ApoE, a glycoprotein, is a structural component of very low density lipoprotein (vLDL) synthesized by the liver and intestinally synthesized chylomicrons . ApoE is also a constituent of a subclass of high density of lipoproteins (HDL) involved in cholesterol transport .ApoE mediates high affinity binding of chylomicrons and vLDL particles to the LDL receptor, allowing for specific uptake of these particles by the liver, preventing the accumulation of cholesterol rich particles in the plasma .Apolipoprotein E combines with fats (lipids) in the body to form molecules called lipoproteins and Apolipoprotein E is a major component of a specific type of lipoprotein called very low-density lipoproteins (VLDLs).
Apolipoprotein H (ApoH) is a 50 kDa variably glycosylated member of the complement control superfamily of proteins. Human ApoH is a major phospholipid binding protein and an important component to measure in the assessment of anti-phospholipid syndrome. Hepatocyte-derived ApoH binds to negatively charged phospholipids . It circulates as a component of lipoprotein particles and as a lipid-free serum protein. Human ApoH is also more specific than anti-cardiolipin antibodies and its presence correlates better with thrombotic risk. Mature human ApoH shares 76% and 82% aa sequence identity with mouse and rat ApoH.
ApoM (apolipoprotein M) is an apolipoprotein and member of the lipocalin protein family. The lipocalins share limited regions of sequence homology and a common tertiary structure architecture. They have an eight-stranded; antiparallel; symmetrical _-barrel fold; which is in essence a beta sheet which has been rolled into a cylindrical shape. Inside this barrel is located a ligand binding site. They transport small hydrophobic molecules such as steroids; bilins; retinoids; and lipids. Lipocalins have been associated with many biological processes; among them immune response; pheromone transport; biological prostaglandin synthesis; retinoid binding; and cancer cell interactions. Lipocalins are comparatively small in size; and are thus less complicated to study as opposed to large; bulky proteins. They can also bind to various ligands for different biological purposes. ApoM is associated with high density lipoproteins and to a lesser extent with low density lipoproteins and triglyceride-rich lipoproteins. ApoM is involved in lipid transport and can bind sphingosine-1-phosphate; myristic acid; palmitic acid and stearic acid; retinol; all-trans-retinoic acid and 9-cis-retinoic acid.
Apolipoprotein M is a secreted protein which belongs to the Lipocalin family. ApoM often presents in high density lipoprotein (HDL) and to a lesser extent in triglyceride-rich lipoproteins (TGRLP) and low density lipoproteins (LDL). The ApoM gene encoded protein is expressed in liver and kidney; secreted through the plasma membrane but remains membrane-bound. ApoM probably involved in lipid transport. ApoM can bind sphingosine-1-phosphate; myristic acid; palmitic acid and stearic acid; retinol; all-trans-retinoic acid and 9-cis-retinoic acid. The expression of ApoM could be regulated by platelet activating factor (PAF); Transforming Growth Factors (TGF); Insulin-Like Growth factor (IGF) and Leptin.
Amyloid precursor protein (APP) is a type I transmembrane protein expressed in many tissues and concentrated in the synapses of neurons, and is suggested as a regulator of synapse formation and neural plasticity. APP can be processed by two different proteolytic pathways. In one pathway, APP is cleaved by β- and γ-secretase to produce the amyloid-β-protein (Aβ, Abeta, beta-amyloid) which is the principal component of the amyloid plaques, the major pathological hallmark of Alzheimer’s disease (AD), while in the other pathway, α-secretase is involved in the cleavage of APP whose product exerts antiamyloidogenic effect and prevention of the Aβ peptide formation. The aberrant accumulation of aggregated beta-amyloid peptides (Abeta) as plaques is a hallmark of AD neuropathology and reduction of Abeta has become a leading direction of emerging experimental therapies for the disease. Abeta may be part of a mechanism controlling synaptic activity, acting as a positive regulator presynaptically and a negative regulator postsynaptically. The pathological accumulation of oligomeric Abeta assemblies depresses excitatory transmission at the synaptic level, but also triggers aberrant patterns of neuronal circuit activity and epileptiform discharges at the network level. There is evidence that beta-amyloid can impair blood vessel function. Vascular beta-amyloid deposition, also known as cerebral amyloid angiopathy, is associated with vascular dysfunction in animal and human studies.
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