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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
23 epatic insulin action in vivo, male C57BL/6J ILK(lox/lox) mice were crossed with Albcre mice to produ
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
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
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
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
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
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
67 ation and metastasis in ovo, where depleting ILK significantly abrogated the tumorigenic and metastat
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
78 ortic lysates from control animals, and eNOS-ILK-shock protein 90 interaction was detected in human n
80 uscle insulin sensitivity relative to HF-fed ILK(lox/lox) mice, as shown by increased rates of glucos
82 Improved muscle insulin action in the HF-fed ILK(lox/lox)HSAcre mice was associated with increased in
85 k-out mice, we demonstrate a requirement for ILK in oligodendrocyte differentiation and axonal myelin
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
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
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
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
114 Most significantly, the IGFBP2/integrin/ILK/NF-kappaB network functions as a physiologically act
117 time, which involves integrin-linked kinase (ILK) and beta-parvin, two integrin:actin-bridging protei
119 s from repression of integrin-linked kinase (ILK) and phosphoinositide-dependent protein kinase-1 (PD
123 profiling identified integrin-linked kinase (ILK) as the most upregulated pathway in sEV-treated epit
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
138 NIFICANCE STATEMENT: Integrin-linked kinase (ILK) is a scaffolding protein involved in integrating si
144 dothelial cells, and integrin-linked kinase (ILK) is important for blood vessel integrity and cardiov
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
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
159 down-regulated both integrin linked kinase (ILK), an activator of smoothened, and phosphorylated gly
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.
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
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
178 pping approaches, we have identified a major ILK binding site involving a 20-residue fragment (residu
180 ng this mutation into the germ line of mice (ILK-VT/GG) caused vasculogenesis defects, resulting in a
183 solated from ILK-VT/GG mice contained mutant ILK in FAs, showed normal adhesion to and spreading on e
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
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
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-
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
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
212 ronment, we detected a parallel induction of ILK and cyclin D1 (CCND1) expression in CLL cells that w
214 Pharmacological or genetic inhibition of ILK in mouse embryonic fibroblasts and macrophages selec
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
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
223 pment hepatic fibrosis with higher levels of ILK, pGSK3b, and Hh activity, as compared with wild-type
226 In this study, we investigated the role of ILK in the context of CLL and observed high ILK expressi
229 s, and genetic or pharmacologic targeting of ILK reversed mitochondrial reprogramming and suppressed
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
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
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
245 transcriptional profiles of cardiac-specific ILK knockout and wild-type hearts from 10-day-old mice b
247 iomyocyte ILK, we generated cardiac-specific ILK knockout mice using alpha-myosin heavy chain-driven
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
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
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
269 Dual immunofluoresence staining showed that ILK expression is co-distributed with p75(NTR) and TrkA
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
276 role in cancer metastasis by activating the ILK-mediated Akt-NF-kappaB-alphavbeta3 signaling axis.
283 es its leucine-rich surface to recognize the ILK pseudokinase domain in a mode that is distinct from
289 er demonstrate that the kindlin-2 binding to ILK is crucial for the kindlin-2 localization to focal a
291 FA in cells expressing endogenous wild-type ILK, implying that paxillin binding to ILK is required f
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
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