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1                                              ILK also regulated osteopontin expression in cardiomyocy
2                                              ILK deletion caused endothelial NOS (eNOS) uncoupling, r
3                                              ILK expression was detected in the endothelial cell laye
4                                              ILK influences the host response to C. rodentium -induce
5                                              ILK is also required for normal melanin transfer, and GS
6                                              ILK is further found to impede interactions between VEGF
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, PINCH1 and pFAK(Tyr397) were significantly decrease
15                                              ILK, PINCH1 and pFAK(Tyr397) were significantly lower in
16                                              ILK, Src, and galectin-3 also mediate EGF stimulation of
17                                              ILK-deficient hair buds also show abnormalities in the d
18                                              ILK-enriched exosomes activated NF-kappaB (nuclear facto
19                                              ILK-ko mice exhibited reduced weight loss at 15 days pos
20 data define a specific mode of the kindlin-2/ILK interaction with mechanistic implications as to how
21 on of integrin with Mn2+ induces galectin-3, ILK, and Src-dependent RhoA activation and caveolin-1 ph
22 active form is promoted by binding to PAT-4 (ILK).
23 epatic insulin action in vivo, male C57BL/6J ILK(lox/lox) mice were crossed with Albcre mice to produ
24 ell types to produce collagen IV to activate ILK (integrin-linked kinase).
25  near the active site and strongly activated ILK kinase activity.
26 a major docking platform in focal adhesions, ILK engages many proteins to dynamically link integrins
27    Because paxillin depletion did not affect ILK localization to FAs, the embryonic lethality and the
28 RC activated the integrin-linked kinase/AKT (ILK/AKT) pathway, likely via integrin interaction, and s
29                                     Although ILK-mediated phosphorylation of p65 at Ser-536 is indepe
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 xpress high levels of endogenous ADAM12L and ILK, the two proteins are redistributed to focal adhesio
35 gh levels of expression of alpha-catulin and ILK were associated with poor overall survival in patien
36                                    ELMO2 and ILK have also separately been implicated in microtubule
37 complexes containing active RhoG, ELMO2, and ILK.
38                                     eNOS and ILK coimmunoprecipitated in aortic lysates from control
39 upregulating ILK enrichment in exosomes, and ILK-mediated activation of NF-kappaB pathway in recipien
40 y response as the top predicted function and ILK and TREM1 as the top predicted canonical pathways.
41 decreased expression of smoothened, GLI2 and ILK compared with cells transfected with nontargeting co
42                   Interplay between KRAS and ILK and the roles of E2F1, c-Myc and heterogeneous nucle
43 t was not different between ILK(lox/lox) and ILK(lox/lox)HSAcre mice.
44 tably, the combined actions of Rif/mDia2 and ILK/beta-parvin/cofilin pathways on FLPs are required no
45 main in a mode that is distinct from another ILK pseudokinase domain binding protein, alpha-parvin.
46  stiffness, ILK, and CSC markers, insofar as ILK and CD44 were expressed in cancer cells located in t
47 tization was associated with increased BDNF, ILK activity, phospho-Akt Ser(473), p75(NTR), and TrkB p
48 ex in which PDLIM5 provides a bridge between ILK and AE1C.
49        Body weight was not different between ILK(lox/lox) and ILK(lox/lox)HSAcre mice.
50 ECM) via beta1 integrins which activate both ILK and Rac1 and are required for STAT5a activation and
51 ugh the induction of TGF-alpha expression by ILK/HIFs-alpha, as well as through MEK/VEGF-A-mediated a
52 lation of LPS-induced TNF-alpha synthesis by ILK does not involve the classical NF-kappaB pathway, be
53 ereas superoxide formation was unaffected by ILK depletion in eNOS-KO cells, indicating eNOS as a pri
54 nuclear translocation are both unaffected by ILK inhibition.
55                                Cardiomyocyte ILK deletion produces a lethal arrhythmogenic cardiomyop
56          To define the role of cardiomyocyte ILK, we generated cardiac-specific ILK knockout mice usi
57  both control and intestinal epithelial cell ILK knockout mice.
