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M-phase inducer phosphatase 1 (CDC25A) belongs to the CDC25 family of phosphatases. CDC25A is essential for progression from G1 to the S phase of the cell cycle. CDC25A activates the cyclin-dependent kinase CDC2 by eliminating 2 phosphate groups. CDC25A is specifically degraded in reaction to DNA damage, which inhibits cells with chromosomal abnormalities from progressing in the course of cell division. CDC25A is an oncogene, though its exact function in oncogenesis has not been determined.

Thioredoxin or TRX contains a single disulfide active site and serves as a general protein disulphide oxidoreductase.Thioredoxins are small disulphide-containing redox proteins (within the conserved Cys-Gly-Pro-Cys active site) that are found in all the kingdoms of living organisms. The proteinis involved in the first unique step in DNA synthesis; It interacts with a wide range of proteins by a redox mechanism based on reversible oxidation of two cysteine thiol groups to a disulphide, along with the transfer of two electrons and two protons. The net result is the covalent interconversion of a disulphide and a dithiol. It has been suggested that thioredoxin may catalyze the formation of correct disulfides during protein folding because of its ability to act as an efficient oxidoreductant.

CTSE or cathepsin E is an intracellular aspartic protease from the pepsin protein family. CTSE has a crucial part in protein degradation, creating bioactive proteins & processing antigens. The enzyme is responsible for cleaving at B site, Swedish mutant of amyloid precursor protein and the enzyme shows reactivity with the wild-type APP.

Ganciclovir (GCV) is a pro-drug nucleoside analog that is activated by phosphorylation. It is useful in the study of gene therapy in cancer research.
Ganciclovir is a synthetic analogue of 2'-deoxy-guanosine. It is initially phosphorylated to a deoxyguanosine triphosphate (dGTP) analogue. This mechanism competitively inhibits the integration of dGTP by viral DNA polymerase, resulting in the termination of elongation of viral DNA. Upon expression of a viral suicide gene encoding thymidine kinase, the non-toxic pro-drug is converted to a phosphorylated active analog and is incorporated into the DNA of replicating eukaryotic cells, causing death of the malignant dividing cell. The cell cycle is irreversibly arrested at the G2-M checkpoint. Gap junction involvement in the ganciclovir bystander effect has been studied. Ganciclovir has been used to study loss of telomeres and to evaluate sensitivity of viruses to antiviral treatments.
Ganciclovir is used in molecular biology for selection against random recombination events when homologous recombination of a gene of interest is required.

Apoptosis-Inducing Factor, Mitochondrion-Associated, 1 (AIFM1) is a mitochondrial protein which translocates to the nucleus once apoptosis has been initiated. AIFM1 causes DNA fragmentation and chromatin condensation and also triggers the release of cytochrome c and caspase-9 from mitochondria. Bcl-2 overexpression prevents the release of AIFM1 from mitochondria, but doesn’t block its apoptogenic activity.

PRDX2 is part of the peroxiredoxin family of antioxidant enzymes, which reduce hydrogen peroxide and alkyl hydroperoxides. PRDX2 takes part as an antioxidant protective role in cells, and contributes to the antiviral activity of CD8(+) T-cells. PRDX2 has proliferative effect in cancer development or progression.
If PRDX2 protection is insufficient against peroxidases, the DNA damage results in neurological disease such as Alzheimer's or DNA damage leading to cancer.

Chitodextrinase is a unique membrane-bound endoenzyme. The chitodextrinase enzyme cleaves soluble oligomers, but not chitin, to the di- and trisaccharides. Chitodextrinase is unable to solubilize chitin, but it can catalyze the hydrolysis of high to low molecular weight soluble chitin oligosaccharides.

BCL2 gene encodes an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants, produced by alternate splicing, differ in their C-terminal ends.

Glutathione reductase (Gor) is a member of the class-I pyridine nucleotide disulfide oxidoreductase family. The main role of the Gor protein is to uphold high levels of reduced glutathione in the cytosol. With the associated oxidation of NADPH, Gor transforms oxidized glutathione to the reduced form. The active site of the Gor protein is a redox-active disulfide bond.

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.

