ライフサイエンスコーパス: ILK

1 ILK also regulated osteopontin expression in cardiomyocy

2 ILK contains a highly degraded kinase active site but it

3 ILK deletion caused endothelial NOS (eNOS) uncoupling, r

4 ILK deletion in primary aortic SMCs results in alteratio

5 ILK expression was detected in the endothelial cell laye

6 ILK influences the host response to C. rodentium -induce

7 ILK is involved in cell-matrix interactions, cytoskeleta

8 ILK is required for LPS-induced activation of nuclear fa

9 ILK mutation/deletion causes cardiomyopathic phenotypes,

10 ILK plays a role in the activation of kinases including

11 ILK reexpression prevented eNOS uncoupling in cKO cells,

12 ILK signaling has also been implicated in oncogenesis an

13 ILK was deleted from the embryonic lens either at the ti

14 ILK, Src, and galectin-3 also mediate EGF stimulation of

15 ILK-1 then induces the Wnt-PCP pathway by binding a prol

16 ILK-deficient hair buds also show abnormalities in the d

17 ILK-ko mice exhibited reduced weight loss at 15 days pos

18 ich then activates integrin-linked kinase 1 (ILK-1) via alpha4-integrins.

19 data define a specific mode of the kindlin-2/ILK interaction with mechanistic implications as to how

20 on of integrin with Mn2+ induces galectin-3, ILK, and Src-dependent RhoA activation and caveolin-1 ph

21 active form is promoted by binding to PAT-4 (ILK).

22 epatic insulin action in vivo, male C57BL/6J ILK(lox/lox) mice were crossed with Albcre mice to produ

23 near the active site and strongly activated ILK kinase activity.

24 e stable expression of constitutively active ILK.

25 a major docking platform in focal adhesions, ILK engages many proteins to dynamically link integrins

26 Because paxillin depletion did not affect ILK localization to FAs, the embryonic lethality and the

27 RC activated the integrin-linked kinase/AKT (ILK/AKT) pathway, likely via integrin interaction, and s

28 Although ILK-mediated phosphorylation of p65 at Ser-536 is indepe

29 Similarly, p-AKT was reduced although ILK was unaffected.

30 An ILK interaction motif of 78 amino acids (amino acids 82-

31 nant negative form of ILK or by injecting an ILK antisense morpholino oligonucleotide.

32 pression, we hypothesized the presence of an ILK-KRAS regulatory loop that enables pancreatic cancer

33 ta1 integrin stabilization, activation of an ILK/EGFR/Ras/NF-kappaB signaling cascade and subsequent

34 and the focal adhesion proteins PINCH-1 and ILK on NF-kappaB activity in this study opens a new wind

35 intracellular binding partners, PINCH-1 and ILK, on NF-kappaB activity after TNF-alpha stimulation.

36 xpress high levels of endogenous ADAM12L and ILK, the two proteins are redistributed to focal adhesio

37 gh levels of expression of alpha-catulin and ILK were associated with poor overall survival in patien

38 Combined knockdown of Cten and ILK had no additive effects on cell motility compared wi

39 ELMO2 and ILK have also separately been implicated in microtubule

40 complexes containing active RhoG, ELMO2, and ILK.

41 eNOS and ILK coimmunoprecipitated in aortic lysates from control

42 y response as the top predicted function and ILK and TREM1 as the top predicted canonical pathways.

43 decreased expression of smoothened, GLI2 and ILK compared with cells transfected with nontargeting co

44 Interplay between KRAS and ILK and the roles of E2F1, c-Myc and heterogeneous nucle

45 t was not different between ILK(lox/lox) and ILK(lox/lox)HSAcre mice.

46 tably, the combined actions of Rif/mDia2 and ILK/beta-parvin/cofilin pathways on FLPs are required no

47 main in a mode that is distinct from another ILK pseudokinase domain binding protein, alpha-parvin.

