ライフサイエンスコーパス: FAK

1 FAK has also been shown to act as a mechanosensor by mod

2 FAK inhibition decreased formation of tumorspheres and r

3 FAK inhibition decreased many characteristics of the mal

4 FAK inhibition was sufficient to decrease fibroblast sti

5 FAK localizes into focal adhesion complexes formed at th

6 FAK phosphorylation is substantially decreased in IP6K1

7 FAK phosphorylation was increased in jejunal epithelium

8 parate studies that focal adhesion kinase-1 (FAK) and the chemokine receptor CXCR4 promote epithelial

9 ented SH3GL2 expression and decreased RAC-1, FAK, A-Actinin and Vinculin expression.

10 K expression, activating PI3K/AKT and ERK1/2 FAK-downstream pathways in MCL.

11 of HER2 signaling cascade, including ERK1/2, FAK, AKT and PAK1 as well as regulation of the growth, c

12 These collective data indicate that VHR is a FAK phosphatase and participates in regulating the forma

13 autocrine loop to promote invasion through a FAK>p130Cas>c-Jun>MMP-9 signaling axis.

14 in activation at the level of RIAM through a FAK-mediated feedforward mechanism that involves reversa

15 ry ligand CD80 sensitizes murine tumors to a FAK inhibitor and show that CD80 is expressed by human c

16 t with ESC-associated integrins and activate FAK more effectively than fibronectin alone.

17 9027 (10-1000 nM) dose-dependently activated FAK phosphorylation, without activating Pyk2-Tyr-402 or

18 sis stimulates beta3 integrins and activates FAK to induce t-SP and promote cue-induced cocaine seeki

19 eases C-MYC protein stability, and activates FAK/SRC signaling.

20 We show that Galphaq activates FAK through TRIO-RhoA non-canonical Galphaq-signaling, a

21 hich beta-arr1 together with STAM1 activates FAK, we used site-directed spin-labeling EPR spectroscop

22 like FAK mimic ZINC40099027, which activates FAK.

23 Active FAK in turn accumulated in the nucleus where it led to t

24 mice, demonstrating that constitutive active FAK signaling downstream of the Pro32Pro33 integrin alph

25 loss resulted in reduced activation of Akt, FAK, ERK, and p38 signaling pathways, which are coordina

26 Activating integrin alpha6-FAK pathway increases STAT3 activity, TET3 expression an

27 er, targeting STAT3 disrupts integrin alpha6-FAK signaling and inhibits TET3(+) GSC maturation in viv

28 m prosignaling kinases, including ERK1/2 and FAK.

29 R through the direct regulation of CXCR4 and FAK expression and FAK/PI3K/AKT pathway activation, cont

30 ow that SOX11 directly upregulates CXCR4 and FAK expression, activating PI3K/AKT and ERK1/2 FAK-downs

31 t regulation of CXCR4 and FAK expression and FAK/PI3K/AKT pathway activation, contributing to a more

32 In fact, expression of WT FAK and FAK/Y180A/M183A (open conformation), but not FAK/Arg(454

33 In turn, focal adhesion formation and FAK/SRC signaling is activated in mesenchymal tumor cell

34 C), activates in parallel the MAP-kinase and FAK/Yes-associated protein pathways.

35 as prevented by beta3 integrin knockdown and FAK inhibition.

36 YAP through inhibition of Rho-ROCK-MLC- and FAK-PI3K-dependent signaling pathways.

37 sically interacts with FAK, and occludin and FAK phosphorylation can be blocked by DSP and occludin a

38 These findings suggest that SFK and FAK exert distinctive molecular hierarchy depending on t

39 to detect subcellular activities of SFK and FAK in three-dimensional (3D) settings.

40 d to tight spatial control of active Src and FAK levels, and so crucially regulates their cancer-asso

41 Blocking calpain cleavage of talin and FAK inhibits repulsive turning from focal uncaging of Ca

42 lear pore proteins, adaptor proteins such as FAK and Akap8, chromatin-modifying proteins, and transcr

43 Because FAK is a critical regulator of integrin-dependent signal

44 potential target for cancer therapy because FAK plays a critical role in the regulation of endotheli

45 This activation event occurs before FAK unfolding at forces within the native range in focal

46 identified a novel molecular complex between FAK and Runx1 in the nucleus of SCC cells and showed tha

47 thus, FHL2 inhibition can selectively block FAK-Rac1 axis in podocyte and prevent proteinuria.

