ライフサイエンスコーパス: ICAM-1

1 ride, and intercellular adhesion molecule-1 (ICAM-1).

2 A-DR) and intercellular adhesion molecule-1 (ICAM-1).

3 e such as intercellular adhesion molecule-1 (ICAM-1).

4 receptor intercellular adhesion molecule-1 (ICAM-1).

5 and ALK2 in the up-regulation of VCAM-1 and ICAM-1.

6 AB and B significantly reduced IE binding to ICAM-1.

7 ll-surface adhesion molecules E-selectin and ICAM-1.

8 on by organizing the spatial distribution of ICAM-1.

9 in annexin A2 as a novel binding partner for ICAM-1.

10 ion of CD56 and high expression of NKp46 and ICAM-1.

11 tion of expression or function of neutrophil ICAM-1.

12 ation, including CD55, CD47, CD18/CD11b, and ICAM-1.

13 d morphology in two-dimensional migration on ICAM-1.

14 MAPKs, and upregulation of adhesion molecule ICAM-1.

15 y is further enhanced by mechanical force on ICAM-1.

16 naling function of the cytoplasmic domain of ICAM-1.

17 in (CD2AP) as a novel interaction partner of ICAM-1.

18 dothelial signaling triggered by adhesion to ICAM-1.

19 dependent increase in vascular expression of ICAM-1.

20 to study the interactions between iRBCs and ICAM-1.

21 cated form lacking the cytoplasmic domain of ICAM-1.

22 LFA-1 to form high-avidity interactions with ICAM-1.

23 AM-1] and intracellular adhesion molecule 1 [ICAM-1]).

24 ARs were constructed targeting overexpressed ICAM-1, a broad tumor biomarker, using its physiological

25 sessment of localization of CD37 and CD18 in ICAM-1-adherent neutrophils demonstrated that these mole

26 human monocytes, CCL2 stimulation coupled to ICAM-1 adhesion led to rapid nuclear-to-cytosolic transl

27 n of rIL-18 led to upregulation of CD11a and ICAM-1 adhesion molecules, which were involved in the co

28 acts with intercellular adhesion molecule 1 (ICAM-1), allowing us to predict binders from a specific

29 ptor interactions of EPCR binding PfEMP1with ICAM-1 amplifies development of severe malaria symptoms.

30 pported lipid bilayers with laterally mobile ICAM-1 and anti-CD3 mAb.

31 could inhibit and reverse binding of IEs to ICAM-1 and CSA receptors.

32 ion of these PfEMP1s, predicted to bind both ICAM-1 and EPCR, is associated with increased risk of de

33 we show that NHERF-1 assembles ERM proteins, ICAM-1 and F-actin into a macromolecule complex that is

34 -dependent leukocyte adhesion to immobilized ICAM-1 and fibronectin.

35 -mediated neutrophil crawling on endothelial ICAM-1 and ICAM-2 is a prerequisite for transcellular ne

36 ICAM-1 and ICAM-3, uropod-directed proteins that do not

37 se (VS), facilitated by interactions between ICAM-1 and LFA-1.

38 It also decreased the upregulation of ICAM-1 and P-selectin.

39 hat the initiation of RhoA activity involves ICAM-1 and the Rho GEFs Ect2 and LARG.

40 ession/activity in EC induces an increase in ICAM-1 and tissue factor expression through the upregula

41 LTC4 upregulated the expressions of ICAM-1 and VCAM-1 in an aspirin-sensitive and TP recepto

42 nflammatory signals, showing upregulation of ICAM-1 and VCAM-1 on their surface, as well as release o

43 Up-regulation of the adhesion molecules ICAM-1 and VCAM-1 resulted in an increased adhesion of p

44 endothelial cells, as well as to immobilized ICAM-1 and VCAM-1.

45 erence and NF-kappaB-dependent expression of ICAM-1 and VCAM-1.

46 cells tested, namely the adhesion molecules ICAM-1 and VCAM-1; the chemokines CCL5, CCL20, CXCL1, CX

47 CAM-1 leads to VE-cadherin dissociation from ICAM-1 and VE-cadherin association with actin, SHP-2 dow

48 surface molecules screened, including CD54 (ICAM-1) and CD71 (transferrin receptor).

