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GHBP is a transmembrane receptor for growth hormone. Binding of growth hormone to the receptor leads to receptor dimerization and the activation of an intra- and intercellular signal transduction pathway leading to growth. A common alternate allele of this gene, called GHRd3, lacks exon three and has been well-characterized. Mutations in this gene have been associated with Laron syndrome, also known as the growth hormone insensitivity syndrome (GHIS), a disorder characterized by short stature. Other splice variants, including one encoding a soluble form of the protein (GHRtr), have been observed but have not been thoroughly characterized.

Resistin, also known as adipose tissue-specific secretory factor (ADSF) is a cysteine-rich peptide derived from adipose tissue. Resistin takes part in the inflammatory response, glucose metabolism, and angiogenesis.Resistin blocks insulinstimulated uptake of glucose by adipocytes and promote glucose release by hepatocytes. As such,Resistin considered to participate in diet‑induced insulin-sensitivity. Resistin causes high levels of lowdensity lipoprotein (LDL), increasing the risk of heart disease.

Tissue factor is well-known as the main cellular initiator of blood coagulation. The Tissue factor gene encodes coagulation factor III which is a cell surface glycoprotein that enables cells to initiate the blood coagulation cascades, and functions as the high-affinity receptor for the coagulation factor VII. Following vessel injury, the Tissue Factor and Factor VIIa complex activates the coagulation protease cascade, which leads to fibrin deposition and activation of platelets. The ensuing complex presents a catalytic event, which is responsible for initiation of the coagulation protease cascades by specific limited proteolysis. Therefore, Tissue factor has a role in normal hemostasis by initiating the cell-surface assembly and propagation of the coagulation protease cascade. Tissue Factor can also be stimulated by the inflammatory mediators interleukin 1 and TNF, as well as by endotoxin, to appear on monocytes and vascular endothelial cells as a component of cellular immune response.
Tissue factor is the only one in the coagulation pathway for which a congenital deficiency has not been described. Certain levels of Tissue Factor are essential for the maintained viability and growth of endothelium and Tissue Factor-expressing tumor cells. Additionally, abnormal Tissue Factor expression inside the vasculature initiates life threatening thrombosis in various diseases, for example sepsis, atherosclerosis, and cancer. Alternative spliced Tissue Factor expression advances tumor growth, and is linked to increased tumor cell proliferation and angiogenesis in pancreatic cancer.

TIE-1 (tyrosine kinase with Ig and EGF homology domains 1) and TIE-2/Tek comprise a receptor tyrosine kinase (RTK) subfamily with unique structural characteristics: two immunoglobulin-like domains flanking three epidermal growth factor (EGF)-like domains and followed by three fibronectin type III-like repeats in the extracellular region and a split tyrosine kinase domain in the cytoplasmic region. These receptors are expressed primarily on endothelial and hematopoietic progenitor cells and play critical roles in angiogenesis, vasculogenesis and hematopoiesis. Human TIE-1 cDNA encodes a 1122 amino acid (aa) residue precursor protein with an 18 residue putative signal peptide, a 726 residue extracellular domain and a 353 residue cytoplasmic domain. Two ligands, angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2), which bind TIE-2 with high-affinity have been identified. Ang2 has been reported to act as an antagonist for Ang1. Mice engineered to overexpress Ang2 or to lack Ang1 or Tie-1 display similar angiogenic defects.

EIF1AX is an important eukaryotic translation initiation factor. EIF1AX is essential for the binding of the 43S complex (a 40S subunit, eIF2/GTP/Met-tRNAi and eIF3) to the 5'' end of capped RNA. EIF1AP1 is needed for maximal rate of protein biosynthesis. EIF1AX increases ribosome dissociation into subunits and stabilizes the binding of the initiator Met-tRNA (I) to 40 S ribosomal subunits.

IFN Regulatory Factor-5, also known as IRF5 belongs to the IFN regulatory factor (IRF) family, a group of transcription factors with various functions, including virus-mediated activation of IFN, and modulation of cell growth, differentiation, apoptosis, and immune system activity. Members of the IRF family are characterized by a conserved N-terminal DNA-binding domain containing tryptophan (W) repeats. Multiple transcript variants encoding different isoforms have been found for this gene. In addition, IRF5 is implicated in the induction of IFNs IFNA and INFB and inflammatory cytokines upon virus infection. IRF5 is activated by TLR7 or TLR8 signaling.

