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1                                              FAK activation is associated with increased expression o
2                                              FAK activation precedes the alpha-SMA expression in HSCs
3                                              FAK activation, via amplification and/or overexpression,
4                                              FAK and other focal adhesion (FA) proteins associate wit
5                                              FAK down-regulation leads to aberrant ciliogenesis due t
6                                              FAK increases key glycolytic proteins, including enolase
7                                              FAK inhibition decreases and overexpression increases in
8                                              FAK inhibition using AZ13256675 blocked FAK(Y397) phosph
9                                              FAK inhibition was sufficient to decrease fibroblast sti
10                                              FAK is directly recruited to active integrins, which enh
11                                              FAK is necessary for CXCL12-induced chemotaxis and assoc
12                                              FAK phosphorylation is substantially decreased in IP6K1
13 parate studies that focal adhesion kinase-1 (FAK) and the chemokine receptor CXCR4 promote epithelial
14 K expression, activating PI3K/AKT and ERK1/2 FAK-downstream pathways in MCL.
15 of HER2 signaling cascade, including ERK1/2, FAK, AKT and PAK1 as well as regulation of the growth, c
16 These collective data indicate that VHR is a FAK phosphatase and participates in regulating the forma
17                          Overexpression of a FAK phosphomimetic and constitutively active mutant p-FA
18        Additionally, combined therapy with a FAK inhibitor and the antiangiogenic agents pazopanib an
19 , but not on 2D substrates, and accordingly, FAK inhibition halts cell migration in 3D microtracks.
20 iveness to the ECM composition and activates FAK/Src pathway signaling by de-repression of the direct
21                                       Active FAK in turn accumulated in the nucleus where it led to t
22 mice, demonstrating that constitutive active FAK signaling downstream of the Pro32Pro33 integrin alph
23                                 Single-agent FAK inhibition using the selective FAK inhibitor VS-4718
24                                     Although FAK inhibition decreased soluble N-ethylmaleimide attach
25                                     Although FAK is known to be required for cell migration through e
26 nhibited TLR4-associated FAK activation, and FAK knockdown prevented MyD88 activation.
27 /67 kDa) and downstream ERK1/2, PI3K/AKT and FAK signalling pathways.
28                    Co-inhibition of BRAF and FAK abolished ERK reactivation and led to more effective
29 late FAK-SRC-CRKL signaling through CRKL and FAK.
30 R through the direct regulation of CXCR4 and FAK expression and FAK/PI3K/AKT pathway activation, cont
31 ow that SOX11 directly upregulates CXCR4 and FAK expression, activating PI3K/AKT and ERK1/2 FAK-downs
32 t regulation of CXCR4 and FAK expression and FAK/PI3K/AKT pathway activation, contributing to a more
33        In turn, focal adhesion formation and FAK/SRC signaling is activated in mesenchymal tumor cell
34 for Crim1 in the regulation of integrin- and FAK-mediated LE cell adhesion during lens development.
35 showed decreased expression of integrins and FAK but stronger FAK and paxillin phosphorylation upon a
36 ctivation of two signalling kinases, JNK and FAK, and stimulating trophoblast migration.
37 resistant point-mutants of talin (L432G) and FAK (V744G), we find that calpain inhibits paxillin-base
38 gration into the tumor microenvironment, and FAK-deficient platelets completely prevented the rebound
39               In vivo, miR-193b mimetics and FAK inhibitor (PF-562271) each inhibited liposarcoma xen
40 sically interacts with FAK, and occludin and FAK phosphorylation can be blocked by DSP and occludin a
41            Coexpression of DSP, occludin and FAK was detected in dental mesenchymal cells during toot
42 n was dependent on expression of p130Cas and FAK activity and was independent of known imatinib targe
43  of paxillin, and suggests that paxillin and FAK function cell-autonomously to control migrating neur
44 important collaboration between paxillin and FAK signaling in the modulation of microtubule acetylati
45 tivation and liver fibrosis progression, and FAK signaling pathway could be a potential target for li
46   Our results suggest that although Pyk2 and FAK are involved in inflammasome activation, only Pyk2 d
47          These findings suggest that SFK and FAK exert distinctive molecular hierarchy depending on t
48                     We observed that SFK and FAK in the lipid rafts and nonrafts are differently regu
49  to detect subcellular activities of SFK and FAK in three-dimensional (3D) settings.