49 uction of intercellular adhesion molecule-1 (ICAM-1) and diminishing the enzymatic activity of urokin

50 increased intercellular adhesion molecule 1 (ICAM-1) and E-selectin expression on HUVECs by 3- and 1.

51 find that intercellular adhesion molecule 1 (ICAM-1) and ICAM-2 on B cells are essential for long-las

52 expressions of pro-inflammatory (IL-6, iNOS, ICAM-1) and pro-fibrogenic (Col1, alpha-SMA, TIMP-1) gen

53 molecules intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1).

54 uction of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).

55 ins CD36, intercellular adhesion molecule-1 (ICAM-1), and endothelial protein C receptor (EPCR); howe

56 L-1beta), intracellular adhesion molecule 1 (ICAM-1), and nitric oxide synthase (NOS2), developed leu

57 levels of intercellular adhesion molecule 1 (ICAM-1), and oxidative stress in the colon are the princ

58 oblasts, which do not constitutively express ICAM-1, and myoblasts and fibroblasts forced to express

59 d from diabetes-induced TNF-alpha, IL-1beta, ICAM-1, and NOS2 upregulation.

60 ed TNFalpha-induced expression of VCAM-1 and ICAM-1, and thus reduced monocyte adherence to human umb

61 of four inflammatory genes (IFN-gamma, IL-6, ICAM-1, and TLR-2), up to four times between 2000 and 20

62 xplained by the greater expression of CCL19, ICAM-1, and VCAM-1 in the mucosal tip compared with the

63 ICAM-1 clustering promotes the ICAM-1-annexin A2 interaction and induces translocation

64 included intercellular adhesion molecule 1 (ICAM-1), anti-LG3, aminopeptidase N, CXCL9, endothelin-1

65 We conjugated catalase to anti-ICAM-1 antibodies and administered the conjugate to 8 wk

66 ectively than non-targeted catalase and anti-ICAM-1 antibody alone.

67 We engineered ICAM-1 antibody conjugated, doxorubicin encapsulating im

68 ation of B cells, while the addition of anti-ICAM-1 antibody partially reduces this proliferation for

69 We synthesized ICAM-1 antibody-conjugated iron oxide nanoparticles (ICA

70 on showed different patterns of migration on ICAM-1, APC interactions, and tissue retention, as well

71 o the cytoskeleton, as its interactions with ICAM-1 are mainly associated with the formation of tethe

72 al adhesion molecules, such as E-selectin or ICAM-1, are connected to the actin cytoskeleton via acti

73 lso show that E-selectin and VCAM-1, but not ICAM-1, are upregulated in response to BMP9 in LPS-stimu

74 We further evaluated ICAM-1 as a MM targeting moiety by characterizing its (1

75 rative flow cytometric screening to identify ICAM-1 as a potential target for metastatic melanoma (MM

76 Identification of ICAM-1 as a TNBC target and biomarker may lead to the de

77 Here, we identify ICAM-1 as an essential receptor for both AHC-causing and

78 ase-1, and costimulatory molecules, CD16/32, ICAM-1, as well as PD-L1 and PD-L2.

79 C and in the presence of an inhibitor of the ICAM-1-associated pathway, rather than inhibitors of the

80 he result of a defect in the detachment from ICAM-1 at the trailing edge when Pyk2 function is inhibi

81 We conclude that ICAM-1 augments myoblast adhesion and fusion through its

82 We report that ICAM-1 augments myoblast adhesion to myoblasts and myotu

83 ugh which intercellular adhesion molecule-1 (ICAM-1) augments the adhesive and fusogenic properties o

84 -reactivity with and cross-inhibition of the ICAM-1 binding capacity of domain cassette 4 PfEMP1s.

85 beta3_D4 with nanomolar affinity and inhibit ICAM-1 binding of domain cassette 4-expressing IE.

86 _D4 has previously been shown to contain the ICAM-1 binding site of DBLbeta domains, suggesting that

87 uggesting that the mAb acts by occluding the ICAM-1 binding surface.

88 t recognizes a panel of PfEMP1s and inhibits ICAM-1 binding.

89 ting intracellular cell adhesion molecule 1 (ICAM-1) binding.

90 conserved mode of receptor engagement among ICAM-1-binding enteroviruses and rhinoviruses.