Cystatins are a superfamily of cysteine proteinase inhibitors found in both plants and animals. They comprise a group of proteinase inhibitors, widely distributed in tissues and body fluids, and form tight complexes with cysteine proteases such as cathepsin B, H, L and S. Cystatin C, a secreted molecule of this family, is of interest from biochemical, medicine and evolutionary points of view. Cystatin C, with molecular weight of 13260 Da, is composed of 120 amino acids, lacks carbohydrate and has two disulfide bridges located near the carboxyl terminus. Cystatin C is increased in patients with malignant diseases, and is related to the insufficiency of renal function and appears to be a better marker than creatinine. On the other hand, low levels of cystatin C involve cause the breakdown of the elastic laminae and, subsequently, the atherosclerosis and abdominal aortic aneurysm.

C1q is the first component of the classical pathway of complement activation. C1q along with the enzymatically active components C1r and C1s forms the C1 complex. When C1 binds to immunoglobulins in the form of immune complexes, it leads to activation of C1r and C1s proteases and a further activates the classical pathway of complement. C1q is a glycoprotein that belongs to the collectin family, having a molecular weight of about 410-462 kDa. C1q is a hexamer composed of globular heads attached to collagen-like triple-helix tails. The globular heads of C1q exclusively bind to the CH2 domain of IgG molecules or the CH3 domain of IgM. Each heavy chain of the immunoglobulin molecule contains a single binding site for C1q. Given that C1q must bind to no less than two heavy chains in order to alter its conformation and activate C1r and C1s, its activation follows only after binding to immunoglobulins in the form of immune complexes bound to multivalent antigens. C1q’s main physiological role is in the clearance of immune complexes and apoptotic bodies from the organism. Interruption of this process may lead to development of autoimmunity. Individuals with genetic deficiencies of C1q or other components of the classical pathway are at risk to develop SLE. C1q specifically binds to apoptotic bodies of human keratinocytes, vascular endothelial cells and lymphocytes. Complement components C1q and bound C3 mediate the clearance of apoptotic bodies. Hence, C1q may advance the clearance of autoantigens, avoiding stimulation of the immune system. Nonetheless, an extended exposition of the immune system to the neoepitope exposed on C1q molecules bound to immune complexes or apoptotic bodies could ultimately lead to an autoimmune response against C1q itself and to an altered complement function. C1q deficiency may also lead to disruption of the negative selection of autoreactive B cells. C1q along with other specific recognition proteins bind to the highly conserved lupus antigens (dsDNA and nuclear proteins) and activate the complement system. Autoantibodies against C1q (anti-C1q) are found in a number of autoimmune and infectious diseases like glomerulonephritis (GN) and lupus erythematosus (SLE), these antibodies are significant in clinical practice due to their negative predictive value.

CUB Domain Containing Protein 1, also known as CDCP1 is a transmembrane protein which contains three extracellular CUB domains. CDCP1 is implicated in cell adhesion and cell matrix association. In addition, CDCP1 takes part in the regulation of anchorage versus migration or proliferation versus differentiation through its phosphorylation. CDCP1 is also a novel marker for leukemia diagnosis as well as for immature hematopoietic stem cell subsets. Furthermore, the extracellular region of human CDCP1 shares amino acid identity sequence with the mouse CDCP1.

HMOX1 cleaves the heme ring at the alpha methene bridge to form Biliverdin. Biliverdin is then converted to Bilirubin by Biliverdin reductase. In physiological state, the highest activity of HMOX1 is found in the spleen, where senescent erythrocytes are sequestrated and destroyed. Heme Oxygenase-1 is involved in the regulation of cardiovascular function and its adaptive response to a variety of stressors. HMOX1 is induced in the colon of ulcerative colitis. HMOX1 is found to overexpress with a higher extent of intraplaque angiogenesis implies a multi-faceted role for HMOX1 in modulating the progression of atherosclerosis. HMOX1 expression reduced LPS-stimulated secretion of MCP-1, IL-6, IL-10, and TNF-alpha in murine and human macrophages.

PRDX2 is part of the peroxiredoxin family of antioxidant enzymes, which reduce hydrogen peroxide and alkyl hydroperoxides. PRDX2 takes part as an antioxidant protective role in cells, and contributes to the antiviral activity of CD8(+) T-cells. PRDX2 has proliferative effect in cancer development or progression.
If PRDX2 protection is insufficient against peroxidases, the DNA damage results in neurological disease such as Alzheimer's or DNA damage leading to cancer.

