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NCR2 is a member of the natural cytotoxicity receptor (NCR) family and holds 1 immunoglobulin-like (Ig-like) domain. NCR2 cooperates with TYROBP/DAP12 and is specifically expressed by activated NK cells and by in vitro cultured TCRg/d lymphoid cells. NCR2 is a cytotoxicity-activating receptor which induces the amplified efficiency of activated natural killer (NK) cells to mediate tumor cell lysis.

Syntaxin-1, synaptobrevin, and SNAP25 cooperate to form the SNARE complex, which is needed for synaptic vesicle docking and fusion SNPH is a neuron-specific protein originally characterized as a binding partner of syntaxin-1. SNPH participates with SNAP25 for the binding to Syntaxin-1 and prevents the construction of the SNARE core complex, thus manageling free syntaxin-1 availability for the assembly of the SNARE complex and potentially regulating synaptic vesicle exocytosis. Expression Syntaphilin appears to be brain-specific. SNPH is an inhibitor of both SNARE-based fusion and dynamin-mediated endocytosis.

GCSAM is a protein which functions in signal transduction pathways and whose expression raises in germinal cell lymphomas. GCSAM contains a putative PDZ-interacting domain, an immunoreceptor tyrosine-based activation motif (ITAM), and two putative SH2 binding sites. In B cells, GCSAM expression is particularly induced by interleukin-4.

Hematological and neurological expressed 1 protein (HN1) is a small protein which is extremely preserved among species. HN1 expression is upregulated in regenerating neural tissues, including the axotomized adult rodent facial motor nerve and dedifferentiating retinal pigment epithelial cells of the Japanese newt. HN1 is also expressed in several tissues during embryonic development as well as in regions of the adult brain which display high plasticity.

Anamorsin, ( CIAPIN) is a member of anamorsin family. CIAPIN mainly expressed in the cytoplasm of liver, pancreas and heart tissue cells and does not show any homology to known apoptosis regulatory molecules of the Bcl-2 or CASP families, or to signal transduction molecules. CIAPIN1 Expression is reliant on growth factor stimulation. It is a ubiquitously expressed protein, and when it is overexpressed, it grants apoptotic resistance.

Nafarelin acetate is a synthetic analog of the naturally occurring gonadotropin-releasing hormone (GnRH). Nafarelin stimulates the release of the pituitary gonadotropins, LH and FSH, resulting in a temporary increase of ovarian steroidogenesis.

Human TNFRSF10A is a type 1 transmembrane protein in the TNF R superfamily. TNFRSF10A is not expressed in rodents. The trimeric ligand Trail binds TNFRSF10A and induces apoptosis, and recombinant, soluble forms of the receptor inhibit Trail-induced apoptosis. TNFRSF10A is expressed generally in damaged, infected, and malignant cells. TNFRSF10A functions in immune surveillance, inducing apoptosis in cancer cells but not normal cells.