91 le Plasmodium falciparum genomes showed that ICAM-1-binding PfEMP1s also interact with endothelial pr

92 irus-ICAM-1 complex, which revealed critical ICAM-1-binding residues.

93 Ab-mediated ICAM-1 blockade triggers neuritis only in young NOD mice

94 d using (3) H-thymidine or CFSE labeling and ICAM-1 blocking.

95 evealed that the rate of association of iRBC-ICAM-1 bonds are ten times lower than iRBC-CD36 (cluster

96 y of intracellular cell adhesion molecule 1 (ICAM-1), but not MHCII.

97 t absolutely required for adhesion of CTL to ICAM-1, but rather delays the initial adhesion.

98 d to myogenic cells, as forced expression of ICAM-1 by fibroblasts did not augment their fusion to IC

99 Expression of ICAM-1 by ocular surface epithelium decreased significan

100 by two-photon microscopy revealed that anti-ICAM-1/catalase prevents the transition of microglia to

101 ential site for MkMP binding, and that CD54 (ICAM-1), CD11b, CD18 and CD43, localized on HSPC uropods

102 a significant increase in adhesion molecule ICAM-1, chemokine ligand (CCL)-2, and cytokine IL-6 mRNA

103 of human intercellular adhesion molecule 1 (ICAM-1) chimera and leukocyte function-associated antige

104 exerted by the T cell cytoskeleton, whereas ICAM-1 clustering enhances valency and further promotes

105 rylation in endothelial cells, which impedes ICAM-1 clustering in response to HLA class I Ab and prev

106 ICAM-1 clustering promotes the ICAM-1-annexin A2 interac

107 Loss of CD2AP stimulates the dynamics of ICAM-1 clustering, which facilitates the formation of IC

108 interaction between filamin and ICAM-1 upon ICAM-1 clustering.

109 rylation, intercellular adhesion molecule 1 (ICAM-1) clustering, and monocyte firm adhesion to HLA I

110 n in the thymic cortex, interacted less with ICAM-1 coated beads, and could overcome TCR stop signals

111 motility of murine CD4(+) primary T cells on ICAM-1-coated plates, an event reversed by a small molec

112 high-resolution cryo-EM structure of a virus-ICAM-1 complex, which revealed critical ICAM-1-binding r

113 ustering, which facilitates the formation of ICAM-1 complexes on the endothelial cell surface.

114 -8, and MCP-1, and the upregulation of CD54 (ICAM-1), consistent with a state of activation.

115 an unusual elongated appearance after 1 h on ICAM-1, consistent with abnormally strong adhesion.

116 adhere firmly, via LFA-1-mediated binding to ICAM-1 constitutively expressed by endothelial cells.

117 o explore whether non-multivalent binding to ICAM-1 could drive endocytosis and/or transcytosis of mo

118 the levels of inflammatory molecules (p-p65, ICAM-1, Cox-2, MMP3, and iNOS), pro-inflammatory cytokin

119 constructed sets of PfEMP1 domains that bind ICAM-1, CSA, or CD36, receptors that commonly support IE

120 d by higher levels of IkBalpha, p65, VCAM-1, ICAM-1, CXCL10, CCL2, TNF, and IL-6 (mostly localized to

121 which associate with actin filaments and the ICAM-1 cytoplasmic domain.

122 These mice, along with true ICAM-1-deficient mice and newly generated ICAM-1-transge

123 Conversely, neutrophils from ICAM-1-deficient mice were defective in these effector f

124 as directly proportional to CAR affinity and ICAM-1 density.

125 inestimulated HBEC to T cells was VCAM-1 and ICAM-1 dependent.

126 MAPKs were involved in ICAM-1-dependent expression of TNF-alpha in cerebral and

127 nt neutrophils to the beta2 integrin ligand, ICAM-1, despite the normal display of high-affinity beta

128 ally, CD2AP is required for mechanosensitive ICAM-1 downstream signaling toward activation of the PI3

129 adhesion molecules, including VCAM-1, IL-6, ICAM-1, E-selectin, and monocyte chemoattractant protein

130 We found that ICAM-1 efficiently marks mammary luminal progenitors com

131 of the CD44/selectin-initiated signaling, as ICAM-1 elevation was inhibited by siRNA targeting PKCalp

132 All three MAPKs were activated by ICAM-1 engagement, either through lymphocyte adhesion or

133 mice leads to disruption of the formation of ICAM-1/ERM/NHERF-1 complex and reduction of hepatic ERM

134 hown that intercellular adhesion molecule-1 (ICAM-1) expressed by endothelial cells is involved in th

135 awling on intercellular adhesion molecule 1 (ICAM-1)-expressing cells.

