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1 line using mass spectrometry, including FAK (focal adhesion kinase).
2 GAP, GRAF1 (GTPase Regulator Associated with Focal Adhesion Kinase).
3 tent and showed increased phosphorylation of focal adhesion kinase.
4 of PI3K signaling mediated by integrins and focal adhesion kinase.
5 integrin-linked kinase but is independent of focal adhesion kinase.
6 rylation of N-WASP at the Tyr-256 residue by focal adhesion kinase.
7 cytoskeleton and reduced phosphorylation of focal adhesion kinase.
8 olipase C, or the gamma-Pcdh binding partner focal adhesion kinase.
9 sions, and attenuated autophosphorylation of focal adhesion kinase.
10 oteolysis of the adhesion proteins talin and focal adhesion kinase.
11 otransduction in primary hepatocytes through focal adhesion kinase.
12 ously expressed non-receptor tyrosine kinase focal adhesion kinase.
13 llin independently of upstream regulation by focal adhesion kinase.
14 the MAP/microtubule affinity regulating and focal adhesion kinases.
15 nt change in mass but a 3-fold increase in P-focal adhesion kinase, 1.5-fold increase in P-Akt, and 5
16 ellular phosphorylation signaling, involving focal adhesion kinase-1 (FAK) and PI3 kinase (PI3K)-depe
17 previously reported in separate studies that focal adhesion kinase-1 (FAK) and the chemokine receptor
19 consists of the integrin subunit betanu and focal adhesion kinase 56 (Fak56), both of which are requ
20 e of RhoH the distribution of phosphorylated focal adhesion kinase, a protein known to coordinate act
22 es several oncogenic pathways, such as early focal adhesion kinase activation upstream of PI3K-mTOR,
23 Additionally, integrin beta1d expression and focal adhesion kinase activation were increased in this
24 SLIT2 treatment stimulated Rac and increased focal adhesion kinase activity to enhance cell tension b
27 teractions led to impaired activation of the focal adhesion kinase, an integrin-mediated regulator of
29 ion of integrin-beta3 and phosphorylation of focal adhesion kinase and AKT, known mediators of integr
31 f angiogenic factors and mechanotransducers (focal adhesion kinase and beta1-integrin) ex vivo A 3-we
33 omes that could be reversed by knocking down focal adhesion kinase and depleting it from the MVs or b
36 A induced cytoskeletal changes and activated focal adhesion kinase and ERKs 1/2, and decreased Src ki
37 lated c-MET, total c-MET, and phosphorylated focal adhesion kinase and increased terminal deoxynucleo
38 f transcription 3-mediated activation of the focal adhesion kinase and its associated focal adhesion
39 evealed that integrin beta5 mediates the Src-focal adhesion kinase and MEK-extracellular signal-regul
40 t in SHP-2 exhibited decreased activation of focal adhesion kinase and mitogen-activated protein kina
41 intracellular signaling cascades, including focal adhesion kinase and mitogen-activated protein kina
42 1 integrin, which subsequently regulates Src/focal adhesion kinase and paxillin and prevents anoikis.
43 ion formation and reduced phosphorylation of focal adhesion kinase and paxillin, which could be resto
44 ibitor protein 1, and the phosphorylation of focal adhesion kinase and paxillin, while enhancing E-ca
47 process required integrin signaling through focal adhesion kinase and relied on an intact microtubul
48 eta3 integrin surface expression, activating focal adhesion kinase and Src kinases, and promoting cel
49 ls, TNFalpha-treated cells exhibited reduced focal adhesion kinase and subsequent plasma membrane per
51 ICOS-Fc downmodulated the phosphorylation of focal adhesion kinase and the expression of beta-Pix in
52 ate that integrin-mediated signaling through focal adhesion kinase and the p38 mitogen-activated prot
53 on integrin beta-3 signals that activate the focal-adhesion kinase and c-Src kinase and their downstr
54 ain of IGFBP-1, through integrin engagement, focal adhesion kinase, and integrin-linked kinase, enhan
55 he migratory proteins rho-associated kinase, focal adhesion kinase, and matrix metalloproteinases.
