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PLAUR is one of 2 activators which convert the extracellular zymogen plasminogen to plasmin, a serine protease involved in a various normal and pathological processes that require cell migration and/or tissue destruction. PLAUR protein is synthesized and released from cells as a single-chain proenzyme with narrow enzymatic activity and is converted to an active two-chain disulfide-linked active enzyme by plasmin and other specific proteinases.

MHC Class II is consists of 2 membrane spanning proteins. Each of these proteins is roughly 30 kDa, and has of two Globular domains, Alpha-1, Alpha-2, Beta-1 and Beta-2. The two regions farthest away from the membrane are alpha-1 and beta-1. The two proteins link without Covalent Bonds. The MHC Class II protein mainly presents peptides, which have been digested from external sources. MHC Class II is normally only expressed by Antigen Presenting Cells (APC) which digest foreign protein. Within the RER the alpha and beta proteins of the molecule, associate with each other, while a third protein called the "invariant chain," is necessary for stabilizing the complex, without it, they will not associate. The MHC-invariant complex is then passed from the RER, into and out of, the Golgi body. It fuses with an Endocytic compartment, where an external protein has been sampled and degraded.

PPARGC1A is transcriptional coactivator for steroid receptors and nuclear receptors which increases the transcriptional activity of PPARG and thyroid hormone receptor on the uncoupling protein promoter. PPARGC1A regulates main mitochondrial genes that contribute to the program of adaptive thermogenesis and plays an important role in metabolic reprogramming in response to dietary availability through coordination of the expression of many genes participate in glucose and fatty acid metabolism. PPARGC1A induces the expression of PERM1 in the skeletal muscle and takes part in the integration of the circadian rhythms and energy metabolism.

PEDF is a noninhibitory serpin with neurotrophic, anti-angiogenic, and anti-tumorigenic properties. PEDF is a 50,000 dalton glycoprotein created and secreted in many tissues all the way through the body. A key component of the anti-angiogenic action of PEDF is the induction of apoptosis in proliferating endothelial cells. Additionally, PEDF is capable to inhibit the activity of angiogenic factors such as VEGF and FGF-2. The neuro-protective effects of PEDF are achieved through suppression of neuronal apoptosis induced by peroxide, glutamate, or other neurotoxins. The recognition of a lipase-linked cell membrane receptor for PEDF (PEDF-R) that binds to PEDF with high affinity should facilitate further elucidation of the underlying mechanisms of this pluripotent serpin. To date, PEDF-R is the only signaling receptor known to be used by a serpin family member. The unique range of PEDF activities associate it as a potential therapeutic agent for the treatment of vasculature related neurodegenerative diseases such as age-related macular degeneration (AMD) and proliferative diabetic retinopathy (PDR). PEDF in addition has the potential to be functional in the treatment of various angiogenesis-related diseases including a number of cancers.

Killer-cell immunoglobulin-like receptors (KIRs), are a family of cell surface glycoproteins found on Natural Killer (NK) Cells, which are important cells of the immune system. They control the killing function of these cells by interacting with MHC class I molecules, which are expressed on all cell types. This interaction allows them to identify virally infected cells or tumor cells that have a distinctive low level of Class I MHC on their surface. The majority of KIRs are inhibitory, which means that their recognition of MHC suppresses the cytotoxic activity of their NK cell. Only a limited number of KIRs have the capacity to activate cells. The KIR genes are found in a cluster on chromosome 19q13.4 within the 1 Mb leukocyte receptor complex (LRC). KIR molecules are extremely polymorphic, meaning their gene sequences differ significantly between individuals, so that different individuals have different arrays/repertoires of KIR genes. The KIR proteins are categorized by the number of

Treponema pallidum is a gram-negative spirochaete bacterium and is considered to be metabolically crippled. There are at least four known subspecies: T. pallidum pallidum, T. pallidum pertenue, T. pallidum carateum and T. pallidum endemicum. The helical structure of T. pallidum pallidum allows it to move in a corkscrew motion through viscous mediums such as mucus. Treponema pallidum sub sp. pallidum has one of the smallest bacterial genomes at 1.14 million base pairs (Mb) and has limited metabolic capabilities, reflecting its adaptation through genome reduction to the rich environment of mammalian tissue.

HCV is a small 50nm, enveloped, single-stranded, positive sense RNAvirus in the family Flaviviridae.
HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, the HCV has an exceptionally high mutation rate, a factor that may help it elude the host's immune response. Hepatitis C virus is classified into six genotypes(1-6) with several subtypes within each genotype. The preponderance and distribution of HCV genotypes varies globally. Genotype is clinically important in determining potential response to interferon-based therapy and the required duration of such therapy. Genotypes 1 and 4 are less responsive to interferon-based treatment than are the other genotypes (2, 3, 5 and 6).

