ライフサイエンスコーパス: FAK

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.