48 In contrast, mice lacking both FAK and Pyk2 develop spontaneous colitis with 100% penet

49 We found that overexpression of both FAK and CAT, but neither FAK nor CAT alone, in mouse liv

50 Ambra1 binds to both FAK and Src in cancer cells.

51 ing negative regulation of integrin beta1 by FAK.

52 D-associated TREM2 R47H variant is caused by FAK/Rac1/Cdc42 signaling disruption, and that activation

53 This phenotype switch is driven by FAK kinase activity, and signaling through the p130Cas>c

54 Accordingly, as indicated by FAK inhibition experiments and in FAK-null fibroblasts,

55 fy the genes/signaling pathways regulated by FAK, CAT, or FAK/CAT.

56 Conclusion: FAK overexpression and beta-catenin mutations often co-o

57 In contrast, FAK-Y861F ECs showed decreased Vegfr2 and Tie2 expressio

58 a unique molecular complex comprising CXCR4, FAK, ASK1, and PP5 in ATII cells during wound healing.

59 In the cytosol, FAK adopts an autoinhibited state but is activated upon

60 at recombinant VHR directly dephosphorylated FAK and paxillin.

61 ntegrin activation, and disrupted downstream FAK/Src/PI3K(p55)/Akt signaling.

62 ferential requirements of EC-FAK-Y397 and EC-FAK-Y861 phosphorylation in the regulation of EC signali

63 ablishes the differential requirements of EC-FAK-Y397 and EC-FAK-Y861 phosphorylation in the regulati

64 Conversely, ECCre+;FAK(Y861F/Y861F) mice exhibit normal tumor growth with a

65 constitutively reduced in inducible, ECCre+;FAK(Y397F/Y397F) -mutant mice.

66 Knockdown of either FAK or Pyk2 reduced TNF-alpha-stimulated ERK and JNK act

67 ntenance can occur in the presence of either FAK or Pyk2, but that both kinases are necessary for epi

68 ptor signaling mediated by AKT2 and elevated FAK-kinase activity and ROCK-RhoA levels but low levels

69 hosphorylation of EGFR family proteins, ERK, FAK, and CSC markers.

70 Our findings establish FAK as a potential therapeutic target for UM and other G

71 Finally, FAK/Pyk2 activity is required for VCAM-1 expression and

72 Following FAK inhibition, cell survival and proliferation decrease

73 Finally, tumor cell stemness following FAK inhibition was evaluated with extreme limiting dilut

74 on and membrane attachment are essential for FAK autophosphorylation and resulting cellular activity

75 d that FAK's kinase activity is required for FAK/CAT-induced tumorigenesis.

76 ether, these results identify a new role for FAK signaling in CAFs that regulate their intercellular

77 ich patients are most likely to benefit from FAK inhibitors, and what the optimal FAK/immunotherapy c

78 iR-16 and miR-148a enriched in exosomes from FAK-null CAFs contribute to the reduced tumor cell activ

79 Furthermore, FAK/Pyk2 activity was not limited to CAM expression but

80 ecting primary tumor development and growth, FAK deletion significantly suppressed breast cancer meta

81 more invasive phenotype through an IL-1beta>FAK>p130Cas>c-Jun >MMP signaling axis, and that combined

82 (EC) is essential for angiogenesis, but how FAK phosphorylation at tyrosine-(Y)397 and Y861 regulate

83 mploy cryo-electron microscopy to reveal how FAK associates with lipid membranes and how membrane int

84 n vivo Collectively, these findings identify FAK as a novel negative regulator of Beclin1-mediated au

85 nflammatory cytokine signaling and implicate FAK/Pyk2 inhibitors as potential therapeutic agents to t

86 Importantly, FAK inhibitor attenuates liver fibrosis in vivo and sign

87 dicated by FAK inhibition experiments and in FAK-null fibroblasts, adhesion-induced FAK activity incr

88 vation by inducing conformational changes in FAK.