58                              In conjunction, ILK-deficient primary oligodendrocytes are defined by a
59 significance in CRC, and we delineate a Cten-ILK pathway controlling cell motility and possibly promo
60  revealed that VT/GG substitutions decreased ILK protein stability leading to decreased ILK levels an
61 d ILK protein stability leading to decreased ILK levels and reduced binding to paxillin and alpha-par
62 lox/lox)) and muscle-specific ILK-deficient (ILK(lox/lox)HSAcre) mice were fed chow or a high-fat (HF
63                           Our results define ILK as a key mechanotransducer in modulating breast CSC
64  produce a hepatocyte-specific ILK deletion (ILK(lox/lox)Albcre).
65              Together, our work demonstrates ILK as necessary for normal oligodendrocyte development,
66                                    Depleting ILK blocked stiffness and hypoxia-dependent acquisition
67 ation and metastasis in ovo, where depleting ILK significantly abrogated the tumorigenic and metastat
68  we report on the role of epithelial derived ILK in response to Citrobacter rodentium infection.
69                                  Diminishing ILK by siRNA decreased the levels of PAR-2-induced p-AKT
70 nts were reduced, possibly related to direct ILK-Kv4.2 subunit interactions.
71 anges associated with cardiomyocyte-directed ILK deletion in mice.
72       Adult mice with cardiomyocyte-directed ILK knockout were compared with littermate controls.
73                                Knocking down ILK in Olig1-Cre-expressing cells reduces the pool of ol
74    These studies suggest that this KRAS-E2F1-ILK-hnRNPA1 regulatory loop enables pancreatic cancer ce
75 highly resembles the phenotype of endogenous ILK inhibition, either by overexpressing a dominant nega
76 MKI67)-positive cells in regions of enhanced ILK expression in lymph nodes from CLL patients.
77                                         eNOS-ILK interaction in endothelial cells was prevented by ge
78 ortic lysates from control animals, and eNOS-ILK-shock protein 90 interaction was detected in human n
79 duced Smad signaling through a Cdc42-Src-FAK-ILK pathway.
80 uscle insulin sensitivity relative to HF-fed ILK(lox/lox) mice, as shown by increased rates of glucos
81                              However, HF-fed ILK(lox/lox)HSAcre mice had improved muscle insulin sens
82 Improved muscle insulin action in the HF-fed ILK(lox/lox)HSAcre mice was associated with increased in
83 ets Akt and GSK3beta is unaffected following ILK loss.
84                     Cells that were null for ILK failed to respond to the induction of invasion by LI
85 k-out mice, we demonstrate a requirement for ILK in oligodendrocyte differentiation and axonal myelin
86                 Our study reveals a role for ILK in extracellular matrix organization, fiber migratio
87 ion of ADAM12L promotes kinase activity from ILK immunoprecipitates.
88                    Fibroblasts isolated from ILK-VT/GG mice contained mutant ILK in FAs, showed norma
89                                 Furthermore, ILK-mediated alternative NF-kappaB activation through p6
90    Results from this study show that hepatic ILK deletion has no effect on insulin action in lean mic
91  ILK in the context of CLL and observed high ILK expression in patient samples, particularly in tumor
92 ted that viral ORF119L might affect the host ILK complex.
93 of a dominant negative inhibitor of the host ILK from ISKNV (an iridovirus).
94 s as a domain-negative inhibitor of the host ILK, providing a novel mechanism for the megalocytivirus
95 is-rich protein (PINCH) and affects the host ILK-PINCH interaction in vitro in fathead minnow (FHM) c
96 identifies three distinct mutations in human ILK, which compromise the function of the gene product i
97  We show that human kindlin-2 binds to human ILK with high affinity.
98 primary epidermal melanocytes and identifies ILK and GSK-3 as important modulators of melanin transfe
99 osome-mediated cardiac repair and identifies ILK as a target kinase for improving progenitor cell exo
100           Comprehensive profiling identifies ILK-dependent transcriptional effects and implicates ost
101                         Our results identify ILK as a regulatory partner of eNOS in vivo that prevent
102                                           If ILK was deleted at a later time-point after initial esta
103 or RhoG stabilizes microtubules, but only if ILK is also present.
104 host PINCH-ILK interaction, and thus impairs ILK signaling.
105                       Our findings implicate ILK as a critical regulatory molecule for the NF-kappaB-
106                                           In ILK-ko mice reduced activation of ser473Akt and reduced
107           The molecular pathways affected in ILK-deficient follicles are similar to those in the abse
108 agonist limited podocyte loss and changes in ILK, Snail, and alpha-actinin-4 expression.
109 apsin response mediator protein 2 (CRMP2) in ILK-deficient melanocytes restored dendricity.
