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Human T-lymphotropic virus (HTLV) is a human, single-stranded RNA retrovirus that causes T-cell leukemia and T-cell lymphoma. The virus activates a subset of T-helper cellscalled Th1cells. The result is a proliferation of Th1 cells and overproduction of Th1 related cytokines (mainly IFN-gamma and TNF-alpha). Feedback mechanisms of these cytokines cause a suppression of the Th2 lymphocytes and a reduction of Th2 cytokine production (mainly IL-4, IL-5, IL-10 and IL-13). The end result is a reduction in the ability of the infected host to mount an adequate immune response to invading organisms that require a predominantly Th2 dependant response (these include parasitic infections and production of mucosal and humoral antibodies).

Helicobacter pylori is a Gram negative bacteria which colonizes in the human stomach and stimulates gastric mucosal inflammations leading to acute gastritis-associated diseases among them are atrophic gastritis, peptic ulcer and gastric cancer.

H. pylori is found in half of the world’s population and is defined as a group I carcinogens. .

An important virulence factor of H. pylori is Cytotoxin-associated gene A (CagA) which is located at the end of an approximately 40-kb cluster of genes called cag pathoge¬nicity island (PAI).

Cag PAI encodes a type-IV secretion system and transfers CagA protein into the intracellular region of gastric epithelial cell.

This relocation induces cellular hyper proliferation, apoptosis and leading to failure of gastric epithelial cell in maintaining its normal cytoskeletal structure. Furthermore it increases the secretion of cytokines such as tumor necrosis factor (TNF) and interleukin (IL) 1, 6 and 8 by the epithelial cells.

The IL-8 leads to extreme inflammatory responses and also stimulates the production of oxygen free radicals that could cause DNA damage to adjacent cells and lead to genetic modifications of gastric epithelial cells which are carcinogenic.

RANKL binds to tnfrsf11b/opg and to tnfrsf11a/rank. Osteoclast differentiation and activation factor. augments the ability of dendritic cells to stimulate naive t-cell proliferation. May be an important regulator of interactions between t-cells and dendritic cells and may play a role in the regulation of the t-cell-dependent immune response. sRANKL may also play an important role in enhanced bone-resorption in humoral hypercalcemia of malignancy.

GCK is an enzyme that expedite the formation of glucose-6-phosphate for glucose by phosphorylation. Humans and other vertebrates have GCK in the cells of the pancreas and liver. In both organs, the enzyme has an important role in carbohydrate metabolism regulation by sensing sugar levels and acting according to the change in glucose levels, that can rise after a meal or fall during fasting. Mutations in the gene that codes for this enzyme can cause hypoglycemia or diabetes.

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Pfu DNA polymeraseenzyme is found in the hyperthermophilic archaeonPyrococcus furiosus, where it functions in vivoto replicate the organism's DNA. In vitro, Pfu is used to swiftly amplify DNAin the Polymerase Chain Reaction, where the enzyme serves the central function of copying a new strand of DNA during each extension step. Pfu DNA polymerase has superior thermostability and 'proofreading' properties compared to other thermostable polymerases. Unlike Taq DNA polymerase, Pfu DNA polymerase possesses 3' to 5' exonuclease proof reading activity, meaning that it works its way along the DNA from the 5' endto the 3' endand corrects nucleotidemisin corporation errors. Pfu DNA polymerase-generated PCRfragments will have fewer errors than Taq-generated PCR inserts. As a result, Pfu is more commonly used for molecular cloning of PCR fragments than the historically popular Taq. Pfu DNA polymerase is superior for techniques that require high-fidelity DNA synthesis, but can also be used in conjunction with Taq polymerase to obtain the fidelity of Pfu with the speed of Taq polymerase activity.