50 reveals intricate interplays between Src and FAK in regulating the dynamic life of single FAs in canc
51 d to tight spatial control of active Src and FAK levels, and so crucially regulates their cancer-asso
52 tion, blocking calpain cleavage of talin and FAK in vivo promotes Rohon-Beard peripheral axon extensi
53       Blocking calpain cleavage of talin and FAK inhibits repulsive turning from focal uncaging of Ca
54 esion assembly through cleavage of talin and FAK, and adhesion disassembly through cleavage of FAK.
55 amics through specific cleavage of talin and FAK.SIGNIFICANCE STATEMENT The proper formation of neuro
56 ar cells decreased during BAPN treatment and FAK inhibition but not Raf inhibition, suggesting that p
57 ood-testis barrier) regulatory genes such as FAK and its phosphomimetic mutants.
58                  Adhesion molecules, such as FAK, are predicted to rescue YAP/TAZ activity in soft en
59 vates surface adhesion receptors, as well as FAK and Src kinases that are essential regulators of the
60  silencing of TLR4 inhibited TLR4-associated FAK activation, and FAK knockdown prevented MyD88 activa
61 GSK3beta(Y216)/beta-catenin regulation axis: FAK and PYK2, elevated in adenomas in APC(min/+) mice an
62                        MUC5AC/integrin beta4/FAK-mediated lung cancer cell migration was confirmed th
63 cells promoted increased association between FAK and CXCR4.
64 identified a novel molecular complex between FAK and Runx1 in the nucleus of SCC cells and showed tha
65 g migration requires the interaction between FAK and Arp2/3, whereas FAK phosphorylation modulates me
66                         Interactions between FAK and CXCR4 were increased upon depletion of ASK1 usin
67      FAK inhibition using AZ13256675 blocked FAK(Y397) phosphorylation but did not alter IAC composit
68 e inhibition of SFK in the non-rafts blocked FAK activation by the cytokines.
69 inin and influencing phosphorylation of both FAK and alpha-actinin through its product 5-IP7.
70                         Ambra1 binds to both FAK and Src in cancer cells.
71                    Phosphorylation of GIV by FAK enhances PI3K-Akt signaling, the integrity of FAs, i
72 hus, we suggest that FHL2 phosphorylation by FAK is a critical, mechanically dependent step in signal
73      These two GEFs are further regulated by FAK/ERK and Src family kinases, respectively.
74 a unique molecular complex comprising CXCR4, FAK, ASK1, and PP5 in ATII cells during wound healing.
75 at recombinant VHR directly dephosphorylated FAK and paxillin.
76             We therefore sought to determine FAK expression in different myeloid cell populations.
77    The discovery of the clinical stage, dual FAK/ALK inhibitor 27b, including details surrounding SAR
78 ncogenic complexes associated with the EGFR, FAK and STAT3 signaling pathways.
79 rol fibroblasts, concomitantly with enhanced FAK(Y397) activity.
80 tivation; knockdown of intestinal epithelial FAK prevented an LPS-induced increase in intestinal perm
81   To distinguish these functions for FIP200 (FAK family-interacting protein of 200 kDa), an Atg in au
82 FAK Y397 autophosphorylation is required for FAK function in vivo and is positively regulated by MYO1
83 in Arp2/3 binding revealed a requirement for FAK in promoting the dense formation, transient stabiliz
84 brane increased, suggesting a novel role for FAK in the progression from assembled SNARE complexes to
85 2 and HSC-CM, suggesting a specific role for FAK.
