Aminopeptidase N (ANPEP or APN), also known as CD13, is a cell-surface metalloprotease located in the small-intestinal and renal microvillar membrane, as well as other plasma membranes. It belongs to the peptidase M1 family. CD13 plays a role in the final digestion of peptides generated from hydrolysis of proteins by gastric and pancreatic proteases and is involved in the metabolism of regulatory peptides by diverse cell types. CD13/APN is a potent regulator of angiogenesis which is essential for tumor invasion and metastasis, and its transcription in activated endothelial cells is induced by angiogenic growth factors via the RAS/MAPK pathway. In addition, this enzyme has been shown to participate in antigen processing and presentation, and accordingly, defects in this gene appear to be a cause of various types of leukemia or lymphoma and carcinomas.
Serum amyloid P component (SAP) is the identical serum form of amyloid P component (AP), a highly preserved plasma protein named for its ubiquitous presence in amyloid deposits. As a normal plasma protein first identified as the pentagonal constituent of in vivo pathological deposits called "amyloid". Serum amyloid P component represents another member of the pentraxin family, a highly conserved group of molecules that may play a role in innate immunity. SAP is a key negative regulator for innate immune responses to DNA and may be partly responsible for the insufficient immune responses after DNA vaccinations in humans. SAP suppression may be a novel strategy for improving efficacy of human DNA vaccines and requires further clinical investigations.
Pentraxin 2 (PTX2), also known as Serum amyloid P (SAP), is a highly conserved, naturally circulating plasma protein and a soluble pattern recognition receptor of the innate immune system. The unique binding activities indicated that it may play an important role in the removal of damaged tissue. PTX2 belongs to the pentraxin family, is universally present in amyloid deposits. Mouse with targeted deletion of the PTX2 gene shows retarded and reduced induction of experimental reactive systemic (AA type) amyloidosis confirmed that it does indeed contribute to pathogenesis of amyloidosis and is a valid therapeutic target. In recent discovery, PTX2 can be used as a powerful antifibrotic agent to regulate certain monocyte differentiation states.
APLP1, also known as amyloid-like protein 1, is a member of the highly conserved amyloid precursor protein gene family. APLP1 is a membrane-associated glycoprotein that is cleaved by secretases in a manner similar to amyloid beta A4 precursor protein cleavage. APLP1, together with APLP2, are important modulators of glucose. APLP1 may also play a role in synaptic maturation during cortical development. Alternatively spliced transcript variants encoding different isoforms have been described. APLP1 also is a mammalian homologue of amyloid precursor protein (APP). APP is a type I membrane protein that is genetically linked to Alzheimer's disease.
ANPEP gene encodes aminopeptidase N (APN) also known as microsomal aminopeptiase, alanyl aminopeptidase, aminopeptidase M, CD13, or membrane protein p161, is a member of the peptidase M1 family. Widely expressed in many cells, tissues and species, APN cleaves the N-terminal amino acids from bioactive peptides, leading to their inactivation or degradation. Probably plays a role in regulating growth and differentiation of early B-lineage cells. It also may play a role in the catabolic pathway of the renin-angiotensin system. It degrades vasoconstricting angiotensin II into angiotensin III and therefore helps to regulate blood pressure.
Apolipoprotein A1 (APOA1) is a member of the apolipoprotein family whose members are proteins bind with lipids and form lipoproteins to translate these oil-soluble lipids such as fat and cholesterol through lymphatic and circulatory system. APOA1 is the main component of high density lipoprotein (HDL) in plasma and is involved in the esterification of cholesterol as a cofactor of lecithin-cholesterol acyltransferase (LCAT) which is responsible for the formation of most plasma cholesteryl esters, and thus play a major role in cholesterol efflux from peripheral cells. As a major component of the HDL complex, APOA1 helps to clear cholesterol from arteries. APOA1 is also characterized as a prostacyclin stabilizing factor, and thus may have an anticlotting effect. Defects in encoding gene may result in HDL deficiencies, including Tangier disease, and with systemic non-neuropathic amyloidosis. Men carrying a mutation may develop premature coronary artery disease.
Apolipoprotein E (Apo-E), is a member of the apolipoprotein A1/A4/E family. ApoE is a major protein component of serum LDL, VLDL, HDL, and chylomicrons. APOE may function in mediating the binding, internalization, and catabolism of lipoprotein particles. It can serve as a ligand for the LDL (apo B/E) receptor and for the specific apo-E receptor (chylomicron remnant) of hepatic tissues. APOE is usually secreted in plasma. Phosphorylation sites are present in the extracellular medium.
Apolipoprotein H (APOH), also known as Beta-2-glycoprotein 1, is a glycoprotein synthesized by liver cells and it is present in the blood associated with plasma lipoproteins. Its carbohydrate content is approximately 19% of the molecular weight and it is present in the blood associated with plasma lipoproteins. Mature mouse ApoH shares 76% and 42% aa sequence identity with human and rat ApoH, respectively. The activity of APOH appears to involve the binding of agglutenating, inhibits agglutination, and negatively charged compounds by the contact activation of the intrinsic blood coagulation pathway. APOH is found be involved in the activation of lipoprotein lipase in lipid metabolism on several classes of lipoproteins.
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