136 was specifically internalized by all tested ICAM-1-expressing cells, including epithelial, fibroblas

137 phox, thereby increasing ROS-NFkappaB-VCAM-1/ICAM-1 expression and monocyte adhesion in ECs inflamed

138 of epoxide hydrolysis, inhibited VCAM-1 and ICAM-1 expression and protein levels; conversely the dio

139 E-selectin and ICAM-1 expression are essential for leukocyte recruitmen

140 D14 and C5 inhibition reduced E-selectin and ICAM-1 expression by 96 and 98% for E. coli and by 70 an

141 y endothelial junction hyperpermeability and ICAM-1 expression during inflammation.

142 f siRNA against MRTF-A and/or MRTF-B induced ICAM-1 expression in HAoECs.

143 ERM knockdown reduces ICAM-1 expression in response to tumor necrosis factor a

144 g LFA expression on NK cells and by inducing ICAM-1 expression on AML cells.

145 remaster muscle and peritoneal cavity led to ICAM-1 expression on intravascular and locally transmigr

146 We have found that variations in ICAM-1 expression on tumor cells influence killing kinet

147 EC activation was measured by E-selectin and ICAM-1 expression using flow cytometry.

148 Interestingly, although ICAM-1 expression was increased in cells lacking ASM act

149 proximately 2.5-fold increase in endothelial ICAM-1 expression, a 4-fold greater monocyte-EC adhesion

150 rientation, markers of ER stress, VCAM-1 and ICAM-1 expression, and monocyte recruitment.

151 disturbed flow regions, reducing endothelial ICAM-1 expression.

152 proinflammatory cytokines and an increase of ICAM-1 expression.

153 and intracellular cell adhesion molecule 1 (ICAM-1) expression in the brain, and chemokine receptor

154 , force spectroscopy experiments reveal that ICAM-1 forms catch bond interactions with Plasmodium fal

155 n this article, we show that ASM coordinates ICAM-1 function in brain endothelial cells by regulating

156 hereas several proteins are known to promote ICAM-1 function, the molecular mechanisms that limit ICA

157 ASM controls T cell migration by regulating ICAM-1 function.

158 actor-kappaB (NF-kappaB) plays a key role in ICAM-1 gene transcription.

159 With respect to the latter, ICAM-1 has been detected on neutrophils in several clini

160 ICAM-1 has been shown to interact with cytoskeletal ezri

161 2 (Pyk2) is required for T cell adhesion to ICAM-1; however, the mechanism by which it regulates adh

162 The fusogenic property of ICAM-1-ICAM-1 interactions was restricted to myogenic ce

163 mRNA expressions of pro-inflammatory genes (ICAM-1, IL-6, TNF-alpha).

164 These studies demonstrate that ICAM-1 immunobiology is highly complex but that individu

165 Mechanical force applied on ICAM-1 impairs CD2AP binding to ICAM-1, suggesting that

166 elated and diapedesis-unrelated functions of ICAM-1 in cerebral and dermal microvascular endothelial

167 integrin LFA-1 cross-linking with its ligand ICAM-1 in human PBMCs or CD4(+) T cells promotes Th1 pol

168 -1 was the prevailing ligand for endothelial ICAM-1 in mediating neutrophil shear resistant arrest, w

169 in adhesion to complement component iC3b and ICAM-1 in shear-free, but not shear-flow, conditions.

170 ockade of EGFR or antibody neutralization of ICAM-1 in TAMs blunted spheroid formation and ovarian ca

171 ession of intercellular adhesion molecule-1 (ICAM-1) in human TNBC cell lines and tissues, and demons

172 binding affinity of LFA-1 whole protein and ICAM-1 increases significantly as the environmental pH d

173 LFA-1 contact with a cognate ligand, such as ICAM-1, independent of the immune synapse activates a la

174 cyte adhesion as well as underflow arrest on ICAM-1 induced by CXCL12.