86                                         Full FAK activation was observed, since phosphorylation was n
87 controlling invadopodium-mediated functions, FAK controls invasiveness of tumor cells by regulating f
88                           On the other hand, FAK-decreased levels of mitochondrial complex I can resu
89 n vivo Collectively, these findings identify FAK as a novel negative regulator of Beclin1-mediated au
90                                 Importantly, FAK inhibitor attenuates liver fibrosis in vivo and sign
91 ably due to the lack of talin involvement in FAK activation and the absence of vinculin in the adhesi
92 -);PyMT tumor cells exhibited a reduction in FAK Y397 phosphorylation.
93 und focal adhesion kinase (FAK) resulting in FAK activation and the formation of lamellipodia.
94 ulate the activity of IL13Ralpha2, including FAK, SRC, PI3K, G-protein-coupled receptors, and TRAIL r
95 ng the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation.
96 lls that signals through an LATS-independent FAK/CDC42/PP1A cascade to control YAP-S397 phosphorylati
97 y with the FAK FERM-kinase linker and induce FAK kinase activity and Y397 phosphorylation.
98 ing growth factor beta-1 (TGF-beta1) induces FAK activation in a time and dose dependent manner.
99 ositive feedback loop that enhances integrin-FAK signaling.
100  progression, and greater levels of integrin-FAK mechanosignaling and Akt signaling in a syngeneic mo
101 ion, and Akt phosphorylation via an integrin/FAK/IGFR-dependent process.
102 metastatic EGFR/Src-dependent beta4 integrin/FAK complex that is involved in breast cancer malignancy
103        Upon disruption of the beta4 integrin/FAK complex, tumorigenesis and metastasis in triple-nega
104 1i inhibited crucial GBM signaling involving FAK and mutant EGFR, EGFRvIII, and abrogated gains in se
105 c-Src and the kinase Syk, but not the kinase FAK, under conditions that precluded extracellular ligan
106 echnology, we identified the tyrosine kinase FAK and the laminin subunit LAMB3 as functional targets
107 c pathways by the Saureus fatty acid kinase (FAK) complex, and FakA is required for virulence.
108 rc activation leading focal adhesion kinase (FAK) activation by 42.6 +/- 12.6 sec.
109 ulin is necessary for Focal Adhesion Kinase (FAK) activation in 3D as vinculin knockdown results in r
110 tified hyperactivated focal adhesion kinase (FAK) activity in neoplastic PDAC cells as an important r
111 enib dephosphorylated focal adhesion kinase (FAK) and extracellular signal-regulated kinases 1/2, whe
112  that is dependent on focal adhesion kinase (FAK) and identify an important collaboration between pax
113 ly, the disruption of focal adhesion kinase (FAK) and paxillin interactions using the small molecule
114 al inhibition of both focal adhesion kinase (FAK) and Raf also induced regression, and levels of phos
115                       Focal adhesion kinase (FAK) and Src family kinases (SFK) are known to play crit
116  signaling components focal adhesion kinase (FAK) and Src.
117 orylation of p130Cas, focal adhesion kinase (FAK) and the downstream adaptor protein paxillin (PXN),
118 y including paxillin, focal adhesion kinase (FAK) and vinculin.
119         We identified focal adhesion kinase (FAK) as a VHR-interacting molecule.
120 previously identified focal adhesion kinase (FAK) as an important regulator of ciliogenesis in multic
121 on proteins talin and focal adhesion kinase (FAK) as proteolytic targets of calpain in Xenopus laevis
122 gnaling downstream of focal adhesion kinase (FAK) autoactivation at the point of Src-mediated phospho
123  in the activation of focal adhesion kinase (FAK) in a protein kinase C dependent manner.
