ライフサイエンスコーパス: ICAM

1 ICAM (intercellular adhesion molecule)-1 and PFKFB3 were

2 ICAM-1 facilitated the restoration of muscle structure a

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

4 ICAM-1 mediated myoblast adhesion and fusion were quanti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 stitutive cell surface expression of ICAM-1, ICAM-2, and E-selectin.

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

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

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

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

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

47 1, VCAM [vascular cell adhesion molecule-1], ICAM [intercellular adhesion molecule-1], and MCP1 [mono

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

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

50 acid and intracellular adhesion molecule 5 (ICAM-5), in neuronal infection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 Anti-ICAM NCs were verified to traffic into the brain after i

93 Anchoring anti-ICAM changed the biodistribution of this antibody simila

94 liposomes exceeded that of anti-TfR and anti-ICAM counterparts by ~27- and ~8-fold, respectively, ach

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

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

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

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

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

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

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

102 we synthesized an oriented, end-to-end anti-ICAM mAb-TM conjugate and found that this therapeutic ha

103 The degree of in vivo targeting for anti-ICAM/3DNA-nanocarriers is unprecedented, for which this

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

105 cumulation increased with the number of anti-ICAM molecules per particle.

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

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

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

109 Immunohistochemistry showed that anti-ICAM and 3DNA components colocalized in the lungs, speci

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 nf) 141 +/- 3.2 vs 12.4 +/- 4.2 ID/g*hrs for ICAM and 188 +/- 90 vs 34.7 +/- 19.9 ID/g*hrs for PECAM)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 M), but not intercellular adhesion molecule (ICAM), suggesting they are early mesenchymal lymphoid ti

182 electin and intercellular adhesion molecule (ICAM)-1 are biomarkers of endothelial activation, which

183 circulating intercellular adhesion molecule (ICAM)-1 was observed.

184 ues from an intercellular adhesion molecule (ICAM)-like motif shared between the SARS viruses from th

185 th elevated levels of the adhesion molecules ICAM and VCAM and the pattern-recognition receptors TLR7

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

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

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

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

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

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

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

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

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

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

196 and AGEs led to significant augmentation of ICAM and VCAM expression, elevated leukocyte adhesion to

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

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

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

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

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

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

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

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

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

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

207 dependent increase in vascular expression of ICAM-1.

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

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

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

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

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

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

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

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

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

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

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

221 eated endothelial cells had higher levels of ICAM (intercellular adhesion molecule)-1 and TF expressi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 icking engagement by the functional receptor ICAM-5, whereas 11G1 exclusively recognizes the A-partic

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

253 namely the mannose receptor and DC-specific ICAM 3 nonintegrin at protein and mRNA levels, thereby a

254 ceptors (CLRs), such as DC-SIGN (DC-specific ICAM-3-grabbing nonintegrin) results in trafficking to s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 ern of infection did not correspond with the ICAM-5 distribution and expression in either human tissu

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

274 dothelial signaling triggered by adhesion to ICAM-1.

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

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

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

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

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

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

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

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

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

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

285 hancer of activated B cells) activity, VCAM, ICAM, and MCP1 levels in hypertensive subjects compared

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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