ライフサイエンスコーパス: ICAM-1

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

2 intercellular adhesion molecule 1 (TfR-1 and ICAM-1).

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

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

5 lation of intercellular adhesion molecule 1 (ICAM-1).

6 y marker expression (PECAM-1, E-selectin and ICAM-1).

7 pectively, to SLB presenting TCR ligands and ICAM-1.

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

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

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

11 dothelial signaling triggered by adhesion to ICAM-1.

12 dependent increase in vascular expression of ICAM-1.

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

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

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

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

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

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

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

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

21 was the level of circulating P-selectin and ICAM-1.

22 am signalling elements such as TNF-alpha and ICAM-1.

23 macrophage-1 antigen (Mac-1), which binds to ICAM-1.

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

25 s against intercellular adhesion molecule-1 (ICAM-1), a glycoprotein overexpressed in the lungs in ma

26 estigated intercellular adhesion molecule-1 (ICAM-1), a membrane protein that mediates cell-to-cell a

27 reases in intercellular adhesion molecule-1 (ICAM-1), a molecule that plays a critical role in regula

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

29 ng through NF-kappaB increased expression of ICAM-1, a pro-inflammatory mediator that recruits macrop

30 Mechanistically, it was found that ICAM-1 actively redistributes to cluster around engulfed

31 seen in vitro and in vivo with inhibition of ICAM-1 adhesive interactions, using a function blocking

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

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

34 rgeted to intercellular adhesion molecule-1 (ICAM-1), an endothelial-surface glycoprotein whose expre

35 ciency of intercellular adhesion molecule 1 (ICAM-1), an established ligand of Mac-1, did not impair

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

37 Local injection of anti-ICAM-1 and anti-ICAM-1/liposomes via carotid artery cath

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

39 of CAR T cells toward both human and murine ICAM-1 and ICAM-1 expression in human and mouse tissues

40 Circulating levels of E-selectin and ICAM-1 and increases in ICAM-1 over the course of young

41 ion increased the cell surface expression of ICAM-1 and induced cell surface expression of P-selectin

42 ntrast, MPs released during crisis increased ICAM-1 and neutrophil adhesion levels, in a PS-dependent

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

44 ecific antibody that binds both cell-surface ICAM-1 and polyethylene glycol (PEG) on the surface of n

45 herogenic and pro-fibrotic targets including ICAM-1 and the connective tissue growth factor CTGF.

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

47 Functional expression of endothelial ICAM-1 and VCAM-1 was confirmed by T-cell interaction wi

48 oinflammatory molecules such as IL-6, MCP-1, ICAM-1 and VCAM-1.

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

50 anscription of proinflammatory genes such as ICAM-1 and, consequently, leukocyte tethering.

51 ticularly intercellular adhesion molecule-1 (ICAM-1) and a subsequent decrease in the number of activ

52 travenous injection of ICAM-1 antibody (anti-ICAM-1) and anti-ICAM-1/liposomes provided nearly an ord

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

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

55 including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1),

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

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

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

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

60 molecule (CAM) expression including VCAM-1, ICAM-1, and E-selectin in human aortic endothelial cells

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

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

63 owing high glucose exposure, including VEGF, ICAM-1, and ROS.

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

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

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

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

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

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

70 y potential therapeutics: annexin V and anti-ICAM-1 antibodies.

71 Systemic intravenous injection of ICAM-1 antibody (anti-ICAM-1) and anti-ICAM-1/liposomes

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

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

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

75 il adhesion was abolished by a blocking anti-ICAM-1 antibody.

76 interactions, using a function blocking anti-ICAM-1 antibody.

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

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

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

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

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

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

83 this uptake induces specific upregulation of ICAM-1 associated with the translocation of NF-kB to the

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

85 also show that A- and BC-type PfEMP1 present ICAM-1 at different angles, perhaps influencing the abil

86 whereas inhibition of ERK1/2 attenuated peak ICAM-1 at high SS (12 dyn/cm(2)).

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

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

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

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

91 s, we show that SIRPalpha, which, similar to ICAM-1, belongs to the Ig superfamily and has previously

92 Additionally, higher Y15 ICAM-1 (beta coefficient per 1 SD higher: 0.18; SE: 0.06

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

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

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

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

97 BMDN with rmCIRP increased the frequency of ICAM-1(+) BMDN, while rmCIRP-treated TREM-1(-/-) BMDN or

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

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

100 not migrate against the direction of flow on ICAM-1, but we hypothesized this was due to the influenc

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

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

103 ot control, RBCs and occurred mostly through ICAM-1, CD11a, and CD18.

