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Endonuclease III (nth) is a DNA repair enzyme which has both DNA N-glycosylase activity and AP-lyase activity. The DNA N-glycosylase activity releases numerous damaged pyrimidines from DNA by cleaving the N-glycosidic bond and leaving an AP (apurinic/apyrimidinic) site. This AP-lyase activity cleaves the phosphodiester bond 3' to the AP site by a beta-elimination, thus leaving a 3'-terminal unsaturated sugar and a product with a terminal 5'-phosphate.

Beta-1,3-N-Acetylglucosaminyltransferase 2 (B3GNT2) is a part of the beta-1,3-N-acetylglucosaminyltransferase family which takes part in the synthesis of poly-N-acetyllactosamine. B3GNT2 is a type II transmembrane protein which prefers the substrate of lacto-N-neotetraose. B3GNT2 catalyzes the initiation and elongation of poly-N-acetyllactosamine chains and comprises the main polylactosamine synthase.

Vascular endothelial growth factor is an important signaling protein involved in both vasculogenesis and angiogenesis. As its name implies, VEGF activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells ). VEGF mediates increased vascular permeability, induces angiogenesis, vasculogenesis and endothelial cell growth, promotes cell migration, and inhibits apoptosis. In vitro, VEGF has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
Elevated levels of this protein is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.

Vascular endothelial growth factor is an important signaling protein involved in both angiogenesis and vasculogenesis.VEGF activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells ).VEGF mediates increased vascular permeability, induces angiogenesis, vasculogenesis and endothelial cell growth, promotes cell migration, and inhibits apoptosis. In vitro, VEGF has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
Elevated levels of VEGF is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in VEGF have been associated with proliferative and nonproliferative diabetic retinopathy.

Granulocyte/Macrophage Colony-Stimulating Factors are cytokines that act in hematopoiesis by controlling the production, differentiation, and function of 2 related white cell populations of the blood, the granulocytes and the monocytes-macrophages. CSF-1 induces cells of the monocyte/macrophage lineage. It plays a role in immunological defenses, bone metabolism, lipoproteins clearance, fertility and pregnancy.

Acetoacetyl-CoA thiolase (ACAT1) is an enzyme member of the membrane-bound acyltransferase family and Sterol o-acyltransferase subfamily. The ACAT1 enzyme catalyzes the reversible formation of acetoacetyl-CoA from 2 molecules of acetyl-CoA. ACAT1 plays a part in lipoprotein compilation and dietary cholesterol absorption. Added to its acyltransferase activity, ACAT1 acts as a ligase.

Angiotensin is an oligopeptide in the blood that causes vasoconstriction, increased blood pressure, and release of aldosterone from the adrenal cortex. It is a powerful dipsogen. It is derived from the precursor molecule angiotensinogen, a serum globulin produced in the liver. It plays an important role in the renin-angiotensin system.
The protein encoded by this gene, pre-angiotensinogen or angiotensinogen precursor, is expressed in the liver and is cleaved by the enzyme renin in response to lowered blood pressure. The resulting product, angiotensin I is then cleaved by angiotensin converting enzyme (ACE) to generate the physiologically active enzyme angiotensin II. The protein is involved in maintaining blood pressure and in the pathogenesis of essential hypertension and preeclampsia.

MMP-3 enzyme is also known as Stromelysin-1or as Transin-1 which hydrolyzes natural collagen at physiological pH and temperature. It dissolves the intervertebral nucleus pulposus and annulus fibrosus of Herniated Lumbar Intervertebral Disk . MMP-3 hydrolyzes components of the extracellular matrix like proteoglycan, laminin, fibronectin, gelatin and collagen types III, IV and IX. It also activates pro-MMP-9 and pro-MMP-8 and superactivates plasmin activated MMP-1. MMP-3 is secreted as a latent proenzyme and is activated by a variety of proteinases, e.g. plasmin, trypsin, chymotrypsin, cathepsin G or human neutrophil elastase. MMP-3 was found to be capable of activating the precursor of IL1-beta.

PDGF-BB is a member of the platelet-derived growth factor family. The four members of this family are mitogenic factors for cells of mesenchymal origin and are characterized by a motif of eight cysteines. This gene product can exist either as a homodimer (PDGF-BB) or as a heterodimer with the platelet-derived growth factor alpha polypeptide (PDGF-AB), where the dimers are connected by disulfide bonds. Mutations in this gene are associated with meningioma. Reciprocal translocations between chromosomes 22 and 7, at sites where this gene and that for COL1A1 are located, are associated with a particular type of skin tumor called dermatofibrosarcoma protuberans resulting from unregulated expression of growth factor. Two splice variants have been identified for this gene.

