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Lewis-antigen-containing ICAM-2/3 on Jurkat leukemia cells interact with DC-SIGN to regulate DC functions.
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exploration of the underlying mechanism demonstrated that ICAM3 not only binds to LFA-1 with its extracellular domain and structure protein ERM but also to lamellipodia with its intracellular domain which causes a tension that pulls cells apart (metastasis).
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Increased expression of PECAM-1, ICAM-3, and VCAM-1 in colonic biopsies from patients with inflammatory bowel disease (IBD) in clinical remission is associated with subsequent flares; this suggests that increases in the expression of these proteins may be early events that lead to flares in patients with IBD
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with larger patient groups and preferably detailed histopathological and clinical evaluations, are needed to explain the severity of ICAM-1, ICAM-2, and ICAM-3 molecules in Barrett's esophagus
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ICAM3 acts as recognition receptors in the phagocytosis portals of macrophages for engulfment of apoptotic neutrophils.
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this data clearly indicate that ICAM-3 promotes drug resistance via inhibition of apoptosis.
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Intercellular adhesion molecule (ICAM)-3 mRNA is upregulated in non-adherent endothelial forming cells.
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Results indicate that the ICAM-3 gene promoter is negatively regulated by RUNX3.
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analysis of activated apoptotic cells induce dendritic cell maturation via engagement of Toll-like receptor 4 (TLR4), dendritic cell-specific intercellular adhesion molecule 3 (ICAM-3)-grabbing nonintegrin (DC-SIGN), and beta2 integrins
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ICAM-3 may be an important adhesion molecule involved in chemotaxis to apoptotic human leukocytes.
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the molecular basis of allergen-induced Th2 cell polarization
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the cross-talk between neutrophils and NK cells is mediated by ICAM-3 and CD11d/CD18, respectively.
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Single nucleotide polymorphisms in ICAM3 gene is associated with lymphoma.
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induction of morphological polarization in primary T lymphocytes and Jurkat cells enhances Kidins220/ARMS colocalization with ICAM-3
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CCR1 antagonist, BX471, did not significantly alter ICAM-3 expression in relapsing-remitting multiple sclerosis patients.
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ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB
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no significant risk association was found for SARS infection for the ICAM-3 Asp143Gly SNP.
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A novel serine-rich motif in the intercellular adhesion molecule 3 is critical for its ezrin/radixin/moesin-directed subcellular targeting
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identification of DC-SIGN binding sites
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interactions with DC-SIGN does not promote DC-SIGN mediated HIV-1 transmission