57 SCs increase phosphorylation of ErbB2, ERK, focal adhesion kinase, and paxillin in response to NRG1,
58 mpaired by inhibitors of NADPH oxidase, Syk, focal adhesion kinase, and proline-rich tyrosine kinase
59 lving vasodilator-stimulated phosphoprotein, focal adhesion kinase, and protein-disulfide isomerase i
62 dynamic competitive interactions between E6, focal adhesion kinase, and the GIT1 ARF-GAP protein for
63 n Shp2 depends on hyperactivation of Akt and focal adhesion kinase as well as mammalian target of rap
64 volves stimulation of Src-family kinases and focal adhesion kinase, as well as the localized accumula
65 on of beta1-integrins and phosphorylation of focal adhesion kinase at synaptic sites, and were preven
67 decreased VEGF-dependent phosphorylation of focal adhesion kinase at Tyr407, but had little effect o
68 amily kinases (SFKs), and phosphorylation of focal adhesion kinase at Y397 (pFAK(Y397)), the latter b
70 tein phosphatase 2A (PP2A) and inhibition of focal adhesion kinase by MEK/ERK to allow the binding be
71 lecularly supported by the regulation of the focal adhesion kinase by p38delta in the human breast ce
72 to adopt a structure similar to that of the focal adhesion kinase C-terminal focal adhesion-targetin
73 ent of vinculin and the formation of a novel focal adhesion kinase complex in response to ErbB2 activ
74 n of ACF7, whose phosphorylation by Src/FAK (focal adhesion kinase) complex is essential for F-actin
75 alpain 1, the primary enzyme responsible for focal adhesion kinase degradation, which becomes induced
76 The intricate interplay of this "MEK/ERK-focal adhesion kinase-DLC1-PP2A" quartet provides a nove
77 molecular changes, such as reduced levels of focal adhesion kinase expression and a misbalance in foc
79 th at baseline and after hemodynamic stress; focal adhesion kinase expression was reduced after stres
80 ion in both cell motility and phosphorylated focal adhesion kinase expression, suggesting a defect in
81 rrent FA assembly and Src activation leading focal adhesion kinase (FAK) activation by 42.6 +/- 12.6
83 ase in cell adhesion, as well as in integrin/focal adhesion kinase (FAK) activation, and exhibit an e
84 cular mechanism, whereby adiponectin targets focal adhesion kinase (FAK) activity and disrupts key fe
86 nctly control force transmission to regulate focal adhesion kinase (FAK) activity, a crucial molecula
90 with increased activating phosphorylation of focal adhesion kinase (FAK) and breast cancer anti-estro
91 sion, axon attraction and phosphorylation of focal adhesion kinase (FAK) and Crk-associated substrate
92 lating the phosphorylation and activation of focal adhesion kinase (FAK) and cytoskeletal reorganizat
93 on and localization as well as activation of focal adhesion kinase (FAK) and enhanced cell spreading.
94 se actions, which prevents the activation of focal adhesion kinase (FAK) and extracellular signal-reg
96 illin at the centrosome that is dependent on focal adhesion kinase (FAK) and identify an important co
97 siRNA knockdown to block phosphorylation of focal adhesion kinase (FAK) and increase the size of foc
98 ar mediators of integrin alpha5/Fn1 activity focal adhesion kinase (FAK) and integrin-linked kinase (
100 the interdependence of the tyrosine kinases focal adhesion kinase (FAK) and Mer tyrosine kinase (Mer
103 A decreased expression of integrin-recruited focal adhesion kinase (FAK) and p-FAK, while increasing
104 emporal relationship between the dynamics of focal adhesion kinase (FAK) and paxillin at FAs in the p
106 a1 integrin and decreased phosphorylation of focal adhesion kinase (FAK) and paxillin resulting in FA
107 ed the glucose-responsive co-localization of focal adhesion kinase (FAK) and paxillin with integrin b
109 ntracellular signaling pathways that include focal adhesion kinase (FAK) and phosphoinositide 3-kinas
110 We demonstrate that Lyn association with focal adhesion kinase (FAK) and phosphorylation of FAK a
111 , we demonstrate that VEGF and NRP2 activate focal adhesion kinase (FAK) and promote FAK-dependent br
112 by a decrease in the phosphorylation of both focal adhesion kinase (Fak) and protein kinase B (Akt).