Connective Tissue Growth Factor belongs to the CCN family of proteins. The CCN family presently consists of six members in human also known as: Cyr61 (Cystein rich 61), CTGF (Connective Tissue Growth Factor), Nov (Nephroblastoma Overexpressed gene), WISP-1, 2 and 3 (Wnt-1 Induced Secreted Proteins). The CCN genes encode secreted proteins associated with the Extracellular Matrix (ECM) and cell membrane. CCN proteins are matricellular proteins which are involved in the regulation of various cellular functions including: proliferation, differentiation, survival, adhesion and migration. They are expressed in derivatives of the three embryonic sheets and are implicated in the development of kidney, nervous system, muscle, bone marrow, cartilage and bone. During adulthood, they are implicated in wound healing, bone fracture repair, and pathologies such as: fibrosis, vascular ailments and tumorigenesis.
Full length secreted CCN proteins can show an antiproliferative activity, whereas truncated isoforms are likely to stimulate proliferation and behave as oncogenes. The full length protein consists of four modulesModule I shares partial identity with the N-terminal part of the Insulin-like Growth Factor Binding Proteins (IGFBPs).
Module II includes a stretch of 70amino acid residues – which shares sequence identity with the Von Willebrand Factor Type C repeat (VWC).
Module III contains sequences sharing identity with the Thrombospondin type 1 repeat (TSP1) (WSXCSXXCG), which is thought to be implicated in the binding of sulfated glycoconjugates and to be important for cell adhesion. Module IV, also designated CT, is encoded by exon5. It is the leasts conserved one of the four domains at the level of nucleotide sequence, but it appears to be critical for several of the biological functions attributed to the CCN proteins. Module IV resembles the CT domain of several extracellular protein including, Von Willebrand's factor and mucins. Sequence similarities to heparin-binding motifs are also found within this domain.
Proteolysis of the secreted full-length CCN proteins that has been reported in the case of CCN2 and CCN3 might result in the production of CCN-derived peptides with high affinity for ligands that full-length CNN proteins bind only poorly. Amino-truncated CCN2 isoforms were biologically active whereas no specific biological activity has been attributed to the truncated CCN3. Although the molecular processes underlying the production of these secreted isoforms is presently unknown, it is important to note that proteolysis occur at the same amino acid residues in both CCN2 and CCN3. An elevated expression of CCN2 has also been detected by Northern blotting in human invasive mammary ductal carcinomas, dermatofibromas, pyogenic granuloma, endothelial cells of angiolipomas and angioleiomyomas, and in pancreatic tumors. A study performed with chondrosarcomas representative of various histological grades established that CCN2 expression was closely correlated with increasing levels of malignancy. In agreement with CCN2 playing a role in brain tumor angiogenesis, immunocytochemistry studies indicated that both glioblastoma tumor cells and proliferating endothelial cells stained positive for CCN2. In astrocytomas, CCN2 expression was particularly elevated in high grade tumors, with a marked effect of CCN2 on cell proliferation. Downregulation of CCN2 expression in these cells was associated with a growth arrest at the G1/S transition while over-expression of CCN2 induced a two-fold increase of the number of cells in the G1 phase. Gene profiling analysis allowed to identify a set of about 50 genes whose expression might account for the proliferative activity of CCN2 in these cells. CCN2 was seen in a higher proportion of mononuclear cells of patients with acute lymphoblastic leukemia.

TNFRSF6B is a member of the Tumor necrosis factor receptor superfamily. TNFRSF6B performs as a decoy receptor which races against death receptors for ligand binding. TNFRSF6B has a regulatory role in suppressing FasL- and LIGHT-mediated cell death and T cell activation in addition to inducing angiogenesis via neutralization of TL1A.

TP53-induced glycolysis and apoptosis regulator (TIGAR or C12ORF5), is a 270 amino acid protein induced by the p53 tumor suppressor pathway that functions to protect against oxidative stress. C12ORF5 specifically functions to block glycolysis, leading the pathway to the pentose phosphate shunt and decreasing the intracellular concentration of reactive oxygen species. Therefore, it is thought that C12ORF5 may act to modulate the apoptotic response to p53, thus allowing cells to survive mild or transient stresses.

The somatomedins, or insulin-like growth factors (IGFs), comprise a family of peptides that takes part in mammalian growth and development. IGF1 mediates various growth-promoting effects of growth hormone (GH; MIM 139250). Early studies showed that growth hormone did not directly stimulate the incorporation of sulfate into cartilage, but rather acted through a serum factor, termed 'sulfation factor,' which later became known as 'somatomedin' (Daughaday et al., 1972). 3 main somatomedins have been characterized: somatomedin C (IGF1), somatomedin A (IGF2; MIM 147470), and somatomedin B (MIM 193190) (Rotwein, 1986; Rosenfeld, 2003).

OSTF1 is an intracellular protein produced by osteoclasts that induces bone resorption, via signaling cascade which results in the secretion of factors enhancing osteoclast formation and activity.

B-Raf Proto-Oncogene, also known as BRAF is a member of the raf/mil family of serine/threonine protein kinases. BRAF participates in regulating the MAP kinase/ERKs signaling pathway, which eventually have an effect on cell division, differentiation, and secretion. Mutations in BRAF have been associated with cardiofaciocutaneous syndrome, which is a disease characterized by heart defects, mental retardation and a distinctive facial appearance. In addition, mutations in BRAF have also been associated with different cancers, including non-Hodgkin lymphoma, colorectal cancer, malignant melanoma, thyroid carcinoma, non-small cell lung carcinoma, as well as adenocarcinoma of lung.