Prolactin is a pituitary hormone involved in the stimulation of milk production, salt and water regulation, growth, development and reproduction. The initial step in its action is the binding to a specific membrane receptor (prolactin receptor) which belongs to the superfamily of class 1 cytokine receptors. The function of the prolactin receptor is mediated, at least in part, by two families of signaling molecules: Janus kinases and signal transducers and activators of transcription. Prolactin (PRL) is a hormone involved in a variety of important functions including ion transport and osmoregulation, stimulation of milk, protein synthesis as well as the regulation of numerous reproductive functions. PRL exerts its influence on different cell types through a signal transduction pathway which begins with the binding of the hormone to a transmembrane PRL receptor. Immunoreactive PRL receptor, a member of the cytokine receptor family, varies in size (short and long forms) with tissue source and species, from ~40 kDa to 100 kDa. The PRL receptor consists of at least three separate domains: an extracellular region with 5 cysteines which contains the prolactin binding site, a single transmembrane domain and a cytoplasmic region, the length of which appears to influence ligand binding and regulate cellular function.

HBsAg is the surface antigen of the Hepatitis-B-Virus (HBV). The capsid of a virus has different surface proteins from the rest of the virus. The antigen is a protein that binds specifically on one of these surface proteins and is commonly referred to as the Australian Antigen. HBsAg is an essential parameter to diagnose hepatitis B disease in the clinic and to monitor antiviral treatment.

TNFR1 belongs to the TNF-receptor superfamily. TNFR1 is a receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha.
There are 2 types of soluble TNF receptors: sTNFR-I and sTNFR-II, which act to neutralize the biological activities of TNF alpha and TNF beta. The levels of these soluble receptors seem to increase as a result of shedding of the extracellular domains of the membrane bound receptors. TNF-a, TNFR1 and TNFR2 have roles in cellular differentiation. TNFR1 and TNFR2 function in cell type-specific renal injury.
TNFR1 is capable of signaling both cell survival and apoptosis. TNFR1-induced apoptosis requires 2 sequential signaling complexes. TNFR1 is capable of activating NF-kappaB, mediate apoptosis, and function as a regulator of inflammation. Oxidative stress promotes TNFR1 and TNFR2 self-interaction, ligand-independent and enhanced ligand-dependent TNF signaling. TNFR1 contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase. Human TNFR1 has a major region which controls cell surface expression. High levels of soluble TNF receptors are found in the amniotic fluid of pregnant women.
Germline mutations of the extracellular domains of TNFR1 are linked to the autosomal dominant periodic fever syndrome. The impaired receptor clearance is believed to be a mechanism of the disease. Familial hibernian fever (FHF) is caused by defects in TNFRSF1A gene.

GH is a member of the prolactin family of hormones which play an important role in growth control. The gene, along with four other related genes, is located at the GH locus on chromosome 17 where they are interspersed in the same transcriptional orientation; an arrangement which is thought to have evolved by a series of gene duplications. The five genes share a remarkably high degree of sequence identity. Alternative splicing generates additional isoforms of each of the five GHs, leading to further diversity and potential for specialization. This particular family member is expressed in the pituitary but not in placental tissue as is the case for the other four genes in the GH locus. Mutations in or deletions of the gene lead to GH deficiency and short stature.

CD70 also known as TNFSF7 is a cytokine which binds to CD27. TNFSF7 takes part in T-cell activation as well as induces the proliferation of costimulated T-cells. Moreover, TNFSF7 enhances the generation of cytolytic T-cells. Among the diseases which are associated with TNFSF7: Include acute myocarditis & Myocarditis.

Gliadin is a common substrate of transglutaminase, which generates neo-epitopes by deamidation of glutamine side chains. In the past, serologic tests for gliadin antibodies usually were not very precise and were not enough for accurate diagnosis due to missing deamidated epitopes within the authentic gliadin fraction traditionally used in diagnostic test kits. ProSpec's deamidated Gliadin isoform matches to the deamidated neo-epitopes, which in the natural antigen are formed by transglutaminase-mediated glutamine side chain deamidation.

