Disease relevance of Alcam

• If the interaction between HDL and HB2 reduces the adhesion-induced inflammatory cellular events that characterize arterial wall injury, thereby achieving the protection associated with higher plasma levels of HDL, these findings may provide a clue to one mitigating effect of HDL in heart disease [1].
• Hypoxia maintained the expression of CD44 (hyaluronan receptor), ALCAM (CD166), and endoglin (transforming growth factor-beta receptor) [2].

High impact information on Alcam

• Differentiation of THP-1 cells into macrophages resulted in a striking increase in HB2 mRNA which was attenuated if cells were cholesterol-loaded by incubation with acetylated low density lipoprotein [1].
• Cloning and characterization of HB2, a candidate high density lipoprotein receptor. Sequence homology with members of the immunoglobulin superfamily of membrane proteins [1].
• It shows significant homology with the adhesion molecules ALCAM and BEN of the immunoglobulin superfamily and the cDNA, when transfected into HepG2 or COS cells, caused specific HDL3 binding to increase by 80-100% [1].
• The level in type II pneumocyte membranes of both binding proteins, MDP and HB2, increased when the plasma lipoprotein concentration was reduced by treatment of rats with 4-aminopyrazolo[3,4-d]-pyrimidine, consistent with a function to facilitate lipid uptake in vivo [3].
• Vitamin E uptake requires interaction between HDL and type II cells, suggesting a role of HB2 and MDP also in this process [3].

Anatomical context of Alcam

• The distribution of a 90 kDa protein, termed KG-CAM, was examined in the developing and adult rat central nervous system (CNS) using the monoclonal antibody 11-59 [4].
• Activated leukocyte cell adhesion molecule is a component of the endothelial junction involved in transendothelial monocyte migration [5].
• Activated leukocyte cell adhesion molecule (ALCAM/CD166) is an Ig CAM expressed by activated monocytes and endothelial cells [5].
• The present study examines the developmentally regulated expression pattern of an Ig superfamily member, KG-CAM, in the neostriatum of the rat [6].
• KG-CAM does not appear to be associated with the guidance of dopaminergic axons from the substantia nigra to the striatum, for this pathway is not immunopositive for this member of the Ig superfamily [6].

Associations of Alcam with chemical compounds

• KG-CAM is a 90-kDa glycoprotein that is related to the DM-GRASP/Neurolin family of adhesion molecules [6].
• Hepatic lipoprotein receptor levels (LDL-receptor and HDL-binding proteins, HB1 and HB2) were not significantly affected by Se deficiency, as assessed by immunoblotting [7].
• Of the various treatments used, only simvastatin or simvastatin plus cholestyramine produced significant changes, with reductions of up to 40% and 60%, respectively, for HB1 and HB2 [8].

Other interactions of Alcam

• Early in neostriatal development, KG-CAM is found in the tyrosine hydroxylase-positive patches [6].

Analytical, diagnostic and therapeutic context of Alcam

• Both antibodies reacted specifically with HB1 and HB2 on the ligand and Western blots, but their binding was not blocked by high-density lipoprotein [9].

References