BCAT1 catalyzes the leading reaction in the catabolism of the indispensable branched chain amino acids isoleucine, leucine and valine.

SSU72 is an extremely conserved homologue of yeast Ssu72, a CTD phosphatase and a component of the polyadenylation/termination machinery. SSU72 interacts with TFIIB, Rb and DNAM-1 and operates to catalyze the dephosphorylation of target proteins, and taking part in RNA processing and termination via dephosphorylation of Pol II. SSU72 is found in multiple alternatively spliced isoforms.

PDIA3 is an enzyme that belongs to the endoplasmic reticulum and interacts with lectin chaperones calreticulin and calnexin to modulate folding of newly synthesized glycoproteins. PDIA3 has protein disulfide isomerase activity. Complexes of lectins and PDIA3 mediate protein folding by promoting formation of disulfide bonds in their glycoprotein substrates. PDIA3 is expressed in the lumbar spinal cord from rats submitted to peripheral lesion during neonatal period. PDIA3 interacts with thiazide-sensitive sodium-chloride cotransporter in the kidney and is induced by glucose deprivation. PDIA3 is part of the major histocompatibility complex (MHC) class I peptide-loading complex (TAP1), which is important for formation of the final antigen conformation and export from the endoplasmic reticulum to the cell surface.

PRDX1 is part of the peroxiredoxin family of antioxidant enzymes, which reduce hydrogen peroxide and alkyl hydroperoxides. PRDX1 is an important protector of red blood cells against reactive oxygen species and in tumor prevention. PRDX1 is antioxidant protective in cells, and contributes to the antiviral activity of CD8(+) T-cells. PRDX1 has a proliferative effect and is involved in cancer development or progression. Peroxiredoxin-1 is plays a role in redox regulation of the cell. Peroxiredoxin decreases peroxides with reducing equivalents provided through the thioredoxin system but not from glutaredoxin. Peroxiredoxin is involved in eliminating peroxides generated during metabolism. Peroxiredoxin participates in the signaling cascades of growth factors and TNF-alpha by regulating the intracellular concentrations of h(2)o(2).

PDCD12 (AVEN) represents a new class of cell death regulator. PDCD12 is a conserved intracellular membrane protein which blocks apoptosis impeded by Apaf-1 mediated caspase activation. BAD and Bcl-2 also interact with PDCD12 to prevent apoptosis. PDCD12 is expressed in a wide variety of normal tissues including the heart, skeletal muscle, kidney, liver, testis, and also in diseases such as cancer.

HCV is a small 50nm, enveloped, single-stranded, positive sense RNAvirus in the family Flaviviridae.
HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, the HCV has an exceptionally high mutation rate, a factor that may help it elude the host's immune response. Hepatitis C virus is classified into six genotypes(1-6) with several subtypes within each genotype. The preponderance and distribution of HCV genotypes varies globally. Genotype is clinically important in determining potential response to interferon-based therapy and the required duration of such therapy. Genotypes 1 and 4 are less responsive to interferon-based treatment than are the other genotypes (2, 3, 5 and 6).

The Fas receptor (CD95) mediates apoptotic signaling by Fas-ligand expressed on the surface of other cells. The Fas-FasL interaction plays an important role in the immune system and lack of this system leads to autoimmunity, indicating that Fas-mediated apoptosis removes self-reactive lymphocytes. Fas signaling is also involved in immune surveillance to remove transformed cells and virus infected cells. Binding of FAS to oligimerized FasL on another cell activates apoptotic signaling through a cytoplasmic domain termed the death domain that interacts with signaling adaptors including FAF, FADD and DAX to activate the caspase proteolytic cascade. Caspase-8 and caspase-10 are first activated, to then cleave and activate downstream caspases, and a variety of cellular substrates that lead to cell death. Caspases cleave nuclear lamins, causing the nucleus to break down and lose its normal structure and another caspase substrate is DFF, inducing cleavage and degradation of the genome. Other caspase substrates are involved in cytoskeletal structure, cell cycle regulation and signaling pathways. Activation of JNK kinase, activation of Jun, and production of ceramide may also play roles in Fas-mediated apoptosis. Activation of fas-mediated apoptosis is opposed by I-FLICE and FAP. Viruses and tumors may escape immune surveillance in part through suppression of fas-mediated apoptosis using similar mechanisms.