48 stiffness, ILK, and CSC markers, insofar as ILK and CD44 were expressed in cancer cells located in t

49 tization was associated with increased BDNF, ILK activity, phospho-Akt Ser(473), p75(NTR), and TrkB p

50 ex in which PDLIM5 provides a bridge between ILK and AE1C.

51 Body weight was not different between ILK(lox/lox) and ILK(lox/lox)HSAcre mice.

52 ECM) via beta1 integrins which activate both ILK and Rac1 and are required for STAT5a activation and

53 ve site conformation as that of the Mg-bound ILK.

54 analysis further confirmed that the Mn-bound ILK adopts the same pseudo active site conformation as t

55 ugh the induction of TGF-alpha expression by ILK/HIFs-alpha, as well as through MEK/VEGF-A-mediated a

56 lation of LPS-induced TNF-alpha synthesis by ILK does not involve the classical NF-kappaB pathway, be

57 ereas superoxide formation was unaffected by ILK depletion in eNOS-KO cells, indicating eNOS as a pri

58 nuclear translocation are both unaffected by ILK inhibition.

59 Cardiomyocyte ILK deletion produces a lethal arrhythmogenic cardiomyop

60 To define the role of cardiomyocyte ILK, we generated cardiac-specific ILK knockout mice usi

61 both control and intestinal epithelial cell ILK knockout mice.

62 In conjunction, ILK-deficient primary oligodendrocytes are defined by a

63 significance in CRC, and we delineate a Cten-ILK pathway controlling cell motility and possibly promo

64 of Cten, thereby demonstrating that the Cten-ILK interaction was functionally relevant.

65 revealed that VT/GG substitutions decreased ILK protein stability leading to decreased ILK levels an

66 d ILK protein stability leading to decreased ILK levels and reduced binding to paxillin and alpha-par

67 lox/lox)) and muscle-specific ILK-deficient (ILK(lox/lox)HSAcre) mice were fed chow or a high-fat (HF

68 Our results define ILK as a key mechanotransducer in modulating breast CSC

69 produce a hepatocyte-specific ILK deletion (ILK(lox/lox)Albcre).

70 Together, our work demonstrates ILK as necessary for normal oligodendrocyte development,

71 Depleting ILK blocked stiffness and hypoxia-dependent acquisition

72 ation and metastasis in ovo, where depleting ILK significantly abrogated the tumorigenic and metastat

73 we report on the role of epithelial derived ILK in response to Citrobacter rodentium infection.

74 Diminishing ILK by siRNA decreased the levels of PAR-2-induced p-AKT

75 nts were reduced, possibly related to direct ILK-Kv4.2 subunit interactions.

76 anges associated with cardiomyocyte-directed ILK deletion in mice.

77 Adult mice with cardiomyocyte-directed ILK knockout were compared with littermate controls.

78 Knocking down ILK dramatically reduced the inhibition of cell growth a

79 Knocking down ILK in Olig1-Cre-expressing cells reduces the pool of ol

80 These studies suggest that this KRAS-E2F1-ILK-hnRNPA1 regulatory loop enables pancreatic cancer ce

81 highly resembles the phenotype of endogenous ILK inhibition, either by overexpressing a dominant nega

82 MKI67)-positive cells in regions of enhanced ILK expression in lymph nodes from CLL patients.

83 eNOS-ILK interaction in endothelial cells was prevented by ge

84 ortic lysates from control animals, and eNOS-ILK-shock protein 90 interaction was detected in human n

85 duced Smad signaling through a Cdc42-Src-FAK-ILK pathway.

86 uscle insulin sensitivity relative to HF-fed ILK(lox/lox) mice, as shown by increased rates of glucos

87 However, HF-fed ILK(lox/lox)HSAcre mice had improved muscle insulin sens

88 Improved muscle insulin action in the HF-fed ILK(lox/lox)HSAcre mice was associated with increased in

89 ets Akt and GSK3beta is unaffected following ILK loss.

