roprotein convertase subtilisin/kexin type 9 (PCSK9), also known as NARC1 (neural apoptosis regulated convertase), which is a newly identified human secretory subtilase belonging to the proteinase K subfamily of the secretory subtilase family. PCSK9 protein is an enzyme which in humans is encoded by the PCSK9 gene with orthologs found across many species. It is expressed in neuroepithelioma, colon carcinoma, hepatic and pancreatic cell lines, and in Schwann cells. PCSK9 protein is highly expressed in the liver and regulates low density lipoprotein receptor (LDLR) protein levels. Inhibition of PCSK9 protein function is currently being explored as a means of lowering cholesterol levels. Thereby, PCSK9 protein is regarded as a new strategy to treat hypercholesterolemia. PCSK9 protein contributes to cholesterol homeostasis and may have a role in the differentiation of cortical neurons.
Causes a rapid but short-lived drop in the level of calcium and phosphate in blood by promoting the incorporation of those ions in the bones.
Programmed Death-1 (PD-1), firstly cloned from mouse T cell hybridoma 2B4.11, is one member of CD28/CTLA-4 superfamily. PD-1 belongs to type I transmembrane protein and acts as an important immunosuppressive molecule. This family also include members of CD28, CTLA-4 and ICOS.The mouse Programmed Death-1 protein, encoded by PD-1 gene, comprises four parts including a putative 20 aa signal peptide, a 149 aa extracellular region, a 21 aa transmembrane domain and a 98 aa cytoplasmic region. The cytoplamsic tail of PD-1 contains two structural motifs, an immunoreceptor tyrosine-based inhibitory motif (ITIM) and an immunoreceptor tyrosine-based switch motif (ITSM) formed by two tyrosine residues which make the difference in PD-1 signal mediating. Mouse PD-1 is expressed in thymus and shares about 69% aa sequence identity with human PD-1. Recently, programmed death-1 (PD-1) with its ligands, programmed death ligand B7H1 (PD-L1) and B7DC (PD-L2), was found to regulate T-cell activation and tolerance, upon ligand binding, inhibiting T-cell effector functions in an antigen-specific manner. PD-1 gene knocked out mice would induce some autoimmune diseases, which suggests that PD-1 acts as a co-inhibitory molecule actively participating in maintaining peripheral tolerance. Thus, PD-1 may be a useful target for the immunologic therapy of carcinoma,infection,autoimmune diseases as well as organ transplantation.
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