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Chymotrypsinogen-B1 (CTRB1) belongs to the serine protease family of enzymes and forms a main precursor of the pancreatic proteolytic enzymes. CTRB1 is located next to a related chymotrypsinogen gene. CTRB1 is a protein coding gene which encodes different isoforms which may undergo similar processing to generate the mature protein.

IFIH1 is a DEAD box protein which is upregulated in response to treatment with beta-interferon and a protein kinase C-activating compound, mezerein. Irreversible reprogramming of melanomas can be attained by therapy with both these agents; treatment with either agent alone only achieves reversible differentiation. DEAD box proteins are implicated in several cellular processes involving alteration of RNA secondary structure such as translation initiation, nuclear and mitochondrial splicing, and ribosome and spliceosome assembly.

Acyl-CoA Thioesterase 7 (ACOT7) belongs to the acyl coenzyme family. ACOT7 hydrolyzes the CoA thioester of palmitoyl-CoA and other long-chain fatty acids. Decreased expression of the ACOT7 protein may be linked to mesial temporal lobe epilepsy.

Protease Serine 22 also known as Prss22 is identified brain-specific expression gene which is expressed mainly in epitheliumrich tissues such as the lung and eye. Prss22 encodes to a serine protease which called BSSP-4 or BSP-2.

Carbonic anhydrase III is part of a multigene family that encodes carbonic anhydrase isozymes which are a class of metalloenzymes that catalyze the reversible hydration of carbon dioxide and are differentially expressed in various cell types. Carbonic anhydrase III expression is strictly tissue specific and present at high levels in skeletal muscle and much lower levels in cardiac and smooth muscle. CA3 catalyses swift conversion of carbon dioxide to bicarbonate and protons (CO2 + H2O = HCO3 + H+). CA3 participates in a variety of biological processes, including respiration, calcifica-tion, acid-base balance, bone resorption and the formation of aqueous humor, cerebrospinal fluid, saliva and gastric juice. CA3 includes a zinc ion in its active site and maintains acid-base balance in blood and other tissues, and to help transport carbon dioxide of tissues.

The protein encoded by this gene is a member of the bone morphogenetic protein family which is part of the transforming growth factor-beta superfamily. The superfamily includes large families of growth and differentiation factors. Bone morphogenetic proteins were originally identified by an ability of demineralized bone extract to induce endochondral osteogenesis in vivo in an extraskeletal site. This particular family member plays an important role in the onset of endochondral bone formation in humans, and a reduction in expression has been associated with a variety of bone diseases, including the heritable disorder Fibrodysplasia Ossificans Progressiva. Alternative splicing in the 5' untranslated region of this gene has been described and three variants are described, all encoding an identical protein.

Tyrosyl-tRNA synthetase (YARS) is a member of the class I tRNA synthetase family. YARS is a vital enzyme which catalyzes the aminoacylation of tRNATrp with tryptophan, a critical function of the cell’s protein synthesis machinery. Expression of YARS is highly stimulated in human cells by the addition of IFN-gamma.

a-Synuclein (amino acids 1-140), an acidic neuronal protein of 140 amino acids, is extremely heat-resistant and is natively unfolded with an extended structure primarily composed of random coils. a-synuclein has been suggested to be implicated in the pathogenesis of Parkinson’s disease and related neurodegenerative disorders, and more recently, to be an important regulatory component of vesicular transport in neuronal cells. Moreover, recent studies have shown that a-synuclein has chaperone activity and that this activity is lost upon removing its C-terminal acidic tail (amino acids 96-140).

Poly (ADP-Ribose) Polymerase 2 (PARP2) contains a catalytic domain which is homologous to that of poly (ADP-ribosyl) transferase but lacks an N-terminal DNA binding domain which activates the C-terminal catalytic domain of poly (ADP-ribosyl) transferase. PARP2 is capable of catalyzing a poly (ADP-ribosyl)ation reaction. The basic residues within the N-terminal area of this protein can bear potential DNA-binding properties, and can be engaged in the nuclear and/or nucleolar targeting of the protein. There has been found two alternatively spliced transcript variants encoding distinct isoforms.

UbcH12 is functional in in vitro NEDDylation reactions. It has been shown to form a thioester linkage with NEDD8 in the presence of the NEDD8 activating enzyme complex Uba3/APP-BP1. APP-BP1 binds to the amyloid precursor protein (APP) carboxy terminal domain and is important in conjunction with Uba3 and UbcH12 in driving cells through the S to M checkpoint. It was demonstrated to be the E2 responsible for the NEDDylation of the Cul-1 component of the SCF (?-TRCP) complex which is important as the E3-ligase in the ubiquitinylation of I?B?. NEDDylation of Cul-1 is essential for conjugation and processing of NF-?B p105 by SCF (?-TRCP) following phosphorylation of the complex. A dominant negative form of UbcH12, previously demonstrated to sequester NEDD8 and inhibit its conjugation, inhibits both conjugation and processing of p105, which is alleviated by wild-type UbcH12.

HCV is a small 50nm, enveloped, single-stranded, positive sense RNA virus 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).

GLRX1 has a glutathione-disulfide oxidoreductase activity in the presence of nadph and glutathione reductase. reduces low molecular weight disulfides and proteins. Glutaredoxin is a glutathione (GSH)-dependent hydrogen donor for ribonucleotide reductase and also catalyzes glutathione-disulfide oxidoreduction reactions in the presence of NADPH and glutathione reductase. GLRX1 is multifunctional enzyme with glutathione-dependent oxidoreductase, glutathione peroxidase and glutathione S-transferase (GST) activity. The disulfide bond functions as an electron carrier in the glutathione-dependent synthesis of deoxyribonucleotides by the enzyme ribonucleotide reductase. In addition, it is also involved in reducing cytosolic protein- and non-protein-disulfides in a coupled system with glutathione reductase. Required for resistance to reactive oxygen species (ROS) by directly reducing hydroperoxides and for the detoxification of ROS-mediated damage.