90 Cells that were null for ILK failed to respond to the induction of invasion by LI

91 k-out mice, we demonstrate a requirement for ILK in oligodendrocyte differentiation and axonal myelin

92 Our study reveals a role for ILK in extracellular matrix organization, fiber migratio

93 ion of ADAM12L promotes kinase activity from ILK immunoprecipitates.

94 Fibroblasts isolated from ILK-VT/GG mice contained mutant ILK in FAs, showed norma

95 Furthermore, ILK-mediated alternative NF-kappaB activation through p6

96 Results from this study show that hepatic ILK deletion has no effect on insulin action in lean mic

97 ILK in the context of CLL and observed high ILK expression in patient samples, particularly in tumor

98 ted that viral ORF119L might affect the host ILK complex.

99 of a dominant negative inhibitor of the host ILK from ISKNV (an iridovirus).

100 s as a domain-negative inhibitor of the host ILK, providing a novel mechanism for the megalocytivirus

101 is-rich protein (PINCH) and affects the host ILK-PINCH interaction in vitro in fathead minnow (FHM) c

102 We show that human kindlin-2 binds to human ILK with high affinity.

103 Comprehensive profiling identifies ILK-dependent transcriptional effects and implicates ost

104 Our results identify ILK as a regulatory partner of eNOS in vivo that prevent

105 If ILK was deleted at a later time-point after initial esta

106 or RhoG stabilizes microtubules, but only if ILK is also present.

107 host PINCH-ILK interaction, and thus impairs ILK signaling.

108 Our findings implicate ILK as a critical regulatory molecule for the NF-kappaB-

109 In ILK-ko mice reduced activation of ser473Akt and reduced

110 The molecular pathways affected in ILK-deficient follicles are similar to those in the abse

111 agonist limited podocyte loss and changes in ILK, Snail, and alpha-actinin-4 expression.

112 ansion of the thoracic aorta was observed in ILK mutant embryos.

113 M mutation, previously thought to inactivate ILK by disrupting ATP binding, significantly impairs the

114 of certain focal adhesion proteins including ILK, PINCH, paxillin, and cdc42, as well as regulating t

115 C. rodentium exposure was shown to increase ILK expression in cell lines, and in murine epithelium i

116 Instead, ILK deletion resulted in secondary fiber migration defec

117 Instead, ILK is involved in an alternative activation of NF-kappa

118 Most significantly, the IGFBP2/integrin/ILK/NF-kappaB network functions as a physiologically act

119 ugh modulation of the integrin-linked kinase ILK.

120 time, which involves integrin-linked kinase (ILK) and beta-parvin, two integrin:actin-bridging protei

121 tain significance in integrin-linked kinase (ILK) and filamin-C (FLNC).

122 s from repression of integrin-linked kinase (ILK) and phosphoinositide-dependent protein kinase-1 (PD

123 simultaneously bind integrin-linked kinase (ILK) and RhoG, forming tripartite ERI complexes.

124 We identify the integrin-linked kinase (ILK) as a new partner for ADAM12L cellular functions.

125 ied septin-5 and the integrin-linked kinase (ILK) as novel calpain substrates.

126 us of myopodin binds integrin-linked kinase (ILK) both in vivo and in vitro.

127 d phosphorylation of integrin-linked kinase (ILK) by TGFBR1.

128 integrin, PINCH, and integrin-linked kinase (ILK) caused formation of multinucleate epidermal cells w

129 1 (kAE1), PDLIM5 and integrin-linked kinase (ILK) form a multiprotein complex in which PDLIM5 provide

130 w that expression of integrin-linked kinase (ILK) in myeloid cells is critical for the epithelial inf

131 genetic deletion of integrin-linked kinase (ILK) increases NSPC proliferation through PINCH1/2-depen