HAT1 is a type B histone acetyltransferase that participates in the rapid acetylation of newly synthesized cytoplasmic histones, which are in turn imported into the nucleus for de novo deposition onto nascent DNA chains. Histone acetylation, mainly of soluble histone H4 at ''Lys-5'' and ''Lys-12'' and acetylates histone H2A at ''Lys-5''. HAT1 takes part in replication-dependent chromatin assembly. HAT1 acetylates soluble but not nucleosomal histone H4 at lysines 5 and 12, and to a lesser degree, histone H2A at lysine 5. HAT1 has intrinsic substrate specificity that modifies lysine in recognition sequence GXGKXG.

Sialic acid-binding Ig-like lectin 7 isoform 1, also known as SIGLEC7, is a newly discovered family of sialic acid-binding lectins of the immunoglobulin (Ig) superfamily. The extracellular portion has two Ig-like domains, with the amino-terminal V-set Ig domain containing amino acid residues which known to be implicated in sialic acid recognition by other Siglecs. The combination of an extracellular sialic acid binding site and an intracellular ITIM motif proposes that SIGLEC7 is involved in trans-membrane regulatory signaling reactions. Furthermore, on the cell surface SIGLEC7 exists as a monomer and is expressed on natural killer cells.

NADH dehydrogenase [ubiquinone] iron-sulfur protein 3 (NDUFS3) is a member of the complex I 30 kDa subunit family. NDUFS3 is one of the iron-sulfur protein (IP) components of mitochondrial NADH:ubiquinone oxidoreductase (complex I). This complex is the first enzyme complex in the electron transport chain of mitochondria. The iron-sulfur protein (IP) fraction of complex I consists of seven subunits. NDUFS3 gene mutations are linked with Leigh syndrome resulting from mitochondrial complex indefficiency.

PRCP is a plasma protein which takes part in the cleavage of C-terminal amino acids linked to proline in proteinfor example angiotensin-2 & 3 at acidic pHenvironment rather than at neutral pHwhich exhibit less activity. This cleavage is important since Angiotensin-2 takes part in regulation of blood pressure & electrolyte balance which is essential to hypertension.

Uromodulin (Tamm–Horsfall protein) is produced mainly by cells in the kidney’s thick ascending limb and is the most abundant protein in normal urine.
Uromodulin takes part in salt and water regulation, helps prevent urinary tract infections and kidney stones, and influences inflammation and immune activity in the kidney.
Reduced Uromodulin levels is associated with chronic kidney disease.
UMOD mutations causes unproper protein folding and thus transported incorrectly, resulting in its accumulation inside kidney tubular cells that damages the tubules and cause kidney disease (ADTKD-UMOD), associated with high uric acid, gout, and progressive kidney failure.

DDT is an enzyme that catayzes the tautomerization of D-dopachrome to give 5,6-dihydroxyindole (DHI). DDT is part of the family of lyases, specifically the carboxy-lyases, which cleave carbon-carbon bonds. DDT shares a homologous amino acid sequence (33% identical) with MIF and has similar tautomerase activity. DDT functions a proinflammatory cytokine.

REV1 Polymerase (REV1) contains a BRCT domain, which is imperative in protein-protein interactions. REV1 is a deoxycytidyl transferase involved in DNA repair. REV1 assists in the 1st step in the bypass of abasic lesions by the incorporation of a nucleotide opposite the lesion. REV1 is essential for normal generation of mutations by physical and chemical agents. REV1 transfers a dCMP residue from dCTP to the 3'-end of a DNA primer in a template-dependent reaction. A role for the human Rev1-like protein has been suggested as a scaffold which recruits DNA polymerases involved in translesion synthesis (TLS) of damaged DNA.

The recombinant Protein A/G/L is a genetically engineered protein which combines the IgG binding profiles of all Protein A, Protein G and Protein L. Protein A/G/L is a gene fusion product. Recombinant fusion protein A/G/L is comprised of 5 Ig-binding regions of protein L (B1-B2-B3-B4-B5), 5 IgG binding domains from Protein A (E-D-A-B-C) and 2 Ig-binding region of protein G (C1-C3). The recombinant Protein A/G/L is ideal for purification of monoclonal or polyclonal IgG antibodies. Protein A/G/L binds to IgG from humans, mice, rats, cows, goats, sheep, rabbits, guinea pigs, pigs, dogs and cats.