Macrophage Inflammatory Proteins (MIP) belong to the family of chemotactic cytokines known as chemokines. In humans, there are two major forms, MIP-1a and MIP-1b that are now officially named CCL3 and CCL4 respectively. Both are major factors produced by macrophages after they are stimulated with bacterial endotoxins. They activate human granulocytes (neutrophils, eosinophils and basophils) which can lead to acute neutrophilic inflammation. They also induce the synthesis and release of other pro-inflammatory cytokines such as interleukin 1 (IL-1), IL-6 and TNF-a from fibroblasts and macrophages. The genes for CCL3 and CCL4 are both located on human chromosome 17.

Cardiotrophin 1 (CT-1) is a 201 amino acid member of the interleukin-6 superfamily. It was identified by its ability to induce hypertrophic response in cardiac myocytes. CT-1 mRNA levels were found both in cardiac myocytes and in cardiac nonmyocytes. CT 1 was also detected in abundance in normal adult human lung and was expressed in both fetal and adult airway smooth muscle cells. CT 1 activates gp130 dependent signaling and stimulates the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway to transduce hypertrophic and cytoprotective signals in cardiac myocytes.
CT 1 has also a neurotrophic function. CTF1 deficiency causes increased motoneuron cell death in spinal cord and brainstem nuclei of mice during a period between embryonic day 14 and the first postnatal week. Moreover, CT-1 is a hepatocyte survival factor that efficiently reduces hepatocellular damage in animal models of acute liver injury. Cardiotrophin 1 expression is augmented after hypoxic stimulation and it can protect cardiac cells when added either prior to simulated ischaemia or at the time of reoxygenation following simulated ischaemia. Cardiotrophin 1 can induce expression of the protective heat shock proteins (hsps) in cardiac cells.
Cardiotrophin-1 increased ventricular expression of ANP, brain natriuretic peptide (BNP) and angiotensinogen mRNA.
Cardiophin 1 levels were significantly elevated in patients with heart failure, patients with dilatative cardiomyopathy, moderate/severe mitral regurgitation, stable and unstable angina and after acute myocardial infarction.

Heme Binding Protein 1 (HEBP1) is an intracellular tetrapyrrole-binding protein. HEBP1 is comprised of a natural chemoattractant peptide of 21 amino acids at the N-terminus, which is a natural ligand for formyl peptide receptor-like receptor 2 (FPRL2) and stimulates calcium mobilization and chemotaxis in monocytes and dendritic cells.

HIF1A has a role as a master transcriptional monitor of the adaptive response to hypoxia. Under hypoxic conditions HIF1A activates the transcription of over 40 genes, including, erythropoietin, glucose transporters, glycolytic enzymes, vascular endothelial growth factor, and genes whose protein products increase oxygen release or facilitate metabolic adaptation to hypoxia. HIF1A functions as an essential role in embryonic vascularization, tumor angiogenesis and pathophysiology of ischemic disease.

Aldo-keto reductase family 1 member C1 or AKR1C1 is an enzyme, part of the aldo/keto reductase family that holds over 40 familiar proteins. AKR1C1 promotes the conversion of ketones & aldehydes to their alcohol forms by using cofactors such as NADH & NADPH. AKR1C1 promotes the progesterone reduction to its inactive molecule form 20-alpha-hydroxy-progesterone.

AKR1C4 is a member of the aldo/keto reductase superfamily that has over 40 known enzymes and proteins. AKR1C4 enables the conversion of aldehydes and ketones to their corresponding alcohols by using NADH and/or NADPH as cofactors. AKR1C4 takes part in the bioreduction of chlordecone, a toxic organochlorine pesticide, to chlordecone alcohol in liver.

CD166 antigen isoform 2 (ALCAM) is a type 1 membrane glycoprotein and belongs to the immunoglobulin superfamily. ALCAM is expressed on thymic epithelium, microvascular endothelium, activated lymphocytes and monocytes, and monocyte-derived dendritic cells. CD166 and CD6 interaction plays a role in T cell development and T cell regulation, as well as in the binding of T cells and B cells to activated leukocytes.

Amine Oxidase Copper Containing 1 or AOC1 is n enzyme, part of the copper-containing amine oxidase group of proteins. AOC1 is responsible for oxidation of many different biogenic amines, such as neurotransmitters, xenobiotic amines & histamine. Dietary histamine intolerance and histaminosis can be caused from AOC1 deficiencies. This enzyme can also cause Tumor Progression by AKT & EMT transduction promotion in stomach cancer.

CCDC101 is known as a subunit of the SAGA (Spt-Ada-Gcn5 acetyltransferase) histone acetyltransferase complex in Saccharomyces cerevisiae. CCDC101 is conserved from yeast to humans.