Placental Lactogen is a polypeptide hormone that is produced by the Syncytiotrophoblasts of the Placenta, also known as chorionic somatomammotropin. It has both Growth Hormone and Prolactin activities on growth, lactation, and luteal steroid production. In women, placental lactogen secretion begins soon after implantation and increases to 1 g or more a day in late pregnancy. Placental lactogen is also an insulin antagonist.
Placental Lactogen Goat is also capable of activating human and other heterologous GH receptors but not ruminat GH receptors.

TFPI is a protease inhibitor which controls the tissue factor (TF)-dependent pathway of blood coagulation. The coagulation process starts with the creation of a factor VIIa-TF complex, that proteolytically triggers additional proteases (factors IX and X) and eventually results in a fibrin clot. TFPI inhibits the activated factor X and VIIa-TF proteases in an autoregulatory loop. TFPI is glycosylated and predominantly located in the vascular endothelium and plasma in both free forms and complexed with plasma lipoproteins. A number of alternatively spliced transcript variants of this gene have are known, however the full-length nature of several of these variants were not yet established.

Crk-like protein (CRKL) is a protein kinase containing SH2 and SH3 (src homology) domains which activates the RAS and JUN kinase signaling pathways and transforms fibroblasts in a RAS-dependent manner. CRKL is a substitute of the BCR-ABL tyrosine kinase, it also has a role in fibroblast transformation by BCR-ABL, and has oncogenic potential.

TCEA1 is a member of the TFS-II family. TCEA1 binds to Pol II and operates to cleave the emerging transcript, thus unlocking the complex and permitting transcription to continue. TCEA1 is localized to the nucleus and holds three independently-folding domains that are essential for accurate binding to Pol II. The arresting sites in are able to trap a certain segment of elongating RNA polymerases that goes through, causing in a locked ternary complex. Cleavage of the emerging transcript by S-II enables the renewal of elongation from the new 3'-terminus.

Interleukin-10 is a multifunctional cytokine produced by a variety of cell types including T helper cells activated B cells and activated macrophages. Interleukin-10 regulates immune-mediated inflammation and modulates the function of cells such as lymphocytes, monocytes, natural killer cells and dendritic cells.

Members of the IFN regulatory factor (IRF) family regulate gene expression critical to immune response, hemopoiesis, and proliferation. IRF-3 is a member of the IRF family, and is distinct from other family members. Its transcriptional activity is regulated solely by posttranslational modifications. It plays a crucial role in activation of innate immunity and inflammation in response to viral infection. IRF-3 mediates IFN-stimulated response element (isre) promoter activation. Functions as a molecular switch for antiviral activity. Dsrna generated during the course of an viral infection leads to IRF3 phosphorylation on the c-terminal serine/threonine cluster. This induces a conformational change, leading to its dimerization, nuclear localization and association with creb binding protein (crebbp) to form dsrna-activated factor 1 (draf1), a complex which activates the transcription of genes under the control of isre. The complex binds to the ie and prdiii regions on the ifn-alpha and ifn-beta promoters respectively. IRF-3 does not have any transcription activation domains.

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.

Osteostat is the cytokine that binds to TNFRSF18/AITR/GITR and is important for interactions between activated T-lymphocytes and endothelial cells and may modulate T-lymphocyte survival in peripheral tissues. Osteostat is expressed at high levels in the small intestine, ovary, testis, kidney and endothelial cells after stimulation by lipopolysaccharides.
Osteostat protein is detectable in human microvascular EC and is highly up-regulated by IFN-alpha and IFN-beta. Osteostat inhibit differentiation of osteoclasts from monocytic precursor cells. Osteostat suppresses the early stage of osteoclastogenesis via inhibition of macrophage colony-stimulating factorinduced receptor activator of NF-kappaB (RANK) expression in the osteoclast precursor cells. Osteostat does not inhibit lipopolysaccharide-induced RANK expression in monocytes and dendritic cells, or activation-induced RANK expression in T cells. Osteostat is a novel regulator of osteoclast generation and substantiate the major role played by the endothelium in bone physiology.