110 of certain focal adhesion proteins including ILK, PINCH, paxillin, and cdc42, as well as regulating t
111  C. rodentium exposure was shown to increase ILK expression in cell lines, and in murine epithelium i
112                                     Instead, ILK deletion resulted in secondary fiber migration defec
113                                     Instead, ILK is involved in an alternative activation of NF-kappa
114      Most significantly, the IGFBP2/integrin/ILK/NF-kappaB network functions as a physiologically act
115                                Intriguingly, ILK knockdown in IL-10 knockout EPC-derived exosome sign
116 ugh modulation of the integrin-linked kinase ILK.
117 time, which involves integrin-linked kinase (ILK) and beta-parvin, two integrin:actin-bridging protei
118 tain significance in integrin-linked kinase (ILK) and filamin-C (FLNC).
119 s from repression of integrin-linked kinase (ILK) and phosphoinositide-dependent protein kinase-1 (PD
120  simultaneously bind integrin-linked kinase (ILK) and RhoG, forming tripartite ERI complexes.
121      We identify the integrin-linked kinase (ILK) as a new partner for ADAM12L cellular functions.
122 ied septin-5 and the integrin-linked kinase (ILK) as novel calpain substrates.
123 profiling identified integrin-linked kinase (ILK) as the most upregulated pathway in sEV-treated epit
124 us of myopodin binds integrin-linked kinase (ILK) both in vivo and in vitro.
125 d phosphorylation of integrin-linked kinase (ILK) by TGFBR1.
126 integrin, PINCH, and integrin-linked kinase (ILK) caused formation of multinucleate epidermal cells w
127 1 (kAE1), PDLIM5 and integrin-linked kinase (ILK) form a multiprotein complex in which PDLIM5 provide
128 pecific depletion of integrin-linked kinase (ILK) in mouse embryos hyper-activates VEGFR3 signalling
129 w that expression of integrin-linked kinase (ILK) in myeloid cells is critical for the epithelial inf
130 l selectively delete integrin linked kinase (ILK) in myeloid cells of mice to show that this integrin
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                      Integrin-linked kinase (ILK) is a scaffold protein that regulates microtubule st
138 NIFICANCE STATEMENT: Integrin-linked kinase (ILK) is a scaffolding protein involved in integrating si
139                      Integrin-linked kinase (ILK) is a serine-threonine kinase that transduces extrac
140                      Integrin-linked kinase (ILK) is a serine/threonine kinase that has been linked t
141                      Integrin-linked kinase (ILK) is a ubiquitously expressed and highly conserved se
142                      Integrin-linked kinase (ILK) is an important protein that is expressed at the in
143                      Integrin-linked kinase (ILK) is an intracellular scaffold protein with critical
144 dothelial cells, and integrin-linked kinase (ILK) is important for blood vessel integrity and cardiov
145                      Integrin-linked kinase (ILK) is one of the few evolutionarily conserved focal ad
146                      Integrin-linked kinase (ILK) localizes to focal adhesions (FAs) where it regulat
147 the kinase domain of integrin-linked kinase (ILK) near the active site and strongly activated ILK kin
148  in the integrin and integrin-linked kinase (ILK) pathways and that these genes are associated with p
149                      Integrin-linked kinase (ILK) represents a relevant target for cancer therapy in
150 ion kinase (FAK) and integrin-linked kinase (ILK) reveals that FAK, but not ILK, is also required for
151  increased levels of integrin-linked kinase (ILK) signaling as demonstrated by the impaired angiogene
152 iviral response, and integrin-linked kinase (ILK) signaling were among the top altered canonical path
153 more, PAR-2, through integrin-linked kinase (ILK) signaling, including the p-AKT, promoted HIF protei
154 ns, the relevance of integrin-linked kinase (ILK) signals in podocyte dysfunction was evaluated.
155   Here, we show that integrin-linked kinase (ILK), a mediator of cell-matrix interactions, is indispe
156 ese processes by the integrin-linked kinase (ILK), a scaffold protein that links the extracellular ma
157 ulin interacted with integrin-linked kinase (ILK), a serine/threonine protein kinase implicated in ca
158                      Integrin-linked kinase (ILK), a serine/threonine protein kinase, has roles in ce
159  down-regulated both integrin linked kinase (ILK), an activator of smoothened, and phosphorylated gly
160 nclude integrins and integrin-linked kinase (ILK), are critical for hair follicle formation.