132 Integrin-linked kinase (ILK) is a distinct intracellular adaptor essential for i

133 Integrin-linked kinase (ILK) is a downstream integrin signaling molecule involve

134 Integrin-linked kinase (ILK) is a major structural adaptor protein governing sig

135 Integrin-linked kinase (ILK) is a mediator of aggressive phenotype in pancreatic

136 Integrin-linked kinase (ILK) is a multifunctional intracellular adaptor protein

137 NIFICANCE STATEMENT: Integrin-linked kinase (ILK) is a scaffolding protein involved in integrating si

138 Integrin-linked kinase (ILK) is a serine-threonine kinase that transduces extrac

139 Integrin-linked kinase (ILK) is a serine/threonine kinase that has been linked t

140 Integrin-linked kinase (ILK) is a ubiquitously expressed and highly conserved se

141 Integrin-linked kinase (ILK) is an important protein that is expressed at the in

142 Integrin-linked kinase (ILK) is an intracellular scaffold protein with critical

143 dothelial cells, and integrin-linked kinase (ILK) is important for blood vessel integrity and cardiov

144 Integrin-linked kinase (ILK) is one of the few evolutionarily conserved focal ad

145 Integrin-linked kinase (ILK) localizes to focal adhesions (FAs) where it regulat

146 the kinase domain of integrin-linked kinase (ILK) near the active site and strongly activated ILK kin

147 in the integrin and integrin-linked kinase (ILK) pathways and that these genes are associated with p

148 Integrin-linked kinase (ILK) represents a relevant target for cancer therapy in

149 ion kinase (FAK) and integrin-linked kinase (ILK) reveals that FAK, but not ILK, is also required for

150 increased levels of integrin-linked kinase (ILK) signaling as demonstrated by the impaired angiogene

151 iviral response, and integrin-linked kinase (ILK) signaling were among the top altered canonical path

152 more, PAR-2, through integrin-linked kinase (ILK) signaling, including the p-AKT, promoted HIF protei

153 ns, the relevance of integrin-linked kinase (ILK) signals in podocyte dysfunction was evaluated.

154 ese processes by the integrin-linked kinase (ILK), a scaffold protein that links the extracellular ma

155 ulin interacted with integrin-linked kinase (ILK), a serine/threonine protein kinase implicated in ca

156 Integrin-linked kinase (ILK), a serine/threonine protein kinase, has roles in ce

157 down-regulated both integrin linked kinase (ILK), an activator of smoothened, and phosphorylated gly

158 nclude integrins and integrin-linked kinase (ILK), are critical for hair follicle formation.

159 ogical inhibition of integrin linked kinase (ILK), EGFR and NF-kappaB, as well as transfection of a d

160 athway that requires integrin-linked kinase (ILK), Engulfment and Cell Motility-2 (ELMO2), integrin b

161 sion and activity of integrin-linked kinase (ILK), level of protein kinase B (Akt) phosphorylation at

162 tter the function of integrin-linked kinase (ILK), we examined the phenotypic consequences of its del

163 te Akt signaling via integrin-linked kinase (ILK), which is antagonistic to endoderm differentiation.

164 we demonstrate that integrin-linked kinase (ILK), which is involved in transmission of the extracell

165 genesis via Src- and integrin-linked kinase (ILK)-dependent signaling.

166 The integrin-linked kinase (ILK)-PINCH-parvin (IPP) complex interacts with the cytop

167 it may interact with integrin-linked kinase (ILK).

168 a(5)beta(1) integrin/integrin-linked kinase (ILK)/Akt pathway.

169 ant negative form of integrin-linked kinase (ILK); i.e., viral ORF119L lacks the ILK kinase domain.

170 se data identify a molecular pathway linking ILK signaling to the contractile SMC gene program.

171 Collectively, these findings identify M-ILK as a critical regulator of epithelial inflammatory s

172 Myeloid ILK (M-ILK) deficiency significantly ameliorates the pathology

173 In contrast, reduced epithelial damage in M-ILK-deficient mice is correlated with elevated levels of

174 matory cytokine production are impaired in M-ILK-deficient mice, and activation of epithelial NF-kapp

175 Moreover, M-ILK-dependent inflammatory signaling in the mucosal epit

176 g colitis and, as a consequence, targeting M-ILK could provide therapeutic benefit.