Hemoglobin Subunit Zeta (Hbz) or Hba-x is a alpha-like hemoglobin and part of the globin family. The protein is expressed and produced in the the yolk sac in early stages of embryonic development. Hemoglobin subunit zeta has 2 pseudogenes and 5 functional genes.

Adenosine Deaminase (ADA), also recognized as ADAT2 is an enzyme that takes part in purine metabolism. ADAT2 is necessary for the breakdown of adenosine from food and for the turnover of nucleic acids in tissues. ADAT2 is involved in the deamination of adenosine-34 to inosine in numerous tRNAs. ADAT2 is part of the cytidine and deoxycytidylate deaminase protein family, ADAT2 employs zinc as a cofactor. ADAT2 is a 191 amino acid enzyme that exists as two isoforms formed by alternative splicing events.

Caused by one of four closely related virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. In cell culture experiments and mice Morpholino antisense oligos have shown specific activity against Dengue virus.

MAT2A is an important enzyme in cellular metabolism and catalyzes the formation of S-adenosylmethionine (SAMe) from L-methionine and ATP. MAT2A is expressed in extrahepatic tissues. In liver, MAT2A expression associates with growth, dedifferentiation, and cancer. NF-kappa B and AP-1 are necessary for basal MAT2A expression in HepG2 cells and mediate the increase in MAT2A expression in response to TNF-alpha. Up-regulation of MAT2A provides growth improvement and s-adenosylmethionine and methylthioadenosine thus can block mitogenic signaling in colon cancer cells. Lower expression of both MAT2A and MAT2beta and interfere with leptin signaling in liver cancer cells.

HPGD is the essential enzyme of prostaglandin degradation. 15-PGDH protein strongly decreases the biologic activity of these molecules by catalyzing the oxidation of the 15-hydroxyl group of prostaglandins to a keto group. GDH1 is involved in numerous physiologic and cellular processes, for instance inflammation.

Dehydrogenase/reductase SDR family member 9 (DHRS9) functions as a homotetramer, which converts both 3-alpha-tetrahydroprogesterone (allopregnanolone) and 3-alpha-androstanediol to dihydroxyprogesterone and is believed to have a part in retinoic acid biosynthesis.

Betaine-Homocysteine Methyltransferase 2 (BHMT2) is involved in the regulation of homocysteine metabolism. Homocysteine is a sulfur-containing amino acid which has a key role in methylation reactions. Transfer of the methyl group from betaine to homocysteine generates methionine, which donates the methyl group to methylate DNA, proteins, lipids, and other intracellular metabolites. BHMT2 is one of two methyl transferases which can catalyze the transfer of the methyl group from betaine to homocysteine. BHMT2 converts homocysteine to methionine using S-methylmethionine (SMM) as a methyl donor. Homocysteine metabolism anomalies are implicated in disorders varying from vascular disease to neural tube birth defects such as spina bifida.

Carbonic anhydrase 12 (CA12) is an enzyme that belongs to the Carbonic anhydrases (CAs) family. This is a large family of zinc metalloenzymes which catalyze the reversible hydration of carbon dioxide. They are involved in various biological processes, including respiration, calcification, acid-base balance, bone resorption, and the formation of aqueous humor, cerebrospinal fluid, saliva, and gastric acid. CA12 is a type I membrane protein which is highly expressed in normal tissues, such as the kidney, colon and pancreas, and is overexpressed in 10% of clear cell renal carcinomas.

6PGD is the 2nd dehydrogenase in the pentose phosphate shift. Pentose is crucial for the biosynthesis of nucleic acid. The pentose phosphate cycle is a prominent source of NADPH. 6PGD deficiency is mostly asymptomatic, and the inheritance of this deasis is autosomal dominant. PGD deficiency elevate the erythrocyte pyruvate kinase levels of activity & decreases glutathione synthetase, which causes hemolysis.