89 ably due to the lack of talin involvement in FAK activation and the absence of vinculin in the adhesi

90 (kinase-dead), augmented Rab5-GTP levels in FAK-null fibroblasts and A549 cells.

91 ut not Rab5/S34N, promoted cell migration in FAK-null fibroblasts.

92 owed alterations of several exosomal miRs in FAK-null CAFs, and further analysis suggested that miR-1

93 g the MIC proliferation and death, including FAK, mTORC1 and NFkappaB, which are validated to be rela

94 ation loops of 37 protein kinases, including FAK and several phosphatases, many of which were not pre

95 ns, and its amplification leads to increased FAK mRNA expression.

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 nd in FAK-null fibroblasts, adhesion-induced FAK activity increased Rab5-GTP levels.

99 Similarly, inhibiting FAK/Src results in chemosensitization.

100 These data indicate that beta3-integrin, FAK and cofilin constitute a signaling pathway downstrea

101 rins and mediates the activation of integrin-FAK signaling in response to irisin.

102 endocytosis or endosomal Met/beta1-integrin/FAK signaling profoundly inhibits the oncogenic effects

103 gent for TNBC by dual inhibition of integrin/FAK and EGFR signaling pathways.

104 us altering the regulation of talin/integrin/FAK/paxillin and integrin/NFkappaB signaling pathways.

105 1i inhibited crucial GBM signaling involving FAK and mutant EGFR, EGFRvIII, and abrogated gains in se

106 c pathways by the Saureus fatty acid kinase (FAK) complex, and FakA is required for virulence.

107 d-type cells, whereas focal adhesion kinase (FAK) activity and Rho/Rac/Cdc42 protein levels were incr

108 eviating the elevated focal adhesion kinase (FAK) activity and the enhanced focal adhesions in the kn

109 taneous inhibition of focal adhesion kinase (FAK) and EGFR signaling pathways.

110 Focal adhesion kinase (FAK) and its close relative Pyk2 are non-receptor tyrosi

111 to the activation of focal adhesion kinase (FAK) and metalloproteinase expression.

112 ly, the disruption of focal adhesion kinase (FAK) and paxillin interactions using the small molecule

113 -integrin to activate focal adhesion kinase (FAK) and phosphorylate the actin binding protein cofilin

114 Focal adhesion kinase (FAK) and Src family kinases (SFK) are known to play crit

115 We identified focal adhesion kinase (FAK) as a VHR-interacting molecule.

116 previously identified focal adhesion kinase (FAK) as an important regulator of ciliogenesis in multic

117 on proteins talin and focal adhesion kinase (FAK) as proteolytic targets of calpain in Xenopus laevis

118 eptor tyrosine kinase/focal adhesion kinase (FAK) axis leads to CDK4/6-independent CDK2 activation, i

119 pecific inhibitors of focal adhesion kinase (FAK) blocked phosphorylation of Tyr45, inhibited stimula

120 eutical inhibition of focal adhesion kinase (FAK) both in vitro and ex ovo.

121 romotes activation of focal adhesion kinase (FAK) by the chemokine receptor CXCR4, facilitating chemo

122 jor PTKs: Src and the focal adhesion kinase (FAK) family kinases - FAK and proline-rich tyrosine kina

123 The focal adhesion kinase (FAK) gene protein tyrosine kinase 2 is amplified in 16.4

124 in the activation of focal adhesion kinase (FAK) in a protein kinase C dependent manner.

125 Expression of focal adhesion kinase (FAK) in endothelial cells (EC) is essential for angiogen

126 Focal Adhesion Kinase (FAK) inhibitors are currently undergoing clinical testin

127 Focal adhesion kinase (FAK) is a central regulator of integrin-dependent cell a

128 Focal adhesion kinase (FAK) is a key component of the membrane proximal signali

129 Focal adhesion kinase (FAK) is a key signaling molecule regulating cell adhesio

130 Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase involved in develo

131 nd that activation of focal adhesion kinase (FAK) is necessary for PE-stimulated autophagy suppressio

132 st-specific inducible focal adhesion kinase (FAK) knockout (cKO) mice in a breast cancer model to stu

133 rin signaling kinases focal adhesion kinase (FAK) or integrin-linked kinase.

