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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
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
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
22 mice, demonstrating that constitutive active FAK signaling downstream of the Pro32Pro33 integrin alph
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
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
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
40 sically interacts with FAK, and occludin and FAK phosphorylation can be blocked by DSP and occludin a
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
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
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
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
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
72 hus, we suggest that FHL2 phosphorylation by FAK is a critical, mechanically dependent step in signal
74 a unique molecular complex comprising CXCR4, FAK, ASK1, and PP5 in ATII cells during wound healing.
77 The discovery of the clinical stage, dual FAK/ALK inhibitor 27b, including details surrounding SAR
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
87 controlling invadopodium-mediated functions, FAK controls invasiveness of tumor cells by regulating f
89 n vivo Collectively, these findings identify FAK as a novel negative regulator of Beclin1-mediated au
91 ably due to the lack of talin involvement in FAK activation and the absence of vinculin in the adhesi
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
100 progression, and greater levels of integrin-FAK mechanosignaling and Akt signaling in a syngeneic mo
102 metastatic EGFR/Src-dependent beta4 integrin/FAK complex that is involved in breast cancer malignancy
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
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
117 orylation of p130Cas, focal adhesion kinase (FAK) and the downstream adaptor protein paxillin (PXN),
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
128 nd that activation of focal adhesion kinase (FAK) is necessary for PE-stimulated autophagy suppressio
130 d the closely related focal adhesion kinase (FAK) regulate tumor cell invasion, albeit via distinct m
133 , which in turn bound focal adhesion kinase (FAK) resulting in FAK activation and the formation of la
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
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
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
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
161 n squamous cell carcinoma (SCC) that nuclear FAK regulates Runx1-dependent transcription of insulin-l
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.
169 the myeloid-specific conditional deletion of FAK on vascular remodeling in the mouse femoral arterial
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
178 tion, silencing of p130Cas and inhibition of FAK activity both strongly reduced imatinib and nilotini
181 ess of liver regeneration, and inhibition of FAK may be a promising strategy to accelerate liver rege
183 ally, through experiments with inhibitors of FAK, Src, and PI3K and rescue experiments in MEFs, we fo
188 of VHR decreased tyrosine phosphorylation of FAK and decreasing VHR promoted FAK tyrosine phosphoryla
191 ine-966, decreased serine phosphorylation of FAK, and decreased association of phosphorylated ASK1 wi
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
199 agents are withdrawn, and dual targeting of FAK and VEGF could have therapeutic implications for ova
202 homimetic and constitutively active mutant p-FAK-Y407E in these cells was capable of rescuing the PFO
204 nic cell signalling, including p-PKCbeta1, p-FAK, p-ERK1/2, p-NFkappabeta, p-PLCgamma1 and p-VEGFR2.
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
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
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
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
225 crease tumor rigidity to indirectly regulate FAK Y397 phosphorylation in tumor cells to promote their
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
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
239 red with SOX11-knockdown cells, and specific FAK and CXCR4 inhibitors impair SOX11-enhanced MCL engra
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
246 domain of ACF7, whose phosphorylation by Src/FAK (focal adhesion kinase) complex is essential for F-a
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
255 r416 phosphorylation of c-Src and subsequent FAK-mediated activation of ERK and AKT signaling pathway
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
262 recovery after photobleaching, we found that FAK inhibition increased the exchange rate of a phosphot
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
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
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
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
285 Akt pathway activities, thereby pointing to FAK/JNK pathway as the downstream effector of MUCL1 sign
290 interaction between FAK and Arp2/3, whereas FAK phosphorylation modulates mechanosensing of ECM stif
295 intestinal permeability was associated with FAK and MyD88 activation; knockdown of intestinal epithe
300 sted this hypothesis by generating mice with FAK Y397-to-phenylalanine (F) mutations in the germline.
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