114 ibition results in altered signaling through focal adhesion kinase (FAK) and RhoA GTPase and a transf
118 creases tyrosine phosphorylation of p130Cas, focal adhesion kinase (FAK) and the downstream adaptor p
119 deletion of gH prevented phosphorylation of focal adhesion kinase (FAK) and the transport of viral c
121 hanges in subcellular distribution of active focal adhesion kinase (FAK) are associated with the fusi
122 Tumor necrosis factor-alpha (TNF-alpha) and focal adhesion kinase (FAK) are key regulators of inflam
126 we identify the adhesion proteins talin and focal adhesion kinase (FAK) as proteolytic targets of ca
127 STRADalpha have increased phosphorylation of focal adhesion kinase (FAK) at Tyr(397)/Tyr(861) and enh
128 C family kinase-dependent phosphorylation of focal adhesion kinase (FAK) at tyrosine 925, FAK associa
129 nhibited alpha3beta1 signaling downstream of focal adhesion kinase (FAK) autoactivation at the point
132 yperoxia were abrogated in cells depleted of focal adhesion kinase (FAK) by treatment with small inhi
133 imulate FN matrix assembly and activation of focal adhesion kinase (FAK) compared with the level of a
134 pathways regulated by keratinocyte-specific focal adhesion kinase (FAK) control dermal remodeling vi
135 tly developed breast cancer mouse model with focal adhesion kinase (FAK) deletion in mammary tumor ce
136 NF1 functions downstream of the Drosophila focal adhesion kinase (FAK) Fak56 and physically interac
137 investigate the proposal that integrins and focal adhesion kinase (FAK) form a complex that has stru
138 mics, and release the cell motility effector focal adhesion kinase (FAK) from inhibition by the autop
141 n and a ligand resulted in the activation of focal adhesion kinase (FAK) in a protein kinase C depend
142 5beta1 integrin and downstream signalling to focal adhesion kinase (FAK) in an endoglin-dependent man
144 Here, we show that conditional deletion of focal adhesion kinase (FAK) in embryonic mammary epithel
157 suppresses autophagy and that activation of focal adhesion kinase (FAK) is necessary for PE-stimulat
159 d dogma, that loss of haematopoietic-derived focal adhesion kinase (FAK) is sufficient to enhance tum
160 rrelates with the number of bound integrins, focal adhesion kinase (FAK) phosphorylation correlates w
161 6-stimulated migration, whereas knockdown of focal adhesion kinase (FAK) preferentially inhibited EGF
166 directly bind paxillin, which in turn bound focal adhesion kinase (FAK) resulting in FAK activation
168 was invasion, which was mediated by both Src-focal adhesion kinase (FAK) signaling and Forkhead box p
169 ssays revealed that S100A4 activates Src and focal adhesion kinase (FAK) signaling events, and inhibi
170 ficantly dysregulated expression of genes in focal adhesion kinase (FAK) signaling, a key pathway reg
173 tyrosine kinase 2 (Pyk2) is a member of the focal adhesion kinase (FAK) subfamily of cytoplasmic tyr
174 we report that Src family kinases (SFK) and focal adhesion kinase (FAK) sustain AKT and MAPK pathway
176 orylation and downstream signals of Akt, and focal adhesion kinase (FAK) thus induced were down-regul
187 ed, we examined the phosphorylation state of focal adhesion kinase (Fak)(Ser732), a known target of C
192 and subsequently to partial inactivation of focal adhesion kinase (FAK), a major effector kinase of
193 nger isoforms exhibited increased binding to focal adhesion kinase (FAK), a molecule important for mi
196 e is similar to that produced by deletion of focal adhesion kinase (FAK), a signaling partner of paxi