Caspase 2 Apoptosis-Related Cysteine Peptidase (CASP2) is a part of the cysteine-aspartic acid protease (caspase) family. CASP2 takes part in the activation cascade of caspases responsible for apoptosis execution. CASP2 is also responsible for inactivating proteins essential for cell survival. The proteolytic cleavage of CASP2 is induced by a variety of apoptotic stimuli.

AKR1C1 transfers progesterone to its inactive state or in other words catalyzes the reaction of 20-alpha-hydroxy progesterone (20-alpha-OHP). In the liver and intestine. AKR1C1 transfers bile and monitors the intrahepatic bile acid concentration though it has a low bile-binding ability. AKR1C1 participates in myelin formation. AKR1C1 is part of the aldo/keto reductase superfamily, which has over 40 known enzymes which catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors thus display overlapping but distinct substrate specificity.

PFKM is a regulatory glycolytic enzyme that converts fructose 6-phosphate and ATP into fructose 1,6-bisphosphate (through PFK-1), fructose 2,6-bisphosphate (through PFK-2) and ADP. Three phosphofructokinase isozymes exist in humans: muscle, liver and platelet. Mutations in PFKM gene have been related with glycogen storage disease type VII, also identified as Tarui disease.

Epoxide Hydrolase 1 Microsomal (EPHX1) is a vital biotransformation enzyme which transfers epoxides from the degradation of aromatic compounds to trans-dihydrodiols that can be conjugated and excreted from the body. Epoxide hydrolase plays a role in both activation and detoxification of epoxides. Mutations in EPHX1 trigger preeclampsia, epoxide hydrolase deficiency or increased epoxide hydrolase activity.

PLA2G7 is a secreted enzyme which catalyzes the degradation of platelet-activating factor to biologically inactive products. The PLA2G7 enzyme is produced by inflammatory cells and hydrolyzes oxidised phospholipids in LDL. In the blood, PLA2G7 goes mainly with LDL and less than 20% is coupled with HDL.
PLA2G7 is implicated in the development of atherosclerosis and is also a marker for cardiac disease. PLA2G7 might have a major physiologic effect in the presence of inflammatory bodily responses.
PLA2G7 alters the action of PAF (platelet-activating factor) by hydrolyzing the sn-2 ester bond to yield the biologically inactive lyso-PAF. PLA2G7 has specificity for substrates with a short residue at the sn-2 position. PLA2G7 is inactive against long-chain phospholipids.
PLA2G7 gene defects are the source of platelet-activating factor acetylhydrolase deficiency, which is a trait that is present in 27% of the Japanese population.

The enzyme Arylsulfatase A, also known as cerebroside-sulfatase, is responsible to break down sulfatides. The main molecule that Arylsulfatase A breaks down is cerebroside 3-sulfate into cerebroside and sulfate. The enzyme is encoded by the ARSA gene in humans. Phosphate can form a covalent bond with the Arylsulfatase A’s active site 3-oxoalanine, thus, inhibits the protein.

Thymine-DNA glycosylase (TDG) is a member of the TDG/mug DNA glycosylase family.
TDG is a nuclear protein that fixes G/T mismatches to G/C pairs by hydrolyzing the carbon-nitrogen bond between the sugar-phosphate backbone of the DNA and the mispaired thymin. In addition, TDG removes uracil and 5-bromouracil from mispairings with guanine. The TDG enzyme has an essential role in cellular defense against genetic mutation triggered by the spontaneous deamination of 5-methylcytosine and cytosine.

Ubiquitin Conjugating Enzyme E2Q2 (UBE2Q2) is a protein coding gene which receives ubiquitin from the E1 complex and catalyzes its covalent attachment to various proteins. UBE2Q2 which is a part of the ubiquitin-conjugating enzyme family is detected in hypopharyngeal head and neck squamous cell carcinoma and in tumor masses.

BLMH is affiliate to the papain superfamily of the cysteine protease and the peptidase C1 family. BLMH is a cytoplasmic cysteinepeptidase usually found as a homohexamer. The standard physiological role of BLMH has not been determined, but it shields normal and malignant cells from the glycopeptide antitumor drug BLM. BLMH catalyzes the inactivation of the antitumor drug BLM (a glycopeptide) by hydrolyzing the carboxyamide bond of its B-aminoalaninamide moiety and in addition demonstrates general aminopeptidase activity.

UDP Glucuronosyltransferase 1 Family Polypeptide A1, also known as UGT1A1 has a main importance in the conjugation as well as subsequent elimination of potentially toxic xenobiotics and endogenous compounds. UGT1A1 is also capable of catalyzing glucuronidation of 17beta, 17alpha, 1-hydroxypyrene, 4-methylumbelliferone, 1-naphthol, paranitrophenol, scopoletin, and umbelliferone.

The three isoenzymes (MM, MB, and BB) are found in muscle, cardiac and brain tissues. These recombinant proteins are ideal for calibrating diagnostic instruments and researching neuromuscular diseases. Creatine Kinases can be used for indications in many neuromuscular applications. These disorders include cardiac disease, mitochondrial disorders, inflammatory myopathies, myasthenia, polymyositis, McArdle's disease, NMJ disorders, muscular dystrophy, ALS, hypo and hyperthyroid disorders, central core disease, acid maltase deficiency, myoglobinuria, rhabdomyolysis, motor neuron diseases, rheumatic diseases, and other that create elevated or reduced levels of Creatine Kinases.