161 ogical inhibition of integrin linked kinase (ILK), EGFR and NF-kappaB, as well as transfection of a d
162 athway that requires integrin-linked kinase (ILK), Engulfment and Cell Motility-2 (ELMO2), integrin b
163 sion and activity of integrin-linked kinase (ILK), level of protein kinase B (Akt) phosphorylation at
164 tter the function of integrin-linked kinase (ILK), we examined the phenotypic consequences of its del
165 te Akt signaling via integrin-linked kinase (ILK), which is antagonistic to endoderm differentiation.
166 genesis via Src- and integrin-linked kinase (ILK)-dependent signaling.
167                  The integrin-linked kinase (ILK)-PINCH-parvin (IPP) complex interacts with the cytop
168 ired the presence of integrin-linked kinase (ILK).
169 ant negative form of integrin-linked kinase (ILK); i.e., viral ORF119L lacks the ILK kinase domain.
170 tein 10 (GRB10), and integrin-linked kinase (ILK)] were significantly associated with Cd concentratio
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                            In the absence of ILK, immature melanosomes are not retained in perinuclea
190               We show that in the absence of ILK, the hair follicle matrix lineage fails to develop,
191 nces FLP formation through the activation of ILK/beta-parvin/cofilin pathway.
192 c, structural, and thermodynamic analysis of ILK.
193 hanical stimulation disrupts the assembly of ILK and beta1 integrin, releasing the integrin to enable
194 L in mediating the functional association of ILK with beta1 integrin to regulate cell adhesion/surviv
195                               Attenuation of ILK or alpha-catulin reciprocally blocked cell migration
196 nase (p38MAPK) activity, the contribution of ILK-p38MAPK signaling to branching morphogenesis in vivo
197    We tested the hypothesis that deletion of ILK in mice on an HF diet would disrupt the ECM-integrin
198 roliferation in vitro Homozygous deletion of ILK in renal collecting ducts (CD) of Ilk(fl/fl) ;Pkhd1-
199                            Early deletion of ILK leads to defects in extracellular matrix deposition
200                                 Depletion of ILK inhibits this effect, which is independent of ADAM12
201                    This effect downstream of ILK signaling is mediated through loss of Ras suppressor
202 ivated Akt-NF-kappaB signaling downstream of ILK, which in turn led to increased expression of fibron
203 phorylation of AKT, a downstream effector of ILK, was remarkably decreased in ORF119L-overexpressing
204  and ERK1/2 that are downstream effectors of ILK pathway.
205                          In vivo efficacy of ILK inhibition was evaluated in two murine xenograft mod
206                        Reduced expression of ILK in Pkd1(fl/fl) ;Pkhd1-Cre mice, a rapidly progressiv
207                       Podocyte expression of ILK increased after the injection of Stx2/LPS and preced
208  and behavior, whereas ectopic expression of ILK stimulated CSC development under softer or normoxic
209 a show that KRAS regulated the expression of ILK through E2F1-mediated transcriptional activation, wh
210 y overexpressing a dominant negative form of ILK or by injecting an ILK antisense morpholino oligonuc
211 extensive literature, the kinase function of ILK is controversial.
212 ronment, we detected a parallel induction of ILK and cyclin D1 (CCND1) expression in CLL cells that w
213 argeted by the pharmacological inhibition of ILK during experimental colitis.
214     Pharmacological or genetic inhibition of ILK in mouse embryonic fibroblasts and macrophages selec
215                                Inhibition of ILK signaling, which is involved in cell motility and cy
216 e knockdown or pharmacological inhibition of ILK suppressed pancreatic tumor growth, in part, by supp
217 re, we have characterized the interaction of ILK with kindlin-2, a key regulator for integrin bidirec
218 e for alpha-parvin (Parva), an interactor of ILK.
219                                 Knockdown of ILK in human LECs triggers VEGFR3 tyrosine phosphorylati
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 s, and genetic or pharmacologic targeting of ILK reversed mitochondrial reprogramming and suppressed
230 ies for other PH domains, including those of ILK and PDK1, were an order-of-magnitude lower.
231 ction gene-expression studies in 10-week-old ILK knockout showed upregulation of structural, remodeli
232 our finding that knockdown of either KRAS or ILK has a reciprocal effect on the other's expression, w
233 ephosphorylation of Akt at Ser-473 and other ILK targets, including glycogen synthase kinase-3beta an
234   Previous reports showed that overexpressed ILK in which Val(386) and Thr(387) were substituted with
235 to the host PINCH, attenuates the host PINCH-ILK interaction, and thus impairs ILK signaling.
