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D-gluconate kinase or idnk is a thermosensitive protein, consists of 187 a.a and part of the gluconokinase gntK/gntV protein family. Idnk enhances the conversion of ATP + D-gluconate => ADP + 6-phospho-D-gluconate. Idnk has a crucial part in determination of gender, removal of a certain portion of 9p may result in the making of male to female (reversal of sex), that leads to a female that has the genotype of male X, Y.

Lymphotoxin alpha, a member of the tumor necrosis factor family, is a cytokine produced by lymphocytes. LTA is highly inducible, secreted, and exists as homotrimeric molecule. LTA forms heterotrimers with lymphotoxin-beta which anchors lymphotoxin-alpha to the cell surface. LTA mediates a large variety of inflammatory, immunostimulatory, and antiviral responses. LTA is also involved in the formation of secondary lymphoid organs during development and plays a role in apoptosis.

CDKN1A holds a key part in the cellular response to DNA mutation. CDKN1A overexpression causes cell cycle to stop. When collaborating with CDK2 complexes, CDKN1A aids to prevent kinase activity and inhibits progression through G1/S. Nevertheless, CDKN1A can additionally increase assembly and activity in complexes of CDK4 or CDK6 and cyclin D. CDKN1A is a vital intermediary by which p53/TP53 facilitates its part as an inhibitor of cellular proliferation as a reaction to DNA impairment.

TNF-related apoptosis-inducing ligand (TRAIL) is a ligand molecule which induces apoptosis. It is a type II transmembrane protein with homology to other members of the tumor necrosis factor family.
In humans, the gene that encodes for TRAIL is located at chromosome 3q26.
TRAIL binds to the death receptors, DR4 and DR5. The process of apoptosis is caspase-8-dependent. This protein preferentially induces apoptosis in transformed and tumor cells, but does not appear to kill normal cells although it is expressed at a significant level in most normal tissues.

Inhibitor of DNA Binding 1 (ID1) is a helix-loop-helix protein which can form heterodimers with members of the basic HLH family of transcription factors. ID1 is lacking DNA binding activity and thus can inhibit the DNA binding and transcriptional activation ability of basic HLH proteins with which it interacts. ID1 participates in cell growth, senescence, and differentiation.

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.

Beta Defensin 116, also known as DEFB116 is a member of the beta-defensin family.DEFB116 has antibacterial activity. The innate immune system includes antimicrobial peptides that protect multicellular organisms from a diverse spectrum of microorganisms. In addition, Beta-Defensins contain one important family of mammalian antimicrobial peptides.

Aurora Kinase B (AURKB) belongs to a family of mitotic serine/threonine kinases. AURKB connects with chromosomes for the period of prophase prior to relocalizing to the spindle at anaphase. AURKB localizes to microtubules near kinetochores, specifically to the specialized microtubules called K-fibers. AURKB controls chromosome segregation through the control of microtubule-kinetochore attachment and cytokinesis. AURKB is required for kinetochore localization of BUB1 and SGOL1. AURKB expression during the G2/M phase transition is firmly coordinated with histone H3 phosphorylation, while overexpression is seen in many kinds of cancers. AURKB phosphorylates 'Ser-10' and 'Ser-28' of histone H3 during mitosis. AURKB is a component of the CPC (chromosomal passenger complex), which is a complex that acts as a key regulator of mitosis.
High level expression of AURKB is seen in the thymus, which is also expressed in the spleen, lung, testis, colon, placenta and fetal liver. AURKB is expressed during S and G2/M phase and expression is up-regulated in cancer cells during M phase.

Herpesvirus entry mediator or HVEM or tumour necrosis factor receptor superfamily member 14 or TNFRSF14, is part of the TNF receptors family that is a receptor located on the cell surface. The cytoplasmic area of this receptor can bind all sorts of TNF receptor associated factor (TRAF) protein. Those proteins can mediate pathways activating an immune response. The MITF is regulating TNFRSF14 gene expression.

Lxn also known as Latexin is a member of the protease inhibitor I47 (latexin) family. Lxn's function is hardly reversible, non-competitive, as well as potent inhibitor of CPA1, CPA2 and CPA4. Furthermore, Lxn plays a role in inflammation. Among the diseases associated with LXN are endocervicitis and listeriosis.

4-1BBR is a member of the TNF-receptor superfamily. 4-1BB receptor contributes to the clonal expansion, survival, and development of T cells.4-1BBRcan also induce proliferation in peripheral monocytes, enhance T cell apoptosis induced by TCR/CD3 triggered activation, and regulate CD28 co-stimulation to promote Th1 cell responses. The expression of this receptor is induced by lymphocyte activation. TRAF adaptor proteins have been shown to bind to this receptor and transduce the signals leading to activation of NF-kappaB.