177 K signaling pathways are restricted by the M-ILK deficiency.

178 pping approaches, we have identified a major ILK binding site involving a 20-residue fragment (residu

179 Hepatocyte-specific ILK knockout mice (ILK/liver-/- mice) and wildtype mice (WT) were given a s

180 ng this mutation into the germ line of mice (ILK-VT/GG) caused vasculogenesis defects, resulting in a

181 Moreover, ILK inhibition blocked KRAS-driven epithelial-mesenchyma

182 Moreover, ILK is required for H. pylori-induced TNF-alpha secretio

183 solated from ILK-VT/GG mice contained mutant ILK in FAs, showed normal adhesion to and spreading on e

184 Myeloid ILK (M-ILK) deficiency significantly ameliorates the pat

185 inked kinase (ILK) reveals that FAK, but not ILK, is also required for lens fiber morphogenesis.

186 -1H-pyrazol-3-yl)propanamide (22) as a novel ILK inhibitor (IC(50), 0.6 muM), which exhibited high in

187 esults suggested that the BDNF-TrkA/p75(NTR)-ILK-Akt signaling pathway may be active in cocaine sensi

188 in which B-cell-specific genetic ablation of ILK resulted in decelerated leukemia development due to

189 We show that in the absence of ILK, the hair follicle matrix lineage fails to develop,

190 nces FLP formation through the activation of ILK/beta-parvin/cofilin pathway.

191 c, structural, and thermodynamic analysis of ILK.

192 L in mediating the functional association of ILK with beta1 integrin to regulate cell adhesion/surviv

193 Attenuation of ILK or alpha-catulin reciprocally blocked cell migration

194 nase (p38MAPK) activity, the contribution of ILK-p38MAPK signaling to branching morphogenesis in vivo

195 We tested the hypothesis that deletion of ILK in mice on an HF diet would disrupt the ECM-integrin

196 roliferation in vitro Homozygous deletion of ILK in renal collecting ducts (CD) of Ilk(fl/fl) ;Pkhd1-

197 Early deletion of ILK leads to defects in extracellular matrix deposition

198 Depletion of ILK inhibits this effect, which is independent of ADAM12

199 This effect downstream of ILK signaling is mediated through loss of Ras suppressor

200 ivated Akt-NF-kappaB signaling downstream of ILK, which in turn led to increased expression of fibron

201 phorylation of AKT, a downstream effector of ILK, was remarkably decreased in ORF119L-overexpressing

202 and ERK1/2 that are downstream effectors of ILK pathway.

203 In vivo efficacy of ILK inhibition was evaluated in two murine xenograft mod

204 Reduced expression of ILK in Pkd1(fl/fl) ;Pkhd1-Cre mice, a rapidly progressiv

205 Podocyte expression of ILK increased after the injection of Stx2/LPS and preced

206 and behavior, whereas ectopic expression of ILK stimulated CSC development under softer or normoxic

207 a show that KRAS regulated the expression of ILK through E2F1-mediated transcriptional activation, wh

208 Expression of ILK, PINCH, PI3K, GSK-3beta, tau, MAP2, synaptophysin an

209 y overexpressing a dominant negative form of ILK or by injecting an ILK antisense morpholino oligonuc

210 extensive literature, the kinase function of ILK is controversial.

211 ronment, we detected a parallel induction of ILK and cyclin D1 (CCND1) expression in CLL cells that w

212 Induction of ILK-dependent kinase activity by integrin alpha7 led to

213 However, inhibition of ILK after forced expression of Cten abrogated the motili

214 argeted by the pharmacological inhibition of ILK during experimental colitis.