Hepatitis B is one of a few known non-retroviralviruses which employ reverse transcriptionas a part of its replication process. (HIV, a completely unrelated virus, also uses reverse transcription, but it is a retrovirus.) HBV invades the cell by binding to surface receptor and become internalized. The viral core particles then migrate to the hepatocyte nucleus and the partially double-stranded, relaxed circular genomes (RC-DNA) are repaired to form a covalently closed circular DNA (cccDNA), which is the template for viral genomic and sub-genomic RNAs by cellular RNA polymerase II. Of these, the pregenomic RNA(pgRNA is selectively packaged into progeny capsids and is then reverse-transcribed into new RC-DNA. The core can either bud into the endoplasmic reticulum to be enveloped or exported from the cell or recycled back into the genome for conversion to cccDNA.

MHC Class II is consists of 2 membrane spanning proteins. Each of these proteins is roughly 30 kDa, and has of two Globular domains, Alpha-1, Alpha-2, Beta-1 and Beta-2. The two regions farthest away from the membrane are alpha-1 and beta-1. The two proteins link without Covalent Bonds. The MHC Class II protein mainly presents peptides, which have been digested from external sources. MHC Class II is normally only expressed by Antigen Presenting Cells (APC) which digest foreign protein. Within the RER the alpha and beta proteins of the molecule, associate with each other, while a third protein called the "invariant chain," is necessary for stabilizing the complex, without it, they will not associate. The MHC-invariant complex is then passed from the RER, into and out of, the Golgi body. It fuses with an Endocytic compartment, where an external protein has been sampled and degraded.

SSU72 is an extremely conserved homologue of yeast Ssu72, a CTD phosphatase and a component of the polyadenylation/termination machinery. SSU72 interacts with TFIIB, Rb and DNAM-1 and operates to catalyze the dephosphorylation of target proteins, and taking part in RNA processing and termination via dephosphorylation of Pol II. SSU72 is found in multiple alternatively spliced isoforms.

TRAIL Receptor-3, also known as TNFRSF10C belongs to theTNF-receptor super family. TNFRSF10C contains an extracellular TRAIL-binding domain as well as a transmembranedomain, however no cytoplasmic death domain. Furthermore, TNFRSF10C is not capable of inducing apoptosis, and is considered toact as an antagonistic receptor which protects cells from TRAIL-induced apoptosis.

Cytotoxicity Triggering Receptor 3 also known as NCR3 is a natural cytotoxicity receptor (NCR) which assists NK cells in the lysis of tumor cells. Moreover, NCR3 interacts with CD3-zeta (CD247), a T-cell receptor. A single nucleotide polymorphism in the 5' untranslated region of NCR3 has been related with mild malaria suceptibility. Three transcript variants encoding various isoforms have been found for this gene.

Ornithine decarboxylase is the preliminary and rate-limiting enzyme in the biosynthetic pathway of polyamines and it takes part in the alteration of ornithine to putrescine. ODC1 is a key member of various biological processes, such as cell growth, transformation, differentiation and apoptosis. Overexpression of the ODC1 gene has a vital part in cell proliferation and the progress of cancer.

GOT1 is a pyridoxal phosphate-dependent enzyme which exists in cytoplasmic and mitochondrial forms, GOT1 and GOT2, which participate in amino acid metabolism and the urea and tricarboxylic acid cycles. Both enzymes are homodimeric and show close homology.

HCV is a small 50nm, enveloped, single-stranded, positive sense RNAvirus in the family Flaviviridae.
HCV has a high rate of replication with approximately one trillion particles produced each day in an infected individual. Due to lack of proofreading by the HCV RNA polymerase, the HCV has an exceptionally high mutation rate, a factor that may help it elude the host's immune response. Hepatitis C virus is classified into six genotypes(1-6) with several subtypes within each genotype. The preponderance and distribution of HCV genotypes varies globally. Genotype is clinically important in determining potential response to interferon-based therapy and the required duration of such therapy. Genotypes 1 and 4 are less responsive to interferon-based treatment than are the other genotypes (2, 3, 5 and 6).

Mycoplasma pneumonia is part of the atypical pneumonia subtype which is caused by the bacteria M. pneumoniae. Mycoplasma pneumonia affects individuals younger than 40. It makes up 15 - 50% of all pneumonia cases in adults and especially in school-aged children. People at great risk for mycoplasma pneumonia comprise of those living or working in busy areas such as schools and homeless shelters, although many people who contract mycoplasma pneumonia have no identifiable risk factor. P1, P30, and P116 of mycoplasma pneumonia membrane proteins have been recognized as adhensive factors, P1 is considered as a main adhension protein of the organism colonization.