Fibrinogen silencer-binding protein (FSBP), interacts with X11alpha. The X11alpha/FSBP complex send signals to the nucleus in order to repress glycogen synthase kinase-3beta promoter activity. X11alpha is a neuronal adaptor protein that interacts with the amyloid precursor protein (APP) via a centrally located phosphotyrosine binding domain to inhibit the production of Abeta peptide that is deposited in Alzheimer's diseased brains.

Peptidase Inhibitor 16 (PI16) which a member of the CRISP family, is a putative serine protease inhibitor. PI16 interacts with PSP94/MSMB. PI16 is expressed in the prostate, testis, ovary and intestine. It also concentrates in prostate cancer patient's sera. PI16 may serve as a marker following prostatectomy for prostate cancer.

RNH1 belongs to the proteinaceous cytoplasmic RNase inhibitors family which occur in many tissues and binds to both intracellular and extracellular RNases. In addition to control of intracellular RNases, the inhibitor may have a part in the regulation of angiogenin. The 50kDa RNH1 binds to ribonucleases and holds them in a latent form. Since neutral and alkaline ribonucleases possibly play a critical role in the turnover of RNA in eukaryotic cells, RNH1 may be vital for control of mRNA turnover; the interaction of eukaryotic cells with ribonuclease may be reversible in vivo.

Akt1, also known as Akt or else protein kinase B (PKB) is an important molecule in mammaliancellular signaling. In humans, there are three genes in the "Akt family": Akt1, Akt2, and Akt3. Moreover, these enzymes are members of the serine/threonine-specific protein kinase family (EC2.7.11.1). Akt1 is involved in cellular survival pathways, by inhibiting apoptoticprocesses. Akt1 is also able to induce protein synthesis pathways, and is therefore a key signaling protein in the cellular pathways which lead to skeletal muscle hypertrophy, and general tissue growth. Since it can block apoptosis, and thereby promote cell survival, Akt1 has been implicated as a most important factor in numerous types of cancer. Akt (now also called Akt1) was at first identified as the oncogenein the transforming retrovirus, AKT8.

SPINT2 is a transmembrane protein acts as an inhibitor of HGF activator. SPINT2 inhibits plasmin, plasma and tissue kallikrein, and factor XIa. SPINT2 has two extracellular Kunitz domains that inhibit few serine proteases. SPINT2 is assumed tumor suppressor, mutations in SPINT2 leads to a congenital sodium diarrhea.

Cytotoxicity Triggering Receptor 3 also known as NCR3 is a natural cytotoxicity receptor (NCR) which assists NK cells in the lysis of tumor cells. Moreover, NCR3 interacts with CD3-zeta (CD247), a T-cell receptor. A single nucleotide polymorphism in the 5' untranslated region of NCR3 has been related with mild malaria suceptibility. Three transcript variants encoding various isoforms have been found for this gene.

KLRC3 belongs to the NKG2 group that can be found mostly in natural killer (NK) cells and encodes a family of transmembrane proteins known for their C-type lectin domain and their type II membrane orientation (extracellular C terminus). The NKG2 gene family is situated inside the NK complex, a region which has quite a few C-type lectin genes mostly expressed on NK cells.

Neurotrophic Receptor Tyrosine Kinase 3 (NTRK3)belongs to the receptor tyrosine kinases family and is a high affinity catalytic receptor of neurotrophin NT-3. NTRK3 mediates multiple effects of this neurotrophic factor, which includes neuronal differentiation and survival. NTRK3 inducesvarious pleiotorpic responses in malignant cells, including enhanced tumor cell invasiveness and chemotoxis.Increased NTRK3 expression was observed in neuroblastoma, medulloblastoma, and in neuroectodermal brain tumors.

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.

TNFRSF14, a member of the TNF receptor superfamily, is a type I transmembrane protein. TNFRSF14 is expressed in peripheral blood T cells, B cells, monocytes and in various tissues enriched in lymphoid cells. TNFRSF14 operates as a co-stimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. Additionally, TNFRSF14 encourages the proliferation of T cells, and triggers apoptosis of various tumor cells.

Members of the Rho (or ARH) protein family and other Ras-related small GTP-binding proteins are involved in various cellular procedures, such as cell cytoskeletal organization, secretion, proliferation, and signaling. The GTPBPs are active only in the GTP-bound state. At least 3 types of proteins firmly regulate cycling between the GTP-bound and GDP-bound states: GDP-dissociation inhibitors (GDIs), GTPase-activating proteins (GAPs) and guanine nucleotide-releasing factors (GRFs). ARHGDIB and the other GDIs lower the level of GDP dissociation from Ras-like GTPases.

The cytokine Macrophage migration inhibitory factor (MIF) has been identified to be secreted by the pituitary gland and the monocyte/macrophage and to play an important role in endotoxic shock. MIF has the unique property of being released from macrophages and T cells in response to physiological concentrations of glucocorticoids. The secretion of MIF is tightly regulated and decreases at high, anti-inflammatory steroid concentration.

Interferon-beta has antiviral, antibacterial and anticancer activities.