FLT3 ligand is a receptor for the fl cytokine has a tyrosine-protein kinase activity & a growth factor that regulates proliferation of early hematopoietic cells. Flt3-Ligand synergizes with other CSFs and interleukins to induce growth and differentiation.

Tumor necrosis factor is a member of a group of cytokines that all stimulate the acute phase reaction. TNF is involved in systemic inflammationand secreted mainly 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.

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, and cancer.

CNTF is a polypeptide hormone whose actions appear to be restricted to the nervous system where it promotes neurotransmitter synthesis and neurite outgrowth in certain neuronal populations. The protein is a potent survival factor for neurons and oligodendrocytes and may be relevant in reducing tissue destruction during inflammatory attacks. A mutation in this gene, which results in aberrant splicing, leads to ciliary neurotrophic factor deficiency, but this phenotype is not causally related to neurologic disease. In addition to the predominant monocistronic transcript originating from this locus, the gene is also co-transcribed with the upstream ZFP91 gene. Co-transcription from the two loci results in a transcript that contains a complete coding region for the zinc finger protein but lacks a complete coding region for ciliary neurotrophic factor.
CNTF is a survival factor for various neuronal cell types. Seems to prevent the degeneration of motor axons after axotomy.

TRAIL Receptor-1 (DR4) and TRAIL Receptor-2(DR5) are members of the TNFR superfamily of transmembrane proteins and contain a cytoplasmic "death domain", which is capable of activating the cell's apoptotic machinery. These receptors are activated by binding to either membrane anchored or soluble TRAIL/Apo2L.

RUNX3 is part of the RUNX family that mediates the expression of genes which participate in cellular differentiation and cell cycle progression. RUNX3 heterodimer and the beta subunit form a complex that binds to the core DNA sequence 5''-PYGPYGGT-3'' found in several enhancers and promoters, and can either activate or suppress transcription. RUNX3 interacts with additional transcription factors. RUNX3 is a good candidate for gastric cancer tumor suppressor diagnosis.

Glia Maturation Factor-Beta (GMF-Beta) is a 17 kDa protein nerve gorwth factor identified as a growth and differentiation factor in the vertebrate brain.

Glia Maturation Factor-Beta stimulates differentiation of normal neurons as well as glial cells. GMFB inhibits the proliferation of the N-18 neuroblastoma line and the C6 glioma line while promoting their phenotypic expression.
GMF-beta inhances the phenotypic expression of glia & neurons thus inhibits the proliferation of their respective tumors when added to cell culture. Although astrocytes produce GMF-b and stores it inside the cells, they don’t secrete the GMF-B into the cultured medium. Cell- surface GMFb acts on the target cells at close range when cells are in direct contact. GMF-Beta is produced by thymic epithelial cells and plays an important role in T cell development in favor of CD4+ T cells.
GMF-Beta is a brain-specific protein which belongs to the actin-binding proteins (ADF) family. GMF-beta appears to play a role in the differentiation, maintenance, and regeneration of the nervous system. It also supports the progression of certain auto-immune diseases, possibly through its ability to induce the production and secretion of various pro-inflammatory cytokines.

cAMP-dependent protein kinase inhibitor beta (PKIB) belongs to the cAMP-dependent protein kinase inhibitor family. PKIB may interact with the catalytic subunit of cAMP-dependent protein kinase and function as a competitive inhibitor.

Canopy 3 homolog (CNPY3) is a 271 a.aToll-like receptor specific co-chaperone for HSP90B1. CNPY3 is necessitated for proper TLR folding, excluding that of TLR3, and so controls TLR exit from the endoplasmic reticulum. Therefore, CNPY3i s required for both innate and adaptive immune responses.

NXT1 operates as a nuclear export factor in both RAN and CRM1 dependent pathways. NXT1 is known to stimulate the export of U1 snRNA in RAN (Ras-related nuclear protein) and CRM1 (chromosome region maintenance) dependent pathways and the export of tRNA and mRNA in a CRM1-independent pathway. This protein heterodimerizes with Tap protein and regulates the ability of Tap protein to intermediate nuclear mRNA export.