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IL-12 is a heterodimeric cytokine that stimulates the production of IFNgamma from T-cells and natural killer cells, and also induces differentiation of Th1 helper cells. It is an initiator of cell-mediated immunity.

Recombinant Human Sonic Hedgehog is part of a small group of secreted proteins that are vital for development in both vertebrates and invertebrates. 3 mammalian hedgehog genes (sonic, desert, Indian) share about 60% homology. The Human Sonic Hedgehog is 99% homologous to the mouse gene. Sonic HedgeHog is a protein that is vital in guding the early embryo. It has been associated as the major inductive signal in patterning of the ventral neural tube, the anterior-posterior limb axis, and the ventral somites. Sonic HedgeHog binds to the patched receptor, which functions in association with smoothened, to activate the transcription of target genes. In the absence of sonic HedgeHog, patched receptor represses the constitutive signaling activity of smoothened. Sonic HedgeHog also regulates another factor, the gli oncogene. Sonic HedgeHog intercellular signal is essential for a various patterning events during development: signal produced by the notochord that induces ventral cell fate in the neural tube and somites, and the polarizing signal for patterning of the anterior-posterior axis of the developing limb bud. Sonic HedgeHog exhibits both floor plate- and motor neuron-inducing activity. Mutations in a long-range Sonic HedgeHog enhancer located in an intron of the limb region 1 gene result in preaxial polydactyly.

FKBP3 is part of a family of immunosuppressant receptors which inhibit T-cell proliferation by arresting two distinct cytoplasmic signal transmission pathways. FKBP3 accelerates the folding of proteins. FKBP3 is part of the immunophilin protein family, which participates in immunoregulation and fundamental cellular processes concerning protein folding and trafficking. FKBP3 is a cis-trans prolyl isomerase enzyme that binds the immunosuppressants FK506 and rapamycin, as well as histone deacetylases, the transcription factor YY1, casein kinase II, and nucleolin. It has a greater affinity for rapamycin than for FK506 and therefore is a significant protein for immunosuppression by rapamycin.

Hemagglutinin-Influenza A Virus H7N9 Anhui 2013 (Anhui H7N9) is a part of the influenza viruses hemagglutinin family. H7N9 Anhui is anantigenic glycoprotein which is responsible for binding the virus to the infected cell. An H7N9 virus was firstreported to have infected humans in March 2013, in China. Although the risk is low, The H7N9 virus has thegreatest potential compared with other influenza A viruses to cause a pandemicbecause like other type A viruses, it is not easily transmitted between people in its current form.

HRAS is part of the Ras oncogene family, whose members are related to the transforming genes of mammalian sarcoma retroviruses. The products encoded by these genes participate in signal transduction pathways. These proteins can bind GTP and GDP, and they have intrinsic GTPase activity. HRAS go trough a continuous cycle of de- and re-palmitoylation, which mediates its rapid exchange between the plasma membrane and the Golgi apparatus. Mutations in HRAS result in Costello syndrome, a disease characterized by increased growth at the prenatal stage, growth deficiency at the postnatal stage, predisposition to tumor formation, mental retardation, skin and musculoskeletal abnormalities, distinctive facial appearance and cardiovascular abnormalities. Defects in this HRAS gene are implicated in a range of cancers, including bladder cancer, follicular thyroid cancer, and oral squamous cell carcinoma.

CAPG is part of the gelsolin/villin family of actin-regulatory proteins. CAPG reversibly blocks the barbed ends of F-actin filaments in a Ca2+ and phosphoinositide-regulated method, though it does not separate preformed actin filaments. By capping the barbed ends of actin filaments, CAPG contributes to the control of actin-based motility in non-muscle cells. CAPG is involved in macrophage function. CAPG is involved in regulating cytoplasmic and/or nuclear structures via possible interactions with actin. CAPG binds DNA. CAPG lacks a nuclear export sequence present in structurally related proteins. CAPG is a tumor suppressor protein that plays a role in the tumorigenic progression of certain cancers. Dysregulated expression of CAPG was found in premalignant and malignant oral carcinogenesis.

JUN N-terminal Kinase 2is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. This kinase targets specific transcription factors, and thus mediates immediate-early gene expression in response to various cell stimuli. It is most closely related to MAPK8, both of which are involved in UV radiation induced apoptosis, thought to be related to the cytochrome c-mediated cell death pathway. This gene and MAPK8 are also known as c-Jun N-terminal kinases. This kinase blocks the ubiquitination of tumor suppressor p53, and thus it increases the stability of p53 in nonstressed cells. Studies of this gene's mouse counterpart suggest a key role in T-cell differentiation. Four alternatively spliced transcript variants encoding distinct isoforms have been reported.