175 JNK activity was critical for ICAM-1-induced F-actin rearrangements.

176 tch pathway activation is dependent on LFA-1/ICAM-1-induced inactivation of glycogen synthase kinase

177 Importantly ICAM-1-induced phosphorylation of paxillin was required

178 Moreover, CD2AP is necessary for ICAM-1-induced Rac1 recruitment and activation.

179 t SHP-2-via association with ICAM-1-mediates ICAM-1-induced Src activation and modulates VE-cadherin

180 CCL1, CCL2, GM-CSF, IL-1alpha, IL-1beta and ICAM-1 inflammatory cytokine expression.

181 We observed that ICAM-1 interacts with Src homology domain 2-containing p

182 ymphocyte function-associated antigen 1) for ICAM-1 (intercellular adhesion molecule 1) but significa

183 MC releasate elevated ICAM-1 (intercellular adhesion molecule-1) expression on

184 III (F3), intercellular adhesion molecule 1 (ICAM-1), interferon gamma (IFN-gamma), interleukin-6 (IL

185 e mobility and prevents the translocation of ICAM-1 into caveolin-1-rich membrane domains.

186 A2 interaction and induces translocation of ICAM-1 into caveolin-1-rich membrane domains.

187 se by inducing the endothelial expression of ICAM-1, intravascular crawling, and extravasation.

188 cell lines and tissues, and demonstrate that ICAM-1 is a potential molecular target and biomarker for

189 for the first time that the mechanoreceptor ICAM-1 is negatively regulated by an actin-binding adapt

190 ICAM-1 is required for firm adhesion of leukocytes to th

191 Intercellular adhesion molecule 1 (ICAM-1) is a cell-surface protein overexpressed in many

192 Intracellular adhesion molecule-1 (ICAM-1) is a transmembrane glycoprotein expressed on the

193 The intercellular adhesion molecule 1 (ICAM-1) is induced in mouse liver after bile duct ligati

194 sharply contrasting disease phenotypes using ICAM-1 isoform mutant mice.

195 e opportunity to begin examining the role of ICAM-1 isoforms (singly or in combination) in various di

196 here are multiple membrane-bound and soluble ICAM-1 isoforms that arise from alternative splicing and

197 Furthermore, activation of endothelial ICAM-1/JNK led to phosphorylation of paxillin, its assoc

198 Moreover, whereas the activation of ICAM-1 leads to VE-cadherin dissociation from ICAM-1 and

199 s the peptides retain its ability to inhibit ICAM-1/LFA-1 interaction.

200 However, the ICAM-1 ligands have never been investigated.

201 important in inducing GN, as anti-CD11b and -ICAM-1 mAb inhibited both proteinuria and macrophage and

202 the lumen of the lymphatic endothelium in an ICAM-1/MAC-1-dependent manner.

203 ntegrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MadCAM-1) and the chemokine receptor CXCR4.

204 e cytoskeleton and that its interaction with ICAM-1 mainly corresponds to force ramps followed by sud

205 Thus, our results suggest that ICAM-1 may not be the sole mediator responsible for cyto

206 Rac inhibition negated ICAM-1 mediated lamellipodia, spreading, and fusion of m

207 ICAM-1 mediated myoblast adhesion and fusion were quanti

208 etase inhibitor substantially inhibits LFA-1/ICAM-1-mediated activation of Notch signaling.

209 unction, the molecular mechanisms that limit ICAM-1-mediated adhesion to prevent excessive leukocyte

210 lar signaling events that originate from the ICAM-1-mediated firm adhesion of neutrophils that regula

211 Mechanistically, ICAM-1-mediated intracellular signaling appeared to supp

212 sion-induced negative feedback loop promotes ICAM-1-mediated neutrophil crawling and paracellular tra

213 ta-catenin, and plakoglobin, and reduced the ICAM-1-mediated phosphorylation of VE-cadherin by immuno

214 We conclude that in the anterior eye, ICAM-1-mediated PMN recruitment to the infected cornea a

215 All previous evidence demonstrating ICAM-1-mediated transport of therapeutics into or across

216 Intercellular adhesion molecule-1 (ICAM-1) mediates the firm adhesion of leukocytes to endo

217 ults suggest that SHP-2-via association with ICAM-1-mediates ICAM-1-induced Src activation and modula

218 l annexin A2 using RNA interference enhances ICAM-1 membrane mobility and prevents the translocation

219 PM2.5 was negatively correlated with ICAM-1 methylation (p = 0.01), but not with other genes.

220 tion in the lower tails of the IFN-gamma and ICAM-1 methylation distributions.