134 reduced the levels of focal adhesion kinase (FAK) phosphorylation at Ser910, whereas the phosphorylat

135 d the closely related focal adhesion kinase (FAK) regulate tumor cell invasion, albeit via distinct m

136 Inhibition of focal adhesion kinase (FAK) rescued SERT function in synapses of KI mice, demon

137 occludin Ser(490) and focal adhesion kinase (FAK) Ser(722) and Tyr(576).

138 integrin-ECM binding, focal adhesion kinase (FAK) signaling, or TGF-beta signaling independently led

139 to activate integrin-focal adhesion kinase (FAK) signaling.

140 eptor tyrosine kinase focal adhesion kinase (FAK) stimulates epithelial motility.

141 ily kinases (SFK) and focal adhesion kinase (FAK) sustain AKT and MAPK pathway signaling under contin

142 caveolin-1 (CAV1) and focal adhesion kinase (FAK) which then interact with AKT and receptor-interacti

143 42 phosphorylation by focal adhesion kinase (FAK), a HDAC5 post-translational modification that contr

144 tein tyrosine kinase, Focal adhesion kinase (FAK), in endothelial cells has implicated its requiremen

145 d that PTK2, encoding focal adhesion kinase (FAK), represents a candidate synthetic lethal gene with

146 light chain (MLC) and focal adhesion kinase (FAK), supporting a role for ROCK activity in regulating

147 rent AKT isoforms and focal adhesion kinase (FAK)-dependent adhesion signaling, which either controll

148 adhesion, including a focal adhesion kinase (FAK)-regulated network mediating the regulation of actin

149 D2's interaction with Focal Adhesion Kinase (FAK).

150 ugh interactions with focal adhesion kinase (FAK).

151 y signaling kinase is focal adhesion kinase (FAK).

152 focal adhesion kinase (FAK) family kinases - FAK and proline-rich tyrosine kinase (Pyk2).

153 We previously showed that mice lacking FAK in the intestinal epithelium are phenotypically norm

154 irtual screen identified the small drug-like FAK mimic ZINC40099027, which activates FAK.

155 pancreatic cancer patients we find that low FAK expression, specifically in the stromal compartment,

156 like features in neuroblastoma PDXs, making FAK a candidate for further investigation as a potential

157 ells infected in the presence of EGFR, MAPK, FAK and ADAM10 inhibitors or with VGF-deleted and F11-de

158 Mechanistically, FAK co-immunoprecipitated with the GTPase-activating pro

159 Mechanistically, FAK-Y397F ECs exhibit increased Tie2 expression, reduced

160 Mechanistically, FAK-Y861F, but not FAK-Y397F ECs showed enhanced p190Rho

161 ling the critical event in integrin mediated FAK activation and signaling at focal adhesions.

162 Matrix stiffness-mediated FAK activation determines Src localization to cell-cell

163 depletion of Beclin1 attenuated PE-mediated/FAK-dependent initiation of myocyte hypertrophy in vivo

164 regulating CDK4/6 kinases and identifies MET/FAK as a tractable route to broaden the utility of CDK4/

165 Combined inhibition of MET/FAK and CDK4/6 eliminates the proliferation capacity of

166 Activation of the MET/FAK axis is known to arise through cancer extrinsic and

167 ects on endogenous ROCK activity and the MLC/FAK/AKT/mTOR signaling pathway, which is involved in aut

168 Small molecule FAK activators can specifically promote epithelial resti

169 rexpression of both FAK and CAT, but neither FAK nor CAT alone, in mouse livers was sufficient to lea

170 Mechanistically, FAK-Y861F, but not FAK-Y397F ECs showed enhanced p190RhoGEF/P130Cas-depende

171 FAK/Y180A/M183A (open conformation), but not FAK/Arg(454) (kinase-dead), augmented Rab5-GTP levels in

172 n squamous cell carcinoma (SCC) that nuclear FAK regulates Runx1-dependent transcription of insulin-l

173 ta-arr1 reduces CXCR4-mediated activation of FAK and chemotaxis.