124                       Focal adhesion kinase (FAK) in platelets regulated their migration into the tum
125                       Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase involved in develo
126                       Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that regulates cel
127               Nuclear focal adhesion kinase (FAK) is a potentially important regulator of gene expres
128 nd that activation of focal adhesion kinase (FAK) is necessary for PE-stimulated autophagy suppressio
129                       Focal adhesion kinase (FAK) promotes anti-tumor immune evasion.
130 d the closely related focal adhesion kinase (FAK) regulate tumor cell invasion, albeit via distinct m
131                       Focal adhesion kinase (FAK) regulates different cellular functions, including c
132         Inhibition of focal adhesion kinase (FAK) rescued SERT function in synapses of KI mice, demon
133 , which in turn bound focal adhesion kinase (FAK) resulting in FAK activation and the formation of la
134 occludin Ser(490) and focal adhesion kinase (FAK) Ser(722) and Tyr(576).
135 ily kinases (SFK) and focal adhesion kinase (FAK) sustain AKT and MAPK pathway signaling under contin
136 ted integrins recruit focal adhesion kinase (FAK) that mediates metastatic downstream signaling pathw
137 f the tyrosine kinase focal adhesion kinase (FAK) upon cell stimulation by the extracellular matrix i
138                       Focal adhesion kinase (FAK), a key transmitter of growth factor and anchorage s
139 oduced by deletion of focal adhesion kinase (FAK), a signaling partner of paxillin, and suggests that
140 ces the activation of focal adhesion kinase (FAK), an integrin downstream regulator which is essentia
141 ed protein 5 (MFAP5), focal adhesion kinase (FAK), ERK, and LPP.
142 ing abrogated phospho-focal adhesion kinase (FAK), Jun NH2-terminal kinase (JNK) and c-Jun signals, b
143 ng axis consisting of focal adhesion kinase (FAK), Src, phosphatidylinositol 3-kinase (PI3K), Akt, an
144 hesion stimulation of focal adhesion kinase (FAK)-Src signaling is another upstream negative regulato
145 o-oncogene (CRKL) and focal adhesion kinase (FAK).
146 utophosphorylation of focal adhesion kinase (FAK).
147 ation of activity for focal adhesion kinase (FAK).
148 D2's interaction with Focal Adhesion Kinase (FAK).
149 wn to be regulated by focal adhesion kinase (FAK).
150 well as phosphorylation by active FA kinase (FAK).
151 nd PTK2 (encoding for focal adhesion kinase [FAK]).
152  report that the cytosolic tyrosine kinases, FAK and Pyk2, are differentially involved in NLRP3 and A
153   Herein, we show that focal-adhesion-kinse (FAK) plays a key role in promoting hepatic stellate cell
154  depletion of Beclin1 attenuated PE-mediated/FAK-dependent initiation of myocyte hypertrophy in vivo
155       Finally, we show that a small-molecule FAK kinase inhibitor, VS-4718, which is currently in cli
156 vated Rho A and the focal adhesion molecules FAK, Pyk2 and paxillin.
157                  Expression of LAMB3 but not FAK was upregulated by mutant KRAS.
158                                Pyk2, but not FAK, could directly phosphorylate ASC at Tyr146, and onl
159                       Here we report a novel FAK/PYK2/GSK3beta(Y216)/beta-catenin regulation axis: FA
160                     Mechanistically, nuclear FAK is associated with chromatin and exists in complex w
161 n squamous cell carcinoma (SCC) that nuclear FAK regulates Runx1-dependent transcription of insulin-l
162                            In the absence of FAK or paxillin, KSHV-TK has no effect on focal adhesion
163 ded by multimerization of DCC, activation of FAK and Src family kinases, and increases in exocytic ve
164 demonstrate that this feedback activation of FAK depends on both guanine nucleotide exchange factor a
165    Unexpectedly, we found that activation of FAK, an upstream component of the integrin Tyr(P) signal
166 2-integrin did not prevent the activation of FAK, nor did EDTA-mediated inactivation of the integrin.
167                               Attenuation of FAK-enhanced glycolysis re-sensitizes cancer cells to gr
168 and adhesion disassembly through cleavage of FAK.
169 the myeloid-specific conditional deletion of FAK on vascular remodeling in the mouse femoral arterial
170 pete with focal adhesion targeting domain of FAK for the binding to LD2 and LD4.