197 t has been shown to regulate the activity of focal adhesion kinase (FAK), a tyrosine kinase activated
198 hat COUP-TFII also reduces the activation of focal adhesion kinase (FAK), an integrin downstream regu
200 ecrease in invasion, less phosphorylation of focal adhesion kinase (FAK), and an approximately 2-fold
201 A and invadopodia-associated proteins talin, focal adhesion kinase (FAK), and cortactin and reduced c
202 evated mRNA and protein expression levels of focal adhesion kinase (FAK), and increased FAK and Src a
205 Cryptococcus also induces phosphorylation of focal adhesion kinase (FAK), ezrin, and protein kinase C
206 in beta1-integrin activation with vinculin, focal adhesion kinase (FAK), FAK(PY397), F actin, and pa
209 er, mifepristone inhibited the expression of focal adhesion kinase (FAK), paxillin, and the formation
210 -mediated protease-independent function; and focal adhesion kinase (FAK), Rac-1, and NF-kappaB were i
211 egrin-associated signaling molecules such as focal adhesion kinase (FAK), Src, c-Cbl, phosphoinositid
212 we show that a signaling axis consisting of focal adhesion kinase (FAK), Src, phosphatidylinositol 3
213 Vbeta5), and EphrinA2 (EphA2), and activates focal adhesion kinase (FAK), Src, phosphoinositol 3-kina
214 ways, leading to tyrosine phosphorylation of focal adhesion kinase (FAK), the tyrosine kinase Src, an
215 both RACK1 and vimentin have been linked to focal adhesion kinase (FAK), we investigated whether thi
216 tivation, such as phosphorylation of ERK and focal adhesion kinase (FAK), were increased after knockd
217 ve conformations of the kinase domain of the focal adhesion kinase (FAK), which are distinguished by
218 how that fibronectin adhesion stimulation of focal adhesion kinase (FAK)-Src signaling is another ups
219 ied by down-regulation of phosphorylated (p)-focal adhesion kinase (FAK)-Tyr(397) and retention of ne
236 epidermal growth factor receptor (EGFR) and focal adhesion kinase (FAK)/protein kinase B (AKT) signa
238 le activated tyrosine kinases, we identified focal adhesion kinase (FAK, PTK2) as a candidate target
239 We establish that specific targeting of focal adhesion kinase (FAK; also known as PTK2) in endot
240 ed kinase (ERK1/2; by approximately 44%) and focal adhesion kinase (FAK; by approximately 46%) as wel
244 tyrosine kinase 2 (Pyk2) is a member of the focal adhesion kinase family and is highly expressed in
246 serve as a regulatable switch downstream of focal adhesion kinase in the integrin outside-in signali
247 n, fibronectin, and impaired accumulation of focal adhesion kinase, indicating that the GPR56-TG2 int
248 ease in intracellular phosphorylated Src and focal adhesion kinase, integrin-dependent cell signaling
250 l-regulated kinase 1 and 2, Elk-1, p38, Akt, focal adhesion kinase, mechanistic target of rapamycin,
251 invadopodia formation through PDGFRalpha and focal adhesion kinase-mediated (FAK-mediated) activation
252 -2 (Has2) are also enhanced upon PN/INTEGRIN/focal adhesion kinase-mediated activation of PI3K and/or
253 hibition promotes reorganization of integrin/focal adhesion kinase-mediated adhesomes, induction of I
254 w that LKB1 kinase activity is essential for focal adhesion kinase-mediated cell adhesion and subsequ
255 t calpain-mediated proteolysis of talin1 and focal adhesion kinase mediates adhesion disassembly in m
256 -WASP via activation of small Rho GTPase and focal adhesion kinase mediates TGF-beta1-induced paracel