236 uced alpha-actinin-4 expression and promoted ILK-dependent nuclear expression of Snail and cell motil
237 of complement and generation of C3a promotes ILK signaling, leading to podocyte dysfunction and loss
238     Among differentially expressed proteins, ILK (integrin-linked kinase) was highly enriched in both
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 transcriptional profiles of cardiac-specific ILK knockout and wild-type hearts from 10-day-old mice b
246                             Cardiac-specific ILK knockout mice spontaneously developed lethal dilated
247 iomyocyte ILK, we generated cardiac-specific ILK knockout mice using alpha-myosin heavy chain-driven
248 e the functional decline in cardiac-specific ILK knockout mice.
249                       Cardiomyocyte-specific ILK deletion leads to a lethal cardiomyopathy characteri
250 Albcre mice to produce a hepatocyte-specific ILK deletion (ILK(lox/lox)Albcre).
251                          Hepatocyte-specific ILK knockout mice (ILK/liver-/- mice) and wildtype mice
252 Wild-type (ILK(lox/lox)) and muscle-specific ILK-deficient (ILK(lox/lox)HSAcre) mice were fed chow or
253 an association between substratum stiffness, ILK, and CSC markers, insofar as ILK and CD44 were expre
254 novel link between EGF receptor stimulation, ILK-containing complexes, and activation of small Rho GT
255 o that prevents eNOS uncoupling, and suggest ILK as a therapeutic target for prevention of endothelia
256                        The newly synthesized ILK protein colocalized to centrosomal structures and wa
257 ovides a mechanistic rationale for targeting ILK to suppress oncogenic KRAS signaling, which might fo
258 ate the translational potential of targeting ILK to suppress oncogenic KRAS signaling in pancreatic c
259                             We conclude that ILK is critical for maintaining the CD epithelium and re
260         The current studies demonstrate that ILK deletion reduces the proliferation and differentiati
261                       This demonstrates that ILK contributes to hepatic insulin resistance and highli
262 in vivo Although in vitro data indicate that ILK controls p38 mitogen-activated protein kinase (p38MA
263  with hair matrix formation, indicating that ILK regulates hair bud cell polarity and functions upstr
264 lymph node microenvironment and propose that ILK promotes leukemogenesis by enabling CLL cells to cop
265                         We further show that ILK interacted with the CD103 intracellular domain, resu
266                            Here we show that ILK is necessary for normal trafficking of melanosomes a
267                    Furthermore, we show that ILK levels correlate with the levels of phos-AKT and ERK
268                           Here, we show that ILK mediates pro-inflammatory signaling in response to l
269  Dual immunofluoresence staining showed that ILK expression is co-distributed with p75(NTR) and TrkA
270                    Thus, our work shows that ILK is a central modulator of melanosome movements in pr
271                   These results suggest that ILK expression in muscle is a critical component of diet
272                        Our data suggest that ILK facilitates mechanically regulated VEGFR3 signalling
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  kinase (ILK); i.e., viral ORF119L lacks the ILK kinase domain.
282 EGF-A) from cancer cells, independent of the ILK/HIFs-alpha pathways.
283 es its leucine-rich surface to recognize the ILK pseudokinase domain in a mode that is distinct from
284 constitution of RSU-1 expression rescued the ILK-dependent effects on NSPC proliferation.
285                    We further found that the ILK-mediated phenotypes induced by stiff and hypoxic mic
286                                   Therefore, ILK deletion impaired the developmental profile, prolife
287 acterial epithelial cell attachment, through ILK-bacterial OspE binding.
288 nd this effect was partly attenuated through ILK knockdown in exosomes.
289 er demonstrate that the kindlin-2 binding to ILK is crucial for the kindlin-2 localization to focal a
290 -type ILK, implying that paxillin binding to ILK is required for its localization to FAs.
291  FA in cells expressing endogenous wild-type ILK, implying that paxillin binding to ILK is required f
292                                   Wild-type (ILK(lox/lox)) and muscle-specific ILK-deficient (ILK(lox
293 sive lymphatic vascular growth observed upon ILK depletion.
294  effect on myocardial repair by upregulating ILK enrichment in exosomes, and ILK-mediated activation
295 F-kappaB pathway in recipient cells, whereas ILK knockdown in exosomes attenuates NF-kappaB activatio
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.

 
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