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IFN regulatory factor 2 is a member of the IFN regulatory transcription factor (IRF) family. IRF2 competitively inhibits the IRF1-mediated transcriptional activation of IFNs alpha and beta, and presumably other genes that employ IRF1 for transcription activation. However, IRF2 also functions as a transcriptional activator of histone H4. IRF2 binds to the upstream regulatory region of type-1 IFN and IFN-inducible MHC class-1 genes (the IFN consensus sequence (ics) and represses those genes.

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.

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.

Ubiquitin-conjugating enzyme E2 H (UBE2H) is a member of the ubiquitin-conjugating enzyme family. Protein modification with ubiquitin is a vital cellular apparatus for directing abnormal or short-lived proteins for degradation. Ubiquitination requires at least 3 classes of enzymes: ubiquitin-activating enzymes (E1s) ubiquitin-conjugating enzymes (E2s) and ubiquitin-protein ligases (E3s). UBE2H receives ubiquitin from the E1 complex and catalyzes its covalent attachment to other proteins. UBE2H protein sequence is 100% identical to the mouse homolog and 98% identical to the frog and zebrafish homologs.

UBE2K belongs to the ubiquitin-conjugating enzymes family which take part in many cellular processes such as selective protein degradation, DNA repair, cell cycle control, and sporulation. In this mechanism, the ATP-coupled activation and subsequent ligation of ubiquitin are catalyzed by separate enzymes functionally linked by ubiquitin carrier protein UBC1. In addition, UBE2K is involved in Alzheimer's disease, Huntington's disease and antigen processing through its interaction with amyloid-?, huntingtin, and MHC-heavy chain proteins.

UbcH12 is functional in in vitro NEDDylation reactions. It has been shown to form a thioester linkage with NEDD8 in the presence of the NEDD8 activating enzyme complex Uba3/APP-BP1. APP-BP1 binds to the amyloid precursor protein (APP) carboxy terminal domain and is important in conjunction with Uba3 and UbcH12 in driving cells through the S to M checkpoint. It was demonstrated to be the E2 responsible for the NEDDylation of the Cul-1 component of the SCF (?-TRCP) complex which is important as the E3-ligase in the ubiquitinylation of I?B?. NEDDylation of Cul-1 is essential for conjugation and processing of NF-?B p105 by SCF (?-TRCP) following phosphorylation of the complex. A dominant negative form of UbcH12, previously demonstrated to sequester NEDD8 and inhibit its conjugation, inhibits both conjugation and processing of p105, which is alleviated by wild-type UbcH12.

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.

CRABP1 is a member of special carrier proteins for members of the vitamin A family. It is believed that CRABP1 has an essential role in retinoic acid-mediated differentiation and proliferation processes. Though, CRABP1 is structurally similar to the cellular retinol-binding proteins, it binds only retinoic acid at specific sites within the nucleus, which may contribute to vitamin A-directed differentiation in epithelial tissue. CRABP1 is constitutively expressed and is thought to have different functions in the cell than the related CRABP2. CRABP1 forms a beta-barrel structure which accommodates hydrophobic ligands in its interior.
Loss of CRABP1 function as a result of hypermethylation of its promoter leads to pathogenesis of papillary thyroid carcinoma. Furthermore, frequent methylation-associated silencing of CRABP1 is linked to esophageal squamous-cell carcinoma.

RERG is a 199 amino acid protein which localizes in the cytoplasm and is a member of the Ras subfamily of small GTPases. RERG is expressed in the pancreas, liver, skin, lung, brain, kidney and heart tissue. RERG is a vital mediator of diverse cell signaling pathways, including those leading to cell proliferation, cytoskeletal organization and secretion.

IFN-tau is also known as TP-1 (trophoblast protein-1) is a new class of type I IFN that is secreted by the trophoblast and is the signal for maternal recognition of pregnancy in sheep. IFN- tau has potent immunosuppressive and antiviral activities similar to other type I IFN but is less cytotoxic than IFN-alpha and IFN-beta. The current investigation concerns the effect of recombinant ovine IFN- tau (rOIFN- tau) on the modulation of MHC class I and II expression on cloned mouse cerebrovascular endothelial (CVE) cells.
IFN-tau induced tyrosine phosphorylation of Stat1 and upregulated the expression of MHC class I on CVE. One proposed action by which type I IFN reduces the relapse rate in MS is via interference with IFN-?-induced MHC class II expression. IFN- tau was shown to downregulate IFN-?-induced MHC class II expression on CVE and, hence, may be of potential therapeutic value in downregulating inflammation in the central nervous system (CNS). IFN- tau did not upregulate the expression of MHC class II on CVE. IFN- tau also inhibited the replication of Theiler's virus in CVE.

ANXA1 is part of the family of Ca(2+)-dependent phospholipid binding proteins which have a Mw between 35kDa-40kDa and are situated on the cytosolic face of the plasma membrane. ANXA1 protein has a Mw of 40kDa, with phospholipase A2 inhibitory activity to bind from two to four calcium ions with high affinity. Since phospholipase A2 is necessary for the biosynthesis of the potent mediators of inflammation, prostaglandins and leukotrienes, ANXA1 might have potential anti-inflammatory activity. ANXA1 promotes membrane fusion and iplays a role in exocytosis. The recognition of ANXA1 protein by immunocytochemical leads a simple, highly sensitive and specific assay for diagnosis of hairy cell leukemia.

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. By injecting soluble RANKL, novel osteopenia model mice were established in only 50 hours. Degree of bone loss can be controlled by changing doses of sRANKL. RANKL can be used in establishing osteopenia model for in vivo screening of drugs for osteoporosis, determination of effect and mechanism, evaluation of bone anabolic drugs.