215 Pharmacological or genetic inhibition of ILK in mouse embryonic fibroblasts and macrophages selec

216 Inhibition of ILK signaling, which is involved in cell motility and cy

217 e knockdown or pharmacological inhibition of ILK suppressed pancreatic tumor growth, in part, by supp

218 Inhibition of ILK, Akt1, and Akt2, and their effector Bcl-2 diminishes

219 re, we have characterized the interaction of ILK with kindlin-2, a key regulator for integrin bidirec

220 n of RASGRP1 and shRNA-mediated knockdown of ILK partially restore cellular senescence in Pparbeta/de

221 armacologic inhibition or shRNA knockdown of ILK prevented periostin-induced Akt/mammalian target of

222 Additionally, CD-specific knockdown of ILK strikingly reduced renal cystic disease and fibrosis

223 pment hepatic fibrosis with higher levels of ILK, pGSK3b, and Hh activity, as compared with wild-type

224 ects are likely due to the reduced levels of ILK-VT/GG and diminished binding to parvins.

225 To determine the role of ILK in hepatic insulin action in vivo, male C57BL/6J ILK

226 In this study, we investigated the role of ILK in the context of CLL and observed high ILK expressi

227 In this study we defined the role of ILK, a key component of the IPP complex, in diet-induced

228 of BV2 cells following targeted silencing of ILK expression by siRNA.

229 rs the structural integrity and stability of ILK, which provides a new basis for understanding how th

230 ies for other PH domains, including those of ILK and PDK1, were an order-of-magnitude lower.

231 dicate that ECM-mediated signaling by way of ILK is essential for adjustment of final liver size and

232 ction gene-expression studies in 10-week-old ILK knockout showed upregulation of structural, remodeli

233 our finding that knockdown of either KRAS or ILK has a reciprocal effect on the other's expression, w

234 ephosphorylation of Akt at Ser-473 and other ILK targets, including glycogen synthase kinase-3beta an

235 Previous reports showed that overexpressed ILK in which Val(386) and Thr(387) were substituted with

236 to the host PINCH, attenuates the host PINCH-ILK interaction, and thus impairs ILK signaling.

237 uced alpha-actinin-4 expression and promoted ILK-dependent nuclear expression of Snail and cell motil

238 of complement and generation of C3a promotes ILK signaling, leading to podocyte dysfunction and loss

239 Recently ILK been shown to have an important role in bacterial ep

240 We show that recombinant ILK from either bacteria or mammalian cells exhibits no

241 ression), we showed that Cten could regulate ILK.

242 1 and downstream invasion pathways, requires ILK to induce cell motility, and activates NF-kappaB.

243 387) were substituted with glycine residues (ILK-VT/GG) could neither interact with paxillin nor loca

244 Treatment of mice with selective ILK inhibitor Cpd22 at Days 22-35 of SU5416/hypoxia expo

245 12 cell lysate did not identify any specific ILK substrates.

246 transcriptional profiles of cardiac-specific ILK knockout and wild-type hearts from 10-day-old mice b

247 Cardiac-specific ILK knockout mice spontaneously developed lethal dilated

248 iomyocyte ILK, we generated cardiac-specific ILK knockout mice using alpha-myosin heavy chain-driven

249 e the functional decline in cardiac-specific ILK knockout mice.

250 Cardiomyocyte-specific ILK deletion leads to a lethal cardiomyopathy characteri

251 Albcre mice to produce a hepatocyte-specific ILK deletion (ILK(lox/lox)Albcre).

252 Hepatocyte-specific ILK knockout mice (ILK/liver-/- mice) and wildtype mice

253 Wild-type (ILK(lox/lox)) and muscle-specific ILK-deficient (ILK(lox/lox)HSAcre) mice were fed chow or

254 an association between substratum stiffness, ILK, and CSC markers, insofar as ILK and CD44 were expre

255 novel link between EGF receptor stimulation, ILK-containing complexes, and activation of small Rho GT

256 o that prevents eNOS uncoupling, and suggest ILK as a therapeutic target for prevention of endothelia

257 The newly synthesized ILK protein colocalized to centrosomal structures and wa

258 ovides a mechanistic rationale for targeting ILK to suppress oncogenic KRAS signaling, which might fo

259 ate the translational potential of targeting ILK to suppress oncogenic KRAS signaling in pancreatic c

260 nase active site but it has been argued that ILK may be an unusual manganese (Mn)-dependent serine-th

261 We conclude that ILK is critical for maintaining the CD epithelium and re

262 The current studies demonstrate that ILK deletion reduces the proliferation and differentiati

263 This demonstrates that ILK contributes to hepatic insulin resistance and highli

264 ively, our data provide strong evidence that ILK lacks intrinsic kinase function.