171 ile Ln-332 and HSC-CM promoted the escape of FAK from ubiquitination, probably inducing a preferentia
172  that mechanistically separable functions of FAK in NA are required for cells to distinguish distinct
173 sion size, measured by immunofluorescence of FAK and zyxin, accompanies the PE-induced changes in cor
174    Our data shed light on the implication of FAK in RABV infection and provide evidence that P-FAK in
175                                Inhibition of FAK activation blocks the alpha-SMA and collagen express
176                   Furthermore, inhibition of FAK activation significantly reduces HSC migration and s
177                  We found that inhibition of FAK activity blocks elevated frequencies of exocytosis i
178 tion, silencing of p130Cas and inhibition of FAK activity both strongly reduced imatinib and nilotini
179                            The inhibition of FAK and Pyk2 with RNA interference or chemical inhibitor
180                                Inhibition of FAK in the lipid rafts blocked SFK response to fluid flo
181 ess of liver regeneration, and inhibition of FAK may be a promising strategy to accelerate liver rege
182 ta3 antibody and pharmacologic inhibitors of FAK, AKT, JNK or ERK.
183 ally, through experiments with inhibitors of FAK, Src, and PI3K and rescue experiments in MEFs, we fo
184                 We show that localization of FAK at CAs depends on interactions taking place at the a
185 in, is essential for correct localization of FAK in multiciliated cells.
186                      Live-cell microscopy of FAK(-/-)cells with expression of phosphorylation deficie
187                           Phosphorylation of FAK (Y397) was decreased in MUC5AC knockdown cells.
188 of VHR decreased tyrosine phosphorylation of FAK and decreasing VHR promoted FAK tyrosine phosphoryla
189 egrin beta4 that mediates phosphorylation of FAK at Y397 leading to lung cancer cell migration.
190 the point of Src-mediated phosphorylation of FAK Y861/Y925.
191 ine-966, decreased serine phosphorylation of FAK, and decreased association of phosphorylated ASK1 wi
192  the interaction with and phosphorylation of FAK.
193           A major mechanism of regulation of FAK activity is an intramolecular autoinhibitory interac
194 vide important new insights into the role of FAK as a scaffolding protein in molecular complexes that
195     Overall these data show that the role of FAK at CAs displays similarities but also important diff
196 or the first time, establish a vital role of FAK in cancer glucose metabolism through alterations in
197                                  The role of FAK in liver regeneration remains unknown.
198                                 Silencing of FAK or LAMB3 recapitulated the synthetic lethal effects
199  agents are withdrawn, and dual targeting of FAK and VEGF could have therapeutic implications for ova
200                   Phosphorylation on Y397 of FAK promotes dense NA formation but is dispensable for t
201 vent the initial activation of either Src or FAK.
202 homimetic and constitutively active mutant p-FAK-Y407E in these cells was capable of rescuing the PFO
203 ury which can be rescued by overexpressing p-FAK-Y407E mutant.
204 nic cell signalling, including p-PKCbeta1, p-FAK, p-ERK1/2, p-NFkappabeta, p-PLCgamma1 and p-VEGFR2.
205 n RABV infection and provide evidence that P-FAK interaction has a proviral function.
206 creased tyrosine phosphorylation of p130Cas, FAK, PXN and radial spheroid invasion in stem cell lines
207 mally high levels of phospho-Src and phospho-FAK accumulate at focal adhesions, positively regulating
208 HSP70 inhibitors decreased levels of phospho-FAK along with impaired migration, invasion, and metasta
209 cularly at advanced stages, and that phospho-FAK (PTK2) and BRAF are HSP70 client proteins.
210  active beta1 integrin and of phosphorylated FAK and ERK.
211 ced regression, and levels of phosphorylated FAK in vascular cells decreased during BAPN treatment an
212  Furthermore, active/tyrosine-phosphorylated FAK directly binds to PKM2 and promotes PKM2-mediated gl
213 egulating phosphorylated-Src, phosphorylated-FAK, and expression of matrix metalloproteinase (MMP) -2
214 promising target for blocking CXCR4-promoted FAK autophosphorylation and chemotaxis.