221 hift in the lower tails of the IFN-gamma and ICAM-1 methylation distributions.

222 Mediation analysis estimated that ICAM-1 methylation mediated 9% of the association of 28-

223 0, -0.06) decrease on the 20th percentile of ICAM-1 methylation, but was not significantly related to

224 ICAM-1 mobility and clustering are regulated by maturati

225 Constrained ICAM-1 mobility is important for DC function, as DCs exp

226 consistent with a model in which constrained ICAM-1 mobility opposes forces on LFA-1 exerted by the T

227 ex and reduction of hepatic ERM proteins and ICAM-1, molecules that are up-regulated and are essentia

228 esent findings suggest that MRTF-A/B inhibit ICAM-1 mRNA expression by forming a complex with NF-kapp

229 function, as DCs expressing a high-mobility ICAM-1 mutant lacking the cytoplasmic domain exhibit dim

230 fibroblasts did not augment their fusion to ICAM-1+ myoblasts/myotubes.

231 The use of chimeric mice deficient in ICAM-1 on myeloid cells demonstrated that neutrophil ICA

232 on regulation of expression and function of ICAM-1 on neutrophils and identify it as an additional r

233 study, we report on the de novo induction of ICAM-1 on the cell surface of murine neutrophils by lipo

234 upregulated alphaMbeta2 integrin on TAMs and ICAM-1 on tumor cells to promote association between tum

235 tering of intercellular adhesion molecule 1 (ICAM-1) on endothelial cells.

236 M-1), and intercellular adhesion molecule 1 (ICAM-1) on endothelial cells.

237 on ligand intercellular adhesion molecule-1 (ICAM-1) on supported planar bilayers recapitulates the d

238 nd fibroblasts forced to express full length ICAM-1 or a truncated form lacking the cytoplasmic domai

239 lates VE-cadherin switching association with ICAM-1 or actin, thereby negatively regulating neutrophi

240 In vitro, neutrophils adherent to ICAM-1 or ICAM-2 rapidly released TNF in response to LTB

241 with monoclonal antibodies to E-selectin or ICAM-1 or treating neutrophils with wortmannin reduced r

242 A and protein expression of PECAM-1, but not ICAM-1 or VCAM-1.

243 cement and probe accumulation in tumors with ICAM-1 overexpression relative to control.

244 Immunohistochemical staining for ICAM-1, P-selectin, nitrotyrosine, and poly(ADP)ribose s

245 platelet-endothelial, and/or vascular CAMs (ICAM-1, PECAM-1, VCAM-1).

246 ple-targeting resulted in binding similar to ICAM-1/PECAM-1 combination and displayed the highest sel

247 In vivo, ICAM-1/PECAM-1-targeted nanocarriers outperformed PECAM-

248 ICAM-1 plays an important role in leukocyte trafficking,

249 hat part of this association was mediated by ICAM-1 promoter methylation.

250 that rmCIRP treatment directly increases the ICAM-1 protein expression and activates NAD(P)H oxidase

251 Quantitation of ICAM-1 protein expression on cells and validation by imm

252 le grass rat (NGR) was associated with lower ICAM-1 protein expression when compared with that in nor

253 mice have lower levels of activated ERM and ICAM-1 protein in the liver accompanied by significantly

254 HDL inhibit ICAM-1 protein levels, but not in cells pretreated with

255 Results indicate that catalase targeted to ICAM-1 reduces markers of oxidative stress, preserves BB

256 Consistent with the ICAM-1 reduction, leukocyte accumulation was significant

257 (mt)DNA, soluble thrombomodulin (sCD141) and ICAM-1, reflecting endothelial damage.

258 how the spatial organization of endothelial ICAM-1 regulates leukocyte adhesion is not well understo

259 and cellular adhesion molecules (VCAM-1 and ICAM-1, respectively), matrix metalloproteinase-9 (MMP-9

260 heroprotective-SS of 12 dynes/cm(2), whereas ICAM-1 rose to a maximum in parallel with SS.

