paradigm validating modulation of paxillin to inhibit angiogenesis.
263 rotrusion by directly binding and recruiting paxillin to nascent adhesions.
264 merization of fibronectin and recruitment of paxillin to sites of lateral integrin alpha5beta1 cluste
265 molecular switch by which GIT1 localization, paxillin trafficking, and cellular protrusive activity a
266 contractility regulated whether vinculin and paxillin turnover dynamics are correlated to each other
267 Galpha13, gastrin-induced FAK Tyr(P)-397 and paxillin Tyr(P)-31 phosphorylation were reduced.
268 n formation, with reduced phosphorylation of paxillin (Tyr(188)).
269 se-induced phosphorylation of FAK (Tyr-397), paxillin (Tyr-118), and ERK1/2 (Thr-202/Tyr-204).
270                                              Paxillin tyrosine phosphorylation and its association wi
271  markedly inhibits cell-ECM adhesion-induced paxillin tyrosine phosphorylation, cell migration, and p
272 ors with reduced tyrosine phosphorylation of paxillin upon orthotopic implantation, compared with Rgn
273  leucine-aspartic acid repeat (LD) motifs in paxillin via its C-terminal calponin homology (CH2) doma
274 role during initial cell spreading: it binds paxillin via the pleckstrin homology and F0 domains to a
275 lassical invadosomes, as they do not contain paxillin, vinculin, and beta1/beta3 integrins.
276                                              Paxillin was also required for pericentrosomal Golgi loc
277                                     Finally, paxillin was also shown to be required for optimal anter
278 rthermore, hypoxia-dependent upregulation of paxillin was HIF-1alpha dependent.
279 mportantly ICAM-1-induced phosphorylation of paxillin was required for lymphocyte TEM and converged f
280                                 Accordingly, paxillin was required for normal growth of human prostat
281                        Myc-Hic-5 but not Myc-paxillin was specifically immunoprecipitated with anti-F
282 llin and chimeric proteins between HIC-5 and paxillin, we demonstrate that a critical difference betw
283                             Using mutants of paxillin, we found that dynamic competitive interactions
284 roundabout4 (Robo4) and the adaptor protein, Paxillin were involved in reducing BBB permeability in S
285  at nascent FAs, FAs containing both FAK and paxillin were quantified by image analysis and time corr
286 enuated the activation of MET, Akt, FAK, and paxillin, which are known to regulate adhesion, migratio
287 phosphorylation of focal adhesion kinase and paxillin, which could be restored by re-expression of GI
288 the behavior of the alpha5beta1-integrin and paxillin, which do not co-flux.
289 d by the ability of kindlin to directly bind paxillin, which in turn bound focal adhesion kinase (FAK
290 La cells is dependent on its ability to bind paxillin, while being negatively impacted by its Arf-GAP
291 phosphorylation of focal adhesion kinase and paxillin, while enhancing E-cadherin expression.
292                          We generated mutant paxillin with a point mutation (S95G) that renders it pa
293 s to enhance the interaction of vinculin and paxillin with each other; however, as with the interacti
294 alization of focal adhesion kinase (FAK) and paxillin with integrin beta1 at the basal cell surface a
295 cificity for the LD1, LD2, and LD4 motifs of paxillin, with K(D) values determined to 27, 42, and 73
296 ia phosphorylated spleen tyrosine kinase and paxillin within focal adhesion complexes.
297           Interestingly, IL-32alpha binds to paxillin without the RGD motif being involved.
298 imilarfold decrease in Src Y421 and Y446 and paxillin Y118 was detected, indicating the far-reaching
299 19N and cdc42 T17N, and non-phosphorylatable paxillin Y118/31F and paxillin DeltaLD4 deletion mutants
300 3 inhibited Src-dependent phosphorylation of paxillin (Y118) and downstream activation of Akt (S473),
301                            Expression of the paxillin-Y31/118F phosphorylation mutant decreased the C

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