Basigin Isoform 2 or BSG is a part of the immunoglobulin superfamily, it is a type 1 transmembrane protein which has a variety of Nand O- glycosylation. BSG has several ligands, such as integrins, cyclophilin proteins Cyp-A & CyP-B. The protein has a crucial role in intercellular recognition, it takes part in many immunologic processes, differentiation and cell development. Also, it regulates numerus cell processes such as production and release of expression of the mono-carboxylate transporter, spermatogenesis, etc. Basigin Isoform 2 promotes invasion, metastasis, growth and survival of malignant cells by producing and releasing matrix metalloproteinases nearby mesenchymal cells and tumor cells.

Enteropeptidase or enterokinase is an enzymeinvolved in human digestion. It is produced by cells in the duodenum wall, and is secreted from duodenum's glands, the crypts of Lieberk?hn, whenever ingested food enters the duodenum from the stomach. Enteropeptidase has the critical job of turning trypsinogen(a zymogen) to trypsin, indirectly activating a number of pancreaticdigestive enzymes.
Enteropeptidase is a serine proteaseenzyme(EC3.4.21.9). Enteropeptidase is a part of the Chymotrypsin-clan of serine proteases, and is structurally similar to these proteins.

NUDT10 belongs to the Nudix hydrolase family of pyrophosphatases. Nudix hydrolases contain a characteristic Nudix domain and are responsible for catalyzing the hydrolysis of nucleoside diphosphate derivatives. NUDT10 functions as a manganese-dependent polyphosphate phosphohydrolase with an optimum pH of 8.5. NUDT10 protein specifically metabolizes diadendosine-polyphosphates and, to a lesser extent, diphosphoinositol polyphosphates.

Ganglioside GM2 activator (GM2A) is a small glycolipid transport protein which functions as a substrate specific co-factor for the lysosomal enzyme beta-hexosaminidase A. GM2A participates in lipid metabolism. GM2A protein is localized in lysosomes. The GM2A protein forms a large binding pocket for a number of single chain phospholipids and fatty acids. GM2A demonstrates calcium-independent phospholipase activity. GM2A stimulates ganglioside GM2 degradation by presenting GM2 to beta-hexosaminidase A. The Beta-hexosaminidase A, along with GM2A, catalyzes the degradation of the ganglioside GM2, and other molecules containing terminal N-acetyl hexosamines. GM2A gene mutations result in GM2-gangliosidosis type AB or the AB variant of Tay-Sachs disease.

CD59 is a cell surface glycoprotein which regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. CD59 is an effective inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the compilation of this complex, thus inhibiting the incorporation of multiple copies of C9 into the complex, which is essential for osmolytic pore formation. In addition, CD59 has a role in signal transduction pathways in the activation of T cells. CD59 gene mutations cause CD59 deficiency, a disease resulting in hemolytic anemia and thrombosis, and which causes cerebral infarction.

IFN-alpha 1b is produced by macrophages, IFN-alpha 1b has antiviral activities and stimulates the production of two enzymes: a protein kinase and an oligoadenylate synthetase.

Mitogen-activated protein kinase 1 (MAPK1) is also known as "extracellular signal-regulated kinase 2" (ERK2). Two similar (85% sequence identity) protein kinases were originally called ERK1 and ERK2. They were found during a search for protein kinases that are rapidly phosphorylated after activation of cell surface tyrosine kinasessuch as the epidermal growth factor receptor. Phosphorylation of ERKs leads to the activation of their kinase activity.
The molecular events linking cell surface receptors to activation of ERKs are complex. It was found that RasGTP-binding proteins are involved in the activation of ERKs. Another protein kinase, Raf-1, was shown to phosphorylate a "MAPK kinase", thus qualifying as a "MAPK kinase kinase". The MAPK kinase was named "MAPK/ERK kinase" (MEK).
Receptor-linked tyrosine kinases, Ras, Raf, MEK and MAPK could be fitted into a signaling cascade linking an extracellular signal to MAPK activation.
Transgenic gene knockoutmice lacking MAPK1 have major defects in early development.

PNMT is an enzyme located in the adrenal medulla and it catalyzes the final step of the catecholamine biosynthesis pathway. PNMT has beta-carboline 2N-methyltransferase activity. PNMT takes part in regulating epinephrine production. Glucocorticoid receptors form multimers of PNMT independent of the DNA binding domain. PNMT expression is regulated late in mouse gestation by AP2-alpha and glucocorticoids.

The somatomedins, or IGFs, comprise a family of peptides that play important roles in mammalian growth and development. IGF1 mediates many of the growth-promoting effects of GH. Early studies showed that GH 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. Three main somatomedins have been characterized: somatomedin C (IGF1), somatomedin A (IGF2), and somatomedin B.

General Transcription Factor IIF Polypeptide 2 (GTF2F2) is a general transcription initiation factor which binds to RNA polymerase II and helps engage it in the initiation complex in collaboration with TFIIB. GTF2F2 promotes transcription elongation. GTF2F2 shows ATP-dependent DNA-helicase activity.

ATF1, a cyclic-AMP dependent transcription factor, is expressed in a large selection of cell types and can dimerize with CREB. MSK1 and MSK2 protein kinases are essential for the stress-induced phosphorylation of transcription factors CREB and ATF1 in primary embryonic fibroblasts. Epidermal growth factor induction of c-jun expression needs ATF1 and MEF2 sites in the c-jun promoter.