174 icantly reduced CXCL12-induced activation of FAK but had no impact on ERK-1/2 activation.

175 2-integrin did not prevent the activation of FAK, nor did EDTA-mediated inactivation of the integrin.

176 and CD81 and proliferate upon activation of FAK-signaling in response to the cold and irisin.

177 feration and migration through activation of FAK/Src and Akt1/mTOR signaling, respectively.

178 Intriguingly, initial binding of FAK to the membrane causes steric clashes that release t

179 eta-catenin (CAT) alone, or a combination of FAK and CAT in the livers of C57/BL6 mice.

180 bolism through pathways under the control of FAK.

181 In mice, depletion of FAK in a subpopulation of CAFs regulates paracrine signa

182 onale supporting the clinical development of FAK inhibitors in combination with patient selection bas

183 assays were used to determine the effect of FAK inhibition on cell motility, which decreased signifi

184 rent studies, we investigated the effects of FAK inhibition on two neuroblastoma PDXs in vitro.

185 hich provide buffering to allow extension of FAK in focal adhesions without compromising functionalit

186 Inhibition of FAK activation blocks the alpha-SMA and collagen express

187 Pharmacological inhibition of FAK and knockdown of YAP abolished m1 and m3-induced cas

188 iated R47H mutation results in inhibition of FAK and Rac1/Cdc42-GTPase signaling critical for cell mi

189 naling axis, and that combined inhibition of FAK and Src has the potential to block this inhibitor-in

190 onstrate that upfront combined inhibition of FAK and Src synergistically inhibits growth and invasion

191 ic ablation or pharmacological inhibition of FAK inhibits UM growth.

192 Inhibition of FAK proved its contribution to IAV infection.

193 5/FN1 expression, resulting in inhibition of FAK/Src signaling, induction of apoptosis and re-sensiti

194 reatment with a pharmacological inhibitor of FAK, PF562,271, in resting A549 cells.

195 We found that a dual inhibitor of FAK/Pyk2 (PF-271) most effectively reduced all three CAM

196 reated with two small molecule inhibitors of FAK, PF-573,228 (PF) and 1,2,4,5-benzentetraamine tetrah

197 er910, whereas the phosphorylation levels of FAK at Tyr397 and Tyr861 were markedly increased.

198 el to study potential role and mechanisms of FAK signaling in CAF to promote breast cancer metastasis

199 comparison with an open and active mutant of FAK, we are able to assign mechanoactivation to an initi

200 nin mutations, suggesting a co-occurrence of FAK overexpression and beta-catenin mutations in HCC.

201 t is not known whether the overexpression of FAK alone is sufficient to induce HCC or whether it must

202 Co-overexpression of FAK and CAT leads to HCC formation in mice through incre

203 f beta3-integrin-mediated phosphorylation of FAK (p-FAK) and cofilin.

204 eased immunoreactivity of phosphorylation of FAK (p-FAK) and p-cofilin in dendrites of reinstated ani

205 of VHR decreased tyrosine phosphorylation of FAK and decreasing VHR promoted FAK tyrosine phosphoryla

206 oscopy to probe the mechanical properties of FAK and examine whether force can trigger activation by

207 vide important new insights into the role of FAK as a scaffolding protein in molecular complexes that

208 Our findings define critical roles of FAK/Pyk2 in mediating inflammatory cytokine signaling an

209 ral details of a key membrane bound state of FAK that is primed for efficient autophosphorylation and

210 the force landscape to partial unfolding of FAK modules.

211 it from FAK inhibitors, and what the optimal FAK/immunotherapy combinations are, is currently unknown

212 signaling pathways regulated by FAK, CAT, or FAK/CAT.

