ライフサイエンスコーパス: ICAM

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

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

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

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

5 ICAM-1 mediated myoblast adhesion and fusion were quanti

6 ICAM-1 mobility and clustering are regulated by maturati

7 ICAM-5 silencing attenuated EV-D68 replication in permis

8 ICAM-targeted Ab/SOD more effectively mitigated inflamma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

27 ppaB) and intercellular adhesion molecule-1 (ICAM) (P < 0.001, respectively) and improved nuclear fac

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 The fusogenic property of ICAM-1-ICAM-1 interactions was restricted to myogenic cells, as

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

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

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

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

47 -specific intercellular adhesion molecule-3 (ICAM-3)-grabbing nonintegrin] and Langerin on immune cel

48 ed by the intercellular adhesion molecule-4 (ICAM-4), which appears on the RBC membrane and binds to

49 -specific intercellular adhesion molecule 5 (ICAM-5/telencephalin) as a cellular receptor for sialic

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

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

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

53 nificant increase in the frequency of active ICAM-4 receptors in both normal RBCs and SS-RBCs.

54 We quantified the frequency of active ICAM-4 receptors on WT-RBC and SS-RBC membranes, as well

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

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

57 h alpha-actinin is critical to conferring an ICAM-2-mediated non-metastatic phenotype in NB cells.

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

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

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

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

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

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

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

65 ICAM-1 and ICAM-3, uropod-directed proteins that do not copatch wit

66 tercellular adhesion molecule 1 (ICAM-1) and ICAM-2 on B cells are essential for long-lasting cognate

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

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

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

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

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

72 egulation of cell surface-expressed CD86 and ICAM.

73 EV-D68 replication in permissive cells, and ICAM-5 expression in non-permissive cells allowed EV-D68

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 Similar to anti-ICAM, anti-ICAM-HRP was specifically internalized and transported a

94 therapeutics linked to non-multivalent anti-ICAM ligands has never been shown, since multivalency wa

95 onjugates coupled to multiple copies of anti-ICAM antibodies or peptides.

96 We observed minimal transport of anti-ICAM to lysosomes, yet prominent and specific transcytos

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

98 We found that anti-ICAM was specifically internalized by all tested ICAM-1-

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

100 enzyme horseradish peroxidase (HRP)) to anti-ICAM and separated a 1:2 antibody:enzyme conjugate for n

101 Similar to anti-ICAM, anti-ICAM-HRP was specifically internalized and tr

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

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

104 mma, GM-CSF, eotaxin, MIP1-alpha, MIP1-beta, ICAM, IL-6, IL-8, IL-10, TNF) in 139 AEC cultures were q

105 s well as the median unbinding force between ICAM-4 and alphavbeta3.

106 However, the unbinding force between ICAM-4 and the corresponding ligand alphavbeta3 remained

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

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

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

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

111 including integrin alpha3beta1, VE-cadherin, ICAM-2, junctional adhesion molecule-B (JAM-B), laminin,

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

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

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

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

116 Thus, B cell ICAMs promote efficient antibody immune response by enha

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

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

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

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

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

122 also from cells that expressed no detectable ICAM-2.

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

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

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

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

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

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

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

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

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

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

133 in vivo characteristics of cells expressing ICAM-2 variants with modified alpha-actinin-binding doma

134 nding domains differed from cells expressing ICAM-2 wild type (WT) and also from cells that expressed

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

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

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

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

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

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

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

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

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

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

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

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

147 , doxorubicin encapsulating immunoliposomes (ICAM-Dox-LPs) to selectively recognize and deliver doxor

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

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

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

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

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

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

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

155 anchoring proteins play an essential role in ICAM-4 activation.

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

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

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

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

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

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

162 Interestingly, ICAM-2 suppressed metastatic but not tumorigenic potenti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 adhesion to intercellular adhesion molecule (ICAM) 1 and vascular cell adhesion molecule (VCAM) 1 and

179 in retinal intercellular adhesion molecule (ICAM)-1 expression and leukocyte accumulation, respectiv

180 ice lacking intercellular adhesion molecule (ICAM)-1 identified a marked decrease in fibrinogen-depen

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

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

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

184 grins bind intercellular adhesion molecules (ICAMs) in cis, which inhibits leukocyte adhesion in vitr

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

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

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

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

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

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

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

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

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

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

195 d SS-RBCs, confirming that the activation of ICAM-4 is regulated by the cAMP-PKA pathway.

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

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

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

199 he likelihood that the cytoplasmic domain of ICAM-2 binds directly to alpha-actinin.

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

201 We hypothesized that the effects of ICAM-2 on NB cell phenotype depend on the interaction of

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

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

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

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

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

207 dependent increase in vascular expression of ICAM-1.

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

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

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

211 or, significantly increased the frequency of ICAM-4 receptors in WT-RBCs and SS-RBCs, confirming that

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

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

214 -binding domains, and compared the impact of ICAM-2 and each variant on NB cell adhesion, migration,

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

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

217 anisms, and indicate that the interaction of ICAM-2 with alpha-actinin is critical to conferring an I

218 cell phenotype depend on the interaction of ICAM-2 with the cytoskeletal linker protein alpha-actini

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

220 One important mechanism of ICAM-4 activation occurs via the cyclic adenosine monoph

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

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

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

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

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

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

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

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

229 We then expressed variants of ICAM-2 with mutated alpha-actinin-binding domains, and c

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

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

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

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

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

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

236 ulation of the cAMP-PKA-dependent pathway on ICAM-4 receptor activation.

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

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

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

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

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

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

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

244 However, unlike the WT protein, ICAM-2 variants did not completely suppress development

245 Like the WT protein, ICAM-2 variants inhibited cell adhesion, migration and c

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

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

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

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

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

251 diverse cell types was inhibited by soluble ICAM-5 fragments.

252 the immune modulatory receptors DC-specific ICAM-3 -: grabbing non integrin (DC-SIGN) and macrophage

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 A1- and H-transferases under control of the ICAM-2 promoter was performed in C57BL/6 (B6) mice.

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

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

274 dothelial signaling triggered by adhesion to ICAM-1.

275 2 (Pyk2) is required for T cell adhesion to ICAM-1; however, the mechanism by which it regulates adh

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

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

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

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

280 luate the impact of alpha-actinin binding to ICAM-2 on the phenotype of NB tumor cells.

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

282 EV-D68 bound specifically and efficiently to ICAM-5, and replication of EV-D68 in diverse cell types

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

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

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

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

287 Further, targeting to ICAM provides higher endocytic efficacy than targeting t

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

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

290 on conjugate size and targeting to PECAM vs. ICAM.

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

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

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

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

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

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

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

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

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

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