261 o found that VE-cadherin associated with the ICAM-1-SHP-2 complex.

262 ther we conclude that during lymphocyte TEM, ICAM-1 signaling diverges into pathways regulating lymph

263 in to MM cells and simultaneously neutralize ICAM-1 signaling via an antibody blockade, demonstrating

264 Therefore, we developed an ICAM-1 specific CAR with broad anti-tumor applicability

265 the inclusion in a vaccine interfering with ICAM-1-specific adhesion of group A PfEMP1 expressed by

266 ouse model, CLIRRTSIC polyplexes carrying si-ICAM-1 specifically bound to endothelium in disturbed fl

267 e applied on ICAM-1 impairs CD2AP binding to ICAM-1, suggesting that a tension-induced negative feedb

268 Quantitative analysis of ICAM-1 surface expression predicted the targeting capabi

269 Therefore, non-multivalent ICAM-1 targeting also provides transport of cargoes into

270 ntibody:enzyme conjugate for non-multivalent ICAM-1 targeting.

271 al malaria were more likely to bind EPCR and ICAM-1 than IE from children with uncomplicated malaria

272 the fibrin(ogen) receptors, alphaMbeta2 and ICAM-1, the myeloid cell integrin-binding site on fibrin

273 ession of intercellular adhesion molecule 1 (ICAM-1) through the transfer of miR-223 to endothelial c

274 F 12 (ARHGEF12) acts downstream of clustered ICAM-1 to increase RhoA activity, and that this pathway

275 demonstrate that these ligands interact with ICAM-1 to mediate cancer cell-endothelial cell adhesion

276 receptor (anti-TCR) monoclonal antibody, and ICAM-1 to represent the surface of HIV Env-bearing antig

277 ue ICAM-1-deficient mice and newly generated ICAM-1-transgenic mice, have provided the opportunity to

278 strictly CCR7-dependent manner; and induces ICAM-1 up-regulation on lymphatic vessels, allowing neut

279 In conclusion, CD44/selectin binding signals ICAM-1 up-regulation on the EC surface through a PKCalph

280 well as the interaction between filamin and ICAM-1 upon ICAM-1 clustering.

281 of which intercellular adhesion molecule 1 (ICAM-1) upregulation in brain microvasculature is the on

282 selectin, intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), pla

283 ession of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and

284 ttenuated intercellular adhesion molecule 1 (ICAM-1)/vascular cell adhesion molecule 1 (VCAM-1)-media

285 on of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 and CD68 macrophages.

286 nflammatory cytokine production (E-selectin, ICAM-1, VCAM-1 and IL-6).

287 The expression of ICAM-1, VCAM-1 and of MCP-1 was elevated and apoptosis w

288 on of the proinflammatory adhesion molecules ICAM-1, VCAM-1, and E-selectin, as well as the proinflam

289 with actin, SHP-2 down-regulation prevented ICAM-1-VE-cadherin association and promoted VE-cadherin-

290 ion and promotes transmigration by enhancing ICAM-1-VE-cadherin interaction.

291 The induction of neutrophil ICAM-1 was associated with enhanced phagocytosis of zymo

292 Accordingly, the expression of ICAM-1 was decreased in IL-1R-deficient and anakinra-tre

293 n myeloid cells demonstrated that neutrophil ICAM-1 was not required for local neutrophil transmigrat

294 Furthermore, the random mobility of CTL on ICAM-1 was severely compromised using all three methods

295 VCAM-1 and ICAM-1 were the endothelial adhesion molecules detected

296 regulates intercellular adhesion molecule 1 (ICAM-1) which binds integrin beta2 on neutrophil membran

297 rate that NOD mice deficient for isoforms of ICAM-1, which comediate costimulatory functions, spontan

298 at F-actin forces are opposed by immobilized ICAM-1, which triggers LFA-1 activation through a combin

299 us to precisely identify the interactions of ICAM-1 with MUC1 or CD43.

300 re compared with that of the interaction (of ICAM-1) with the LFA-1 whole protein.

301 cells to the intercellular adhesion molecule ICAM-1, with little effect on cells expressing mutant Lc