Tumor necrosis factor receptor superfamily member 8 (TNFRSF8) is a receptor for TNFSF8/CD30L. TNFRSF8 has a role in the regulation of cellular growth and transformation of activated lymphoblasts. In addition, the TNFRSF8 protein regulates gene expression via activation of NF-kappa-B. TNFRSF8 being a regulator of apoptosis, induces cell death or proliferation, depending on the cell type.

TNFR1 belongs to the TNF-receptor superfamily. TNFR1 is a receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha.
There are 2 types of soluble TNF receptors: sTNFR-I and sTNFR-II, which act to neutralize the biological activities of TNF alpha and TNF beta. The levels of these soluble receptors seem to increase as a result of shedding of the extracellular domains of the membrane bound receptors. TNF-a, TNFR1 and TNFR2 have roles in cellular differentiation. TNFR1 and TNFR2 function in cell type-specific renal injury.
TNFR1 is capable of signaling both cell survival and apoptosis. TNFR1-induced apoptosis requires 2 sequential signaling complexes. TNFR1 is capable of activating NF-kappaB, mediate apoptosis, and function as a regulator of inflammation. Oxidative stress promotes TNFR1 and TNFR2 self-interaction, ligand-independent and enhanced ligand-dependent TNF signaling. TNFR1 contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase. Human TNFR1 has a major region which controls cell surface expression. High levels of soluble TNF receptors are found in the amniotic fluid of pregnant women.
Germline mutations of the extracellular domains of TNFR1 are linked to the autosomal dominant periodic fever syndrome. The impaired receptor clearance is believed to be a mechanism of the disease. Familial hibernian fever (FHF) is caused by defects in TNFRSF1A gene.

Hydroxymethylglutaryl-CoA lyase (HMGCL) is a mitochondrial matrix protein which is a member of the HMG-CoA lyase family. HMGCL is a homodimer and participates in leucine catabolism and ketogenesis, the hepatic synthesis of ketone bodies which, during fasting, provides a major source of energy for the heart, brain and kidney. More precisely, HMGCL catalyzes the final step of these processes, the cleavage of 3-hydroxy-3-methylglutaryl-CoA to acetoacetic acid and acetyl-CoA.

Tumor necrosis factor is a cytokine involved in systemic inflammation and is a member of a group of cytokines that all stimulate the acute phase reaction. TNF is mainly secreted by macrophages.
TNF causes apoptotic cell death, cellular proliferation, differentiation, inflammation, tumorigenesis and viral replication, TNF is also involved in lipid metabolism, and coagulation. TNF's primary role is in the regulation of immune cells.
Dysregulation and, in particular, overproduction of TNF have been implicated in a variety of human diseases- autoimmune diseases, insulin resistance, and cancer.

Vascular endothelial growth factor is an important signaling protein involved in both vasculogenesis and angiogenesis. As its name implies, VEGF activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells ).VEGF mediates increased vascular permeability, induces angiogenesis, vasculogenesis and endothelial cell growth, promotes cell migration, and inhibits apoptosis. In vitro, VEGF has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
Elevated levels of this protein is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.

C1QTNF1 is a novel adipokine, providing a significant framework to further address the physiological functions and mechanisms of the action of this family of secreted glycoproteins in normal and disease states. C1QTNF1 increases the production of aldosterone. C1QTNF1 is vastly expressed in obese subjects as well as up-regulated in hypertensive patients, C1QTNF1 is identified molecular link between obesity and hypertension. C1QTNF1 expression may be associated with a low-grade chronic inflammation status in adipose tissues.

FGF-basic is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. This protein functions as a modifier of endothelial cell migration and proliferation, as well as an angiogenic factor. It acts as a mitogen for a variety of mesoderm- and neuroectoderm-derived cells in vitro, thus is thought to be involved in organogenesis. Three alternatively spliced variants encoding different isoforms have been described. The heparin-binding growth factors are angiogenic agents in vivo and are potent mitogens for a variety of cell types in vitro. There are differences in the tissue distribution and concentration of these 2 growth factors.

Vascular endothelial growth factor is an important signaling protein involved in both vasculogenesis and angiogenesis. As its name implies, VEGF activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/ macrophagemigration, neurons, cancer cells, kidney epithelial cells ).VEGF mediates increased vascular permeability, induces angiogenesis, vasculogenesis and endothelial cell growth, promotes cell migration, and inhibits apoptosis. In vitro, VEGF has been shown to stimulate endothelial cell mitogenesisand cell migration. VEGF is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.
Elevated levels of this protein are linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.