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

105 cell adhesion molecules, PECAM-1 (CD31) and ICAM-1 (CD54).

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

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

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

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

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

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

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

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

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

115 -8, and MCP-1, and the upregulation of CD54 (ICAM-1), consistent with a state of activation.

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

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

118 Myogenic cell expression of ICAM-1 contributed to the restoration of muscle structur

119 ermed efferocytosis, it was examined whether ICAM-1 contributes to this process.

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

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

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

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

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

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

126 expression of key inflammatory factors (eg, ICAM-1, E-selectin, MCP-1) in endothelial cells or vascu

127 AM-1) and intercellular adhesion molecule-1 (ICAM-1), endothelial dysfunction, and smooth muscle cell

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

129 ings provide support for a paradigm in which ICAM-1 expressed by myogenic cells after muscle injury a

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

131 Intercellular adhesion molecule-1 (ICAM-1) expressing neutrophils produce excessive amounts

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

133 macrophage polarization and high numbers of ICAM-1-expressing macrophages were noted in inflamed col

134 ation in dysbiotic mice was able to increase ICAM-1 expression and leukocyte trafficking into the tum

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

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

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

138 ells toward both human and murine ICAM-1 and ICAM-1 expression in human and mouse tissues to demonstr

139 tical role in the eCIRP-mediated increase of ICAM-1 expression in neutrophils, leading to the increas

140 This phenotype was attributed to elevated ICAM-1 expression in the presence of HBZ.

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

142 more profoundly suppressed KLF2 and enhanced ICAM-1 expression than single exposure in the lung at 24

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

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

145 We found that ICAM-1 expression was induced during inflammatory macrop

146 g ability to TM and eNOS promoters, enhanced ICAM-1 expression, and decreased expression of upstream

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

148 oxicity in normal cells with basal levels of ICAM-1 expression.

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

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

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

152 lineages, in part through the beta2-integrin/ICAM-1/ezrin pathway.

153 ICAM-1 facilitated the restoration of muscle structure a

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 vated NK cell phenotype (eg, increased CD69, ICAM-1, HLADR, and CCR5 expression), and decreased capac

159 ntly, macrophages have been shown to express ICAM-1, however, their role in macrophage function is un

160 ited constitutive cell surface expression of ICAM-1, ICAM-2, and E-selectin.

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

162 this response as well as increase in VCAM-1, ICAM-1, IL-6, and IL-8 levels.

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

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

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

166 nockout mice) or siRNA-mediated knockdown of ICAM-1 in isolated murine and human macrophages signific

167 Our findings define a new role for ICAM-1 in promoting macrophage efferocytosis, a critical

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

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

170 omoted alphaLbeta2-dependent slow rolling on ICAM-1 in vitro and in vivo.

171 ssion of Inter-Cellular Adhesion Molecule-1 (ICAM-1) in mice.

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

173 presenting T cell receptor (TCR) ligands and ICAM-1 induce budding of extracellular microvesicles enr

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 Blocking intercellular adhesion molecule-1 (ICAM-1) inhibited the cytolytic response of CD4-MBL CAR-

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

182 ene expression for ACE2 and TMPRSS2, and for ICAM-1 (intercellular adhesion molecule 1) (rhinovirus r

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

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

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 ICAM-1 is best known for its role in mediating leukocyte

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

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

191 Intercellular adhesion molecule-1 (ICAM-1) is up-regulated during inflammation by several c

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

193 Genetic deletion (ICAM-1 knockout mice) or siRNA-mediated knockdown of ICA

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

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

196 on of ICAM-1 antibody (anti-ICAM-1) and anti-ICAM-1/liposomes provided nearly an order of magnitude h

197 Local injection of anti-ICAM-1 and anti-ICAM-1/liposomes via carotid artery catheter provided an

198 rts was markedly lower (e.g., uptake of anti-ICAM-1/liposomes was 100-fold higher vs IgG/liposomes).