215 orylation of FAK and decreasing VHR promoted FAK tyrosine phosphorylation.
216          5-IP7, a product of IP6K1, promotes FAK autophosphorylation.
217 1 is recruited to focal adhesions, promoting FAK-regulated cancer cell direction-sensing and invasion
218   Here, we show that focal adhesion proteins FAK, paxillin, and vinculin but not the cytoskeletal pro
219              Dual targeting of EGFR and PYK2/FAK inhibited complementary key growth and survival path
220  a strategy of cotargeting the EGFR and PYK2/FAK kinases to improve TNBC therapy.
221 FR and the nonreceptor tyrosine kinases PYK2/FAK synergistically inhibits the proliferation of basal-
222     Moreover, the clinical-trial-tested Pyk2/FAK dual inhibitor PF-562271 reduced monosodium urate-me
223  3D as vinculin knockdown results in reduced FAK activation in both 3D uniform collagen matrices and
224 omotes Arp2/3 localization to NA and reduces FAK activity.
225 crease tumor rigidity to indirectly regulate FAK Y397 phosphorylation in tumor cells to promote their
226  which we propose act in concert to regulate FAK signaling.
227               miR-193b was found to regulate FAK-SRC-CRKL signaling through CRKL and FAK.
228  motifs of Crim1 are required for regulating FAK phosphorylation.
229 zation and advance of the cell edge requires FAK-Arp2/3 interaction, which promotes Arp2/3 localizati
230 on the alpha3beta1/Ln-332 axis and requiring FAK ubiquitination, providing new insights into personal
231                     Focal adhesion kinase's (FAK) role in regulating cell migration has recently been
232 gle-agent FAK inhibition using the selective FAK inhibitor VS-4718 substantially limited tumor progre
233  that the concomitant inhibition of both SFK/FAK and EGFR may be a promising therapeutic strategy for
234                                 Combined SFK/FAK inhibition exhibited the most potent effects on grow
235 w selectively decreased cytokine-induced SFK/FAK activation.
236                                    Silencing FAK, but not extracellular signal-regulated kinases 1/2,
237                                     Specific FAK inhibition blocks downstream PI3K/AKT- and ERK1/2-me
238                       Additionally, specific FAK and PI3K inhibitors reduce SOX11-enhanced MCL cell m
239 red with SOX11-knockdown cells, and specific FAK and CXCR4 inhibitors impair SOX11-enhanced MCL engra
240 ion occurs independently of myeloid specific FAK.
241  utilizing a phosphorylation (Y397)-specific FAK inhibitor.
242  of aerobic glycolysis and more specifically FAK-reprogrammed glucose metabolism will disrupt the bio
243 aling pathways (e.g., Ca(2+) release, c-Src, FAK, MAPK, and PI3K); and (c) association with Rho GTPas
244 on of intracellular signaling molecules SRC, FAK, AKT, JNK and ERK.
245 2-induced Smad signaling through a Cdc42-Src-FAK-ILK pathway.
246 domain of ACF7, whose phosphorylation by Src/FAK (focal adhesion kinase) complex is essential for F-a
247 cancer cells, which may involve the EGFR/SRC/FAK signalling.
248 ribed 'spatial rheostat' controlling the Src/FAK pathway.
249 ed that VEGF-dependent activation of the Src/FAK/paxillin signalsome is required for human retinal en
250 al support for the use of the clinical stage FAK/PYK2 inhibitors for treatment of MM, especially in a
251 acts with alpha6/beta4 integrin to stimulate FAK and Src signaling, leading to PI3K activation of pho
252 expression of integrins and FAK but stronger FAK and paxillin phosphorylation upon attachment to fibr
253             VHR-knockout cells have stronger FAK phosphorylation in cell adhesions, long-lasting trai
254 motes an interaction with FAK and subsequent FAK activation.
255 r416 phosphorylation of c-Src and subsequent FAK-mediated activation of ERK and AKT signaling pathway
256  leading edge of motile cells and suppresses FAK.