213 Knockdown of beta3 integrin or FAK inhibitor, but not beta1 integrin or integrin-linked

214 We overexpressed FAK alone, constitutively active forms of beta-catenin (

215 CK1 had no significant effect on p-MLC and p-FAK levels, mTOR signaling, or autophagy at baseline.

216 howed increased phosphorylated (p)-MLC and p-FAK levels, which were mostly attributable to a compensa

217 -integrin-mediated phosphorylation of FAK (p-FAK) and cofilin.

218 mmunoreactivity of phosphorylation of FAK (p-FAK) and p-cofilin in dendrites of reinstated animals co

219 We found that p-FAK was increased during drug seeking in both D1 and D2-

220 ith extinguished and yoked saline, and the p-FAK and cofilin depended on beta3-integrin signaling.

221 by pericytes that is controlled by pericyte FAK.

222 ogenesis and tumour growth, but how pericyte FAK regulates tumour angiogenesis is unknown.

223 a and provide evidence that loss of pericyte FAK enhances Gas6-stimulated phosphorylation of the rece

224 We show that pericyte FAK regulates tumour growth and angiogenesis in multiple

225 0% or more tumour blood vessels are pericyte-FAK negative, melanoma patients are stratified into thos

226 Pharmacologic FAK catalytic inhibition reduces Sost mRNA expression in

227 mally high levels of phospho-Src and phospho-FAK accumulate at focal adhesions, positively regulating

228 nd point-like adhesions that contain phospho-FAK and phosphopaxillin, located in small protrusions.

229 DMSO, staining the mucosa for phosphorylated FAK and Ki-67 and measuring mucosal ulcer area, serum cr

230 Using a small molecule inhibitor to prevent FAK activation, we blocked cued-induced cocaine reinstat

231 iated knockdown of endogenous Rab5 prevented FAK-induced A549 cell migration, whereas expression of W

232 hat non-dynamic (N) hydrogels do not promote FAK signaling and that stiff D- and N-hydrogels are cons

233 sed and multiple interfaces align to promote FAK oligomerization on the membrane.

234 orylation of FAK and decreasing VHR promoted FAK tyrosine phosphorylation.

235 5-IP7, a product of IP6K1, promotes FAK autophosphorylation.

236 We assessed whether ZINC40099027 promotes FAK-Tyr-397 phosphorylation and wound healing in Caco-2

237 1 is recruited to focal adhesions, promoting FAK-regulated cancer cell direction-sensing and invasion

238 a strategy of cotargeting the EGFR and PYK2/FAK kinases to improve TNBC therapy.

239 FR and the nonreceptor tyrosine kinases PYK2/FAK synergistically inhibits the proliferation of basal-

240 n-dependent signaling and Rab5 recapitulates FAK-mediated effects, we evaluated the possibility that

241 Depletion of CAP1 also reduced FAK activity and cell adhesion, but did not cause signif

242 th TNF-alpha and IL-1beta signaling requires FAK/Pyk2 activity to activate ERK and JNK MAPKs leading

243 Combined SFK/FAK inhibition exhibited the most potent effects on grow

244 w selectively decreased cytokine-induced SFK/FAK activation.

245 Additionally, specific FAK and PI3K inhibitors reduce SOX11-enhanced MCL cell m

246 aling pathways including CREB, mTOR, and Src-FAK.

247 activator receptor (uPAR)/integrin beta1/Src/FAK signal circuit converges to regulate ERK1/2 phosphor

248 ed that VEGF-dependent activation of the Src/FAK/paxillin signalsome is required for human retinal en

249 including cancer cell invasion, while stable FAK oligomerization appears to be needed for optimal can

250 criptomic level in patients with low stromal FAK.

251 motes an interaction with FAK and subsequent FAK activation.

252 Osteocyte cell adhesion supports FAK tyrosine phosphorylation, and FFSS triggers FAK deph

253 C-J9, an AR degradation enhancer, suppressed FAK/CAT-induced HCC formation.

254 leading edge of motile cells and suppresses FAK.