Based on sequence similarity to VEGF-A, a gene encoding a VEGF homologue has recently been discovered in the genome of Orf virus (OV) (Lyttle et al., 1994). Different isolates of Orf virus show significant amino acid sequence similarity to VEGF-A and described as a viral virulence factor that appears to be derived from captured host genes. All eight cysteine residues of the central cysteine knot motif characteristic of members of the VEGF family are conserved among other residues in the VEGF-E proteins (Dehio et al., 1999; Wise et al., 1999). Alignment of all mammalian VEGF sequences indicated that VEGF-E is distinct from the previously described VEGFs but most closely related to VEGF-A. Like VEGF-A, VEGF-E was found to bind with high affinity to VEGF receptor-2 (KDR) resulting in receptor autophosphorylation, whilst in contrast to VEGF-A, VEGF-E can not bind to VEGF receptor-1 (Flt-1). Furthermore VEGF-E can also not bind to VEGF receptor-3 (FLT-4). Therefore VEGF-E is a potent angiog

Cytochrome c oxidase assembly factor 4 (COA4) is the last enzyme of the mitochondrial respiratory chain which needs a great number of accessory factors. COA4 is vital for oxidative phosphorylation and comprises multiple complexes including cytochrome c oxidase, assembled in macromolecular supercomplexes. COX4 is a protein-coding gene which defect in it causes an acute human encephalomyopathies.

Ipamorelin is a peptide selective agonist of the ghrelin/growth hormone secretagogue receptor and a growth hormone secretagogue. Ipamorelin is a pentapeptide that was derived from GHRP1. Ipamorelin significantly increases plasma growth hormone levels in both animals and humans. Like pralmorelin and GHRP-6, ipamorelin does not affect prolactin, FSH, LH or TSH levels. However, unlike GHRP2 and GHRP6, but as growth hormone-releasing hormone (GHRH), ipamorelin does not stimulate the secretion of adrenocorticotropic hormone (ACTH) or cortisol, and is highly selective for inducing the secretion only of GH.

GDF8 is a member of the bone morphogenetic protein (BMP) family and the TGF-beta superfamily. This group of proteins is characterized by a polybasic proteolytic processing site which is cleaved to produce a mature protein containing seven conserved cysteine residues. The members of this family are regulators of cell growth and differentiation in both embryonic and adult tissues. This gene is thought to encode a secreted protein which negatively regulates skeletal muscle growth.

Gastric Inhibitory Polypeptide (GIP) which is a significant hormone of the enteroinsular axis has a functional profile of possible therapeutic value for type 2 diabetes. GIP is an important incretin hormone released into the circulation from endocrine K-cells of the duodenum and jejunum after ingestion of food1. GIP was evaluated for his ability to elevate cellular cAMP production. GIP promotes plasma triglyceride clearance in response to oral fat loading.

GDF15 is part of the TGF-Beta superfamily which is involved in regulating inflammatory and apoptotic pathways in injured tissues and throughout disease processes. GDF15 is most abundant in the liver. Its expression in liver can be considerably up-regulated in during injury of organs such as liver, kidney, heart and lung. GDF-15 promotes proliferation or growth arrest and differentiation due to differences in cellular differentiation. GDF15 prevents apoptosis in cerebellar granule neurons by activating Akt and inhibiting endogenously active ERK. GDF15 is a novel autocrine/endocrine factor that antagonizes the hypertrophic response and loss of ventricular performance.

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.

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. MCSF induces cells of the monocyte/macrophage lineage. MCSF plays a role in immunological defenses, bone metabolism, lipoproteins clearance, fertility and pregnancy.

NAPA is part of the SNAP (Soluble NSF Attachment Protein) family. SNAPs, acting together with SNAREs (SNAP receptors) and the N-ethylmaleimide-sensitive fusion protein (NSF), are necessary for the fusion of transport vesicles to their objective membranes in synaptic transmission, intra-Golgi transport, endosome-to-endosome fusion and transcytotic vesicles-to-plasma membrane transport. NAPA is in charge of the binding of NSF and therefore the formation of a 20S fusion particle.

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).

SNRPF is a member of the snRNP Sm proteins family. There are at least seven isoforms, E, F, G, D1, D2, D3 and B/B. This type of common proteins have a crucial part in the biogenesis of the snRNPs. Moreover, they represent the major targets for the so-called anti-Sm auto-antibodies that are diagnostic for systemic lupus erythematosus (SLE). SNRPF assist in the cytoplasmic construction of the UsnRNPs by binding to aconserved Sm site on UsnRNA and forming a stable snRNP core complex.