257      Our results also support that targeting FAK(Y397) may rescue normal mechanobiology in IPF.
258                  These data demonstrate that FAK plays an essential role in HSC activation and liver
259 d carbon-13 tracing studies demonstrate that FAK promotes glucose consumption and glucose-to-lactate
260  provide evidence that despite the fact that FAK is in the active, open conformation at CAs, its kina
261                                We found that FAK activity was elevated in human PDAC tissues and corr
262 recovery after photobleaching, we found that FAK inhibition increased the exchange rate of a phosphot
263                           We also found that FAK inhibition rendered the previously unresponsive KPC
264                                We found that FAK is expressed at equally low levels in Ly6C(hi) and L
265   Extracellular flux analysis indicates that FAK enhances glycolysis and decreases mitochondrial resp
266 ogenesis and ciliary function revealing that FAK plays a scaffolding role in multiciliated cells.
267  in the nucleus of SCC cells and showed that FAK interacted with a number of Runx1-regulatory protein
268              Mechanistically, we showed that FAK phosphorylates Beclin1, a core autophagy protein, on
269                      These data suggest that FAK inhibition increases immune surveillance by overcomi
270       Ultimately, these results suggest that FAK is not required for monocyte migration to the periva
271       In summary, these results suggest that FAK may be a unique target in situations in which antian
272  and the actin cytoskeleton, suggesting that FAK is an important regulator of the CA complex.
273 ess and collagen expression, supporting that FAK(Y397) hyperactivation may underlie the aberrant mech
274 ly, the Postn-Itgav interaction inhibits the FAK/PI3K/AKT pathway in HSCs, leading to increase in p27
275      IL13Ralpha2-triggered activation of the FAK and PI3K/AKT/mTOR pathways was mediated by FAM120A,
276  tendon generation, we demonstrated that the FAK/ERK1/2 signaling pathway regulates CTGF-induced prol
277 escue experiments in MEFs, we found that the FAK/Src/PI3K/Akt signaling pathway to control rRNA trans
278 east cancer cells, probably mediated via the FAK/JNK signaling pathway.
279 lecular motor, to interact directly with the FAK FERM-kinase linker and induce FAK kinase activity an
280  activity controls membrane dynamics through FAK since loss of LKB1 kinase activity results in morpho
281                                        TLR4, FAK, and MyD88 were colocalized.
282 tinal inflammation was dependent on the TLR4/FAK/MyD88 signal transduction axis.
283 and died during mesoderm development akin to FAK kinase-dead mice.
284          However, when Ambra1 cannot bind to FAK, abnormally high levels of phospho-Src and phospho-F
285  Akt pathway activities, thereby pointing to FAK/JNK pathway as the downstream effector of MUCL1 sign
286 amma-Pcdh inhibition of (but not binding to) FAK.
287               Sorafenib down-regulated total FAK, inducing its proteasomal degradation, while Ln-332
288 yrosine (Y) 397, is not required for in vivo FAK function until late midgestation.
289                                         When FAK is present, Ambra1 is recruited to focal adhesions,
290  interaction between FAK and Arp2/3, whereas FAK phosphorylation modulates mechanosensing of ECM stif
291                        We determined whether FAK can act as an intrinsic driver to promote aerobic gl
292            Our data support a model in which FAK Y397 autophosphorylation is required for FAK functio
293         However, the mechanism through which FAK functions in the complex is not clear, and in this s
294 ased association of phosphorylated ASK1 with FAK.
295  intestinal permeability was associated with FAK and MyD88 activation; knockdown of intestinal epithe
296 n using AZD0530 alone or in combination with FAK inhibition.
297 inase activations lead the disassembly, with FAK being activated earlier than Src.
298  reduced, which promotes an interaction with FAK and subsequent FAK activation.
299           Occludin physically interacts with FAK, and occludin and FAK phosphorylation can be blocked
300 sted this hypothesis by generating mice with FAK Y397-to-phenylalanine (F) mutations in the germline.

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