257 luding transforming growth factor-beta/SMAD, focal adhesion kinase, MRTFs, Wnt/beta-catenin and YAP/T
258 pha resulted in increased phosphorylation of focal adhesion kinase on Tyr-407, which induced the recr
259 otein tyrosine kinase 2 (ptk2, also known as focal adhesion kinase or FAK), is reduced in the neuromu
260 ation experiments revealed that Yes bound to focal adhesion kinase or p130Cas more strongly in GD3+ c
261 simultaneous depletion of alpha-catenin and focal adhesion kinase or p21-activated kinase eliminates
263 gration away from the lipid raft-independent focal adhesion kinase pathway and toward a lipid raft-de
266 e prominent tyrosine-phosphorylated proteins focal adhesion kinase, paxillin, and cortactin were iden
267 Shc, phospholipase Cgamma, protein kinase C, focal adhesion kinase, paxillin, and mitogen-activated p
268 hosphorylation and/or dampened activation of focal adhesion kinase, paxillin, Rac1, and Erk1/2 during
269 dingly, BA caused an increase in the size of focal-adhesion-kinase/paxillin-positive peripheral adhes
270 initiation factor eIF5A and upregulates the focal adhesion kinase PEAK1, which transmits integrin an
271 msk mutants fail to localize phosphorylated focal adhesion kinase (pFAK) to the sites of muscle-tend
272 Perlecan augments the reduction in phospho-focal adhesion kinase (phospho-FAK) levels that result f
274 T lymphocytes, which induces ATP secretion, focal adhesion kinase phosphorylation, cell polarization
276 hesion kinase expression and a misbalance in focal adhesion kinase phosphorylation, which may lead to
277 ractions, in part dependent on activation of focal adhesion kinases, promote delivery of basophil-der
278 s and myosin phosphatase activity, including focal adhesion kinase, protein tyrosine kinase-2, Janus
279 the present study show the importance of the focal adhesion kinase Pyk2 downstream of G-protein-coupl
280 yze the contribution of the Ca(2+)-dependent focal adhesion kinase Pyk2 in platelet activation and th
282 ein tyrosine kinases (PTKs), Src family PTK, focal adhesion kinase, Rho GTPase Rac1, and neural Wisko
284 s proliferation of CPCs via beta(1)-integrin-focal adhesion kinase-signal transducer and activator of
285 can bind to INTEGRINs and activate INTEGRIN/focal adhesion kinase signaling pathways and downstream
286 of extracellular signal-regulated kinase and focal adhesion kinase signaling pathways that are critic
288 matrix stiffness and activation of the FAK (focal adhesion kinase)/SRC-signaling pathway, with a sti
289 Importantly LAMB1 stimulated ITG-dependent focal adhesion kinase/Src proto-oncogene non-receptor ty
290 ing Exo(fib+), two major events are induced: focal adhesion kinase/Src-dependent signaling pathways a
291 terference (RNAi) depletion of myosin II and focal adhesion kinase, suggesting that this behavior req
293 lving vasodilator-stimulated phosphoprotein, focal adhesion kinase, the H(+)/K(+) ATPase beta (flippa
294 uding vasodilator-stimulated phosphoprotein, focal adhesion kinase, the membrane phospholipid translo
296 rombin treatment led to increases in phospho-focal adhesion kinase (tyrosine 397), ERK1/2 phosphoryla
298 rgets, epidermal growth factor receptors and focal adhesion kinase, were significantly reduced in c-C
299 eral application, here we apply the model to focal adhesion kinase, which initiates the chemical sign
300 nd activate the non-receptor tyrosine kinase focal adhesion kinase, which plays a key role in signali
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