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the effect of modulation of the cAMP-PKA-dependent pathway on ICAM-4 receptor activation
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Cytometry analysis evidenced a specific expression profile on reticulocytes of SCA infants, with notably an increased expression of the adhesion molecules Lu/BCAM, ICAM-4 and LFA-3, both in percentage of positive cells and in surface density.
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ICAM-1 and ICAM-4 play roles in host cell invasion by M. tuberculosis and P. falciparum, respectively.
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Seven variant ICAM4 alleles were found, distinct from the wild-type ICAM4 allele (GenBank KF712272), known as LW*05 and encoding LW(a) .
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Data from differentiating cultured erythroid precursor cells suggest that RhAG (Rh-associated glycoprotein) knockdown abolishes Rh blood group expression (ICAM4; RhoD [ras homolog family member D]; CD47 Rh-related antigen) in erythroid cells.
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Erythrocyte plasma membrane-bound ERK1/2 activation promotes ICAM-4-mediated sickle red cell adhesion to endothelium.
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In a transgenic mouse model of sickle cell disease ICAM-4 is implicated in abnormal adhesiveness of erythrocytes to endothelium.
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LWa allele occurs with incidence of 100% of donors in this study, while LWb allele has not been found in Chinese population.
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ICAM-4 as the first red blood cells protein ligand of platelets that may have relevant physiological significance
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binds to the I domains of the CD11a/CD18 and CD11b/CD18 leukocyte integrins
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12 single amino-acid changes in ICAM4 affected the interaction of ICAM-4 with alpha(V) integrins
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LW on sickle but not on normal erythrocytes undergoes increased PKA-dependent serine phosphorylation as a result of activation. The major counter receptor for LW was identified as the alphavbeta3 integrin on ECs
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Different integrins bind to different but partly overlapping sites on ICAM4, and ICAM4 may accommodate multiple integrin receptors present on leukocytes, platelets and endothelial cells.
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Review. LW antigen contributes to RBC adhesion, thrombosis, and (in sickle cell disease) vaso-occlusion.
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We show that ICAM-4 functions as a ligand for the monocyte/macrophage-specific CD11c/CD18. Deletion of the individual immunoglobulin domains of ICAM-4 demonstrated that both its domains contain binding sites for CD11c/CD18.
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LW play potentially pathophysiological roles in sickle cell disease