265 in vivo Although in vitro data indicate that ILK controls p38 mitogen-activated protein kinase (p38MA

266 with hair matrix formation, indicating that ILK regulates hair bud cell polarity and functions upstr

267 lymph node microenvironment and propose that ILK promotes leukemogenesis by enabling CLL cells to cop

268 We further show that ILK interacted with the CD103 intracellular domain, resu

269 Furthermore, we show that ILK levels correlate with the levels of phos-AKT and ERK

270 Here, we show that ILK mediates pro-inflammatory signaling in response to l

271 Dual immunofluoresence staining showed that ILK expression is co-distributed with p75(NTR) and TrkA

272 These results suggest that ILK expression in muscle is a critical component of diet

273 pha, and TGF-alpha; our results suggest that ILK is involved in the PAR-2-mediated TGF-alpha via an H

274 ur knowledge we show for the first time that ILK disruption results in non-apoptotic cell death in vi

275 The ILK/liver-/- mice, on the other hand, showed a prolonged

276 role in cancer metastasis by activating the ILK-mediated Akt-NF-kappaB-alphavbeta3 signaling axis.

277 Calpain activation also disrupted the ILK-PINCH-Parvin complex and altered platelet adhesion a

278 independently of reduced colonization in the ILK knockout mice.

279 tosis failed to promote cell survival in the ILK-deleted lens epithelium.

280 ated fibronectin expression was found in the ILK-ko mice.

281 The prolonged proliferative response in the ILK/liver-/- mice seems to be due to sustained induction

282 A mutant of myopodin lacking the ILK interaction motif is inactive in suppressing the gro

283 kinase (ILK); i.e., viral ORF119L lacks the ILK kinase domain.

284 EGF-A) from cancer cells, independent of the ILK/HIFs-alpha pathways.

285 es its leucine-rich surface to recognize the ILK pseudokinase domain in a mode that is distinct from

286 constitution of RSU-1 expression rescued the ILK-dependent effects on NSPC proliferation.

287 We further found that the ILK-mediated phenotypes induced by stiff and hypoxic mic

288 5-fold increase in liver weight, whereas the ILK/liver-/- mice showed a 3.7-fold increase in liver we

289 Therefore, ILK deletion impaired the developmental profile, prolife

290 rvival and suppresses cell apoptosis through ILK-induced phosphorylation of Akt1, Akt2, and up-regula

291 acterial epithelial cell attachment, through ILK-bacterial OspE binding.

292 er demonstrate that the kindlin-2 binding to ILK is crucial for the kindlin-2 localization to focal a

293 -type ILK, implying that paxillin binding to ILK is required for its localization to FAs.

294 FA in cells expressing endogenous wild-type ILK, implying that paxillin binding to ILK is required f

295 Wild-type (ILK(lox/lox)) and muscle-specific ILK-deficient (ILK(lox

296 t Ser-473 was RICTOR-mTOR-dependent, whereas ILK and PAK1/2 were dispensable.

297 Falpha-NF-kappaB-mediated mechanism by which ILK expression is induced in the lymph node microenviron

298 trate that ADAM12L coimmunoprecipitates with ILK in cells and that its cytoplasmic tail is required f

299 gic effects through direct interactions with ILK, a signal transduction pathway firmly linked to cell

300 out postnatal development in Olig1Cre(+/-) x ILK(fl/fl) mice.