255 Mechanistically we demonstrate that FAK-depletion in CAFs increases chemokine production, wh

256 We further demonstrated that FAK's kinase activity is required for FAK/CAT-induced tu

257 our work also provides further evidence that FAK is a promising potential target for cancer therapy b

258 We found that FAK overexpression dramatically enhances binding of beta

259 d effects, we evaluated the possibility that FAK activates Rab5 and contributes to cell migration.

260 Taken together, these results reveal that FAK activates Rab5, leading to cell migration.

261 on of the underlying mechanism revealed that FAK regulates YAP by tyrosine phosphorylation of MOB1, i

262 hibition and mutant expression, we show that FAK kinase activity, along with its proximity to and pot

263 We further showed that FAK ablation in CAFs decreased exosome functions to prom

264 in the nucleus of SCC cells and showed that FAK interacted with a number of Runx1-regulatory protein

265 m cKO mice as well as human CAFs showed that FAK is required for their activity to promote mammary tu

266 Mechanistically, we showed that FAK phosphorylates Beclin1, a core autophagy protein, on

267 ess and collagen expression, supporting that FAK(Y397) hyperactivation may underlie the aberrant mech

268 The FAK inhibitor PF-573228 prevented ZINC40099027-stimulate

269 provides persistent signals to activate the FAK/p130Cas pathway, thereby promoting CRC cell migratio

270 s a link between SSEA3/SSEA4/Globo-H and the FAK/CAV1/AKT/RIP complex in tumor progression and apopto

271 ly inhibition of the MAPK branch but not the FAK branch synergizes with inhibition of the proximal ca

272 Phosphorylation of the FAK family member Pyk2 at tyrosine 402 is decreased in N

273 Analysis of the FAK-regulated transcriptome demonstrated that GNAQ stimu

274 ll membrane and subsequent activation of the FAK-RhoA pathway.

275 nal-driven CRPC progression by targeting the FAK-YAP signaling axis.

276 lecular motor, to interact directly with the FAK FERM-kinase linker and induce FAK kinase activity an

277 3 stimulation induces YAP activation through FAK, whose encoding gene, PTK2 is frequently amplified i

278 ulates endothelial barrier integrity through FAK activity, providing one mechanism by which extracell

279 ned whether beta3-integrin signaling through FAK and cofilin (actin depolymerization factor) is neces

280 activation of ERK or JNK is specific through FAK and Pyk2.

281 emonstrated that GNAQ stimulates YAP through FAK.

282 rt that forces in focal adhesions applied to FAK via known interactions can induce conformational cha

283 However, when Ambra1 cannot bind to FAK, abnormally high levels of phospho-Src and phospho-F

284 NF-alpha or IL-1beta stimulation compared to FAK or Src specific inhibitors (PF-228 or Dasatinib), wh

285 tem cell (CSC) markers and susceptibility to FAK inhibitor.

286 tyrosine phosphorylation, and FFSS triggers FAK dephosphorylation.

287 mbranes and how membrane interactions unlock FAK autoinhibition to promote activation.

288 ced podocyte cytoskeleton reorganization via FAK-Rac1 axis, FHL2 binds with FAK and is an important m

289 re the origin of intracellular signaling via FAK and paxillin.

290 l beta3-integrin loss enhances signaling via FAK-p-HGFR-p-Akt-p-p65, driving CXCL1, CCL2, and TIMP-1

291 When FAK is present, Ambra1 is recruited to focal adhesions,

292 not understood, and it is not clear whether FAK is activated directly by force or downstream to the

293 and some hematological malignancies in which FAK inhibitors have not been tested clinically.

294 However, the mechanism through which FAK functions in the complex is not clear, and in this s

295 anization via FAK-Rac1 axis, FHL2 binds with FAK and is an important mediator of Ang II induced Rac1

296 rticular OX-40 and 4-1BB in combination with FAK, can drive enhanced anti-tumor immunity and even com

297 good prognosis and reversely correlates with FAK and EGFR activation status in TNBC.

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 e found that 34.8% of human HCC samples with FAK amplification also show beta-catenin mutations, sugg

301 In fact, expression of WT FAK and FAK/Y180A/M183A (open conformation), but not FAK