199 oscopy via cranial window revealed that anti-ICAM-1/liposomes, but not IgG/liposomes bind to the lume

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

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

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

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

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

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

206 ICAM-1 mediated myoblast adhesion and fusion were quanti

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

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

209 We found that ICAM-1-mediated cell clustering enabled CD8(+) T cells t

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 d, we demonstrate that WAT-MSCs also support ICAM-1-mediated proliferation and activation of LFA-1-ex

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

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

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

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

218 Compared with AA MPs, SS MPs increased EC ICAM-1 messenger RNA and protein levels, as well as neut

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

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

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

222 Higher E-selectin (n = 1,810) and ICAM-1 (n = 1,548) at Y7 were associated with black race

223 The frequencies of ICAM-1(+) neutrophils in blood and lungs were markedly d

224 xpressed on myeloid cells-1 (TREM-1) and the ICAM-1(+) neutrophils involve Rho GTPase to promote NETo

225 We reveal that eCIRP generates ICAM-1(+) neutrophils through triggering receptor expres

226 P17 significantly decreased the frequency of ICAM-1(+) neutrophils.

227 Coculture of ICAM-1(-/-) neutrophils or wild-type (WT) neutrophils wi

228 Treatment of ICAM-1(-/-) neutrophils with rmCIRP resulted in reduced

229 evaluated the associations of E-selectin and ICAM-1, obtained at year (Y) 7 (Y7) and Y15 examinations

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

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

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

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

234 of the target cell engaging with its ligand, ICAM-1, on the surface of the infected cell (effector ce

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

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

237 However, suppression of ICAM-1 or its binding site, the alpha subunit of lymphoc

238 ls of E-selectin and ICAM-1 and increases in ICAM-1 over the course of young adulthood are associated

239 have shown a significant correlation between ICAM-1 overexpression and malignancy in thyroid cancer,

240 We showed that ICAM-1 overexpression was primarily caused by MPs derive

241 L1/KC, CXCL2/MIP-2, MCP-1/CCL2, CXCR2, IL-6, ICAM-1, P-selectin, and C5aR) was suppressed by anti-G-C

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

243 E-selectin and ICAM-1 partially mediated the associations between highe

244 GM-CSF, M-CSF, TNF-alpha, IFN-gamma, VCAM-1, ICAM-1, PD-L1 and ICOS-L.

245 In sum, both LFA-1 and Mac-1 binding ICAM-1 play a critical role in determining the direction

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

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

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

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

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

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

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

253 re of a domain from a B-type PfEMP1 bound to ICAM-1, revealing a complex binding site.

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

255 sting structure of an A-type PfEMP1 bound to ICAM-1 shows that the 2 complexes share a globally simil

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

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

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

259 RP-induced Rho activation, while blockade of ICAM-1 significantly decreased Rho activation.

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

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

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

263 We demonstrate this both on ICAM-1 surfaces and on activated endothelium.

264 grate against the direction of fluid flow on ICAM-1 surfaces via LFA-1 if Mac-1 is blocked; otherwise

265 the direction of shear flow once adherent on ICAM-1 surfaces.

266 cifically accumulated in the lungs, the main ICAM-1 target.

267 hyroid cancer, and have pioneered the use of ICAM-1 targeted CAR T cells as a novel treatment modalit

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

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

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

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

272 ompatibility complex molecules (pMHC) and of ICAM-1-the ligand of beta(2)-integrins-we show that the

273 However, while the A-type PfEMP1 bind ICAM-1 through a highly conserved binding surface, the B

274 micromolar rather than nanomolar affinity to ICAM-1 to avoid cytotoxicity in normal cells with basal

275 is anterior muscles of wild-type mice caused ICAM-1 to be expressed by a population of satellite cell

276 -affinity conformation, which interacts with ICAM-1 to mediate arrest.

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

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

279 -affinity conformation, which interacts with ICAM-1 to slow rolling.

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

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

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

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

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

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

286 8), systemic and vascular inflammation (CRP, ICAM-1, VCAM-1), and SAA (all P < .001).

287 ll homing and activation proteins, including ICAM-1, VCAM-1, HLA class I and II, and interferon gamma

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

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

290 Neither E-selectin nor ICAM-1 was associated with measures of LV diastolic func

291 CAM-1 and intercellular adhesion molecule 1 (ICAM-1) was regulated by the spatiotemporal activation o

292 ly, while intercellular adhesion molecule 1 (ICAM-1) was significantly upregulated on activated HLMVE

293 These findings differed from those for ICAM-1, where gene expression was increased in asthma an

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

295 known as intercellular adhesion molecule 1 (ICAM-1), which helps initiate and stabilize contact (doc

296 eptors is intracellular adhesion molecule-1 (ICAM-1), which is bound by 2 distinct groups of PfEMP1,

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

298 longitudinal associations of E-selectin and ICAM-1 with subclinical alterations in cardiac function.

299 temporal associations between E-selectin and ICAM-1 with subclinical cardiac dysfunction are unclear.

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