Candida albicans is a diploid fungus, which grows both as yeast and filamentous cells and a contributory agent of opportunistic oral and genital infections in humans, and candidal onychomycosis (an infection of the nail plate). Systemic fungal infections (fungemias) including those by C. albicans are regarded as key causes of morbidity and mortality in immunocompromised patients (e.g., AIDS, cancer chemotherapy, organ or bone marrow transplantation). C. albicans biofilms may develop on the surface of implantable medical devices. C. albicans is commensal and a constituent of the normal gut flora containing microorganisms which live in the human mouth and gastrointestinal tract. Overgrowth of the fungus leads to in candidiasis (candidosis). Candidiasis is frequently detected in immunocompromised persons, including HIV-infected patients. To infect host tissue, the habitual unicellular yeast-like form of C. albicans reacts to environmental signals and changes into an invasive, multicellular filamentous form, a phenomenon which is known as dimorphism.

IL4 is a pleiotropic cytokine produced by activated T cells. IL4 is a ligand for interleukin 4 receptor. The interleukin 4 receptor also binds to IL13, which contributes to various overlapping roles of this cytokine and IL13. STAT6, a signal transducer and activator of transcription plays a main role in mediating the immune regulatory signal of this cytokine. IL4, IL3, IL5, IL13, and CSF2 form a cytokine gene cluster on chromosome 5q, with this gene particularly close to IL13. IL4, IL13 and IL5 are regulated co-ordinately by several long-range regulatory elements in an over 120 kilobase range on the chromosome.

CXADR is a component of the epithelial apical junction complex which operates as an homophilic cell adhesion molecule and is crucial for tight junction integrity. CXADR also takes part in transepithelial relocation of leukocytes through adhesive interactions with AMICA1/JAML a transmembrane protein of the plasma membrane of leukocytes. A number of transcript variants encoding different isoforms were identified for this gene. Pseudogenes of this gene were located on chromosomes 15, 18, and 21.

FKBP1A is a 12kDa protein initially discovered on an immune cells on the basis of its capability to bind as well as mediate the intracellular effect of the immunosuppressant FK506. FKBP1A is also known to mediate the action of Rapamycin-immunosuppressive agent. FKBP1A is part of the family of immunophilins, which have in common high affinity for immunosuppressant drugs and a peptidyl-prolyl cis-trans isomerase (PPIase). Activity which participates in folding of proline-containing protein. In the absence of immunosuppressive ligands, FKBP1A is involved in intracellular calcium regulation by associating with 3 types of Ca2+ release channel complexes: skeletal ryanodine receptors, cardiac ryanodine receptors and the inositol 1,4,5-triphosphate receptor. FKBP1A also interact with TGF-beta type I receptor exerting an inhibitory effect on the TGF-beta signaling pathway. FKBP12 plays a role in modulation of ryanodine receptor isoform-1 (ryr-1), a component of the calcium release channel of skeletal muscle sarcoplasmic reticulum. FKBP1A increase the folding of proteins and catalyzes the cis-trans isomerization of proline imidic peptide bonds in oligopeptides.

KGF-2 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. FGF-10 exhibits mitogenic activity for keratinizing epidermal cells, but essentially no activity for fibroblasts, which is similar to the biological activity of FGF7. Studies of the mouse homolog of suggested that this gene is required for embryonic epidermal morphogenesis including brain development, lung morphogenesis, and initiation of lim bud formation. This gene is also implicated to be a primary factor in the process of wound healing.

Phosphomannomutase 1 (PMM1) is an enzyme involved in the synthesis of the GDP-mannose and dolichol-phosphate-mannose required for a number of critical mannosyl transfer reactions. PMM1 catalyzes the conversion between D-mannose 6-phosphate and D-mannose 1-phosphate which is a substrate for GDP-mannose synthesis. GDP-mannose is used for the synthesis of dolichol-phosphate-mannose, which is crucial for N-linked glycosylation and accordingly the secretion of several glycoproteins as well as for the synthesis of glycosyl-phosphatidyl-inositol (GPI) anchored proteins. Additionally, PMM1 may be responsible for the degradation of glucose-1,6-bisphosphate in ischemic brain.

TSG101 is a member of apparently inactive homologs of ubiquitin-conjugating enzymes. TSG101 contains a coiled-coil domain that interacts with stathmin, a cytosolic phosphoprotein implicated in tumorigenesis. TSG101 is involved in cell growth and differentiation and acts as a negative growth regulator. TSG101 in vitro steady-state expression is important for maintenance of genomic stability and cell cycle regulation. TSG101 mutations and alternative splicing occur in high rate in breast cancer and implicate that defects occur during breast cancer tumorigenesis and/or progression. TSG101 is a factor of the ESCRT-I complex, a monitor of vesicular trafficking process. TSG101 binds to ubiquitinated cargo proteins and is needed for the sorting of endocytic ubiquitinated cargos into multivesicular bodies. TSG101 is needed for completion of cytokinesis and is involved in cell growth and differentiation.

IL2 is a secreted cytokine that is important for the proliferation of T and B lymphocytes. The receptor of this cytokine is a heterotrimeric protein complex whose gamma chain is also shared by interleukin 4 (IL4) and interleukin 7 (IL7). The expression of this gene in mature thymocytes is monoallelic, which represents an unusual regulatory mode for controlling the precise expression of a single gene. The targeted disruption of a similar gene in mice leads to ulcerative colitis-like disease, which suggests an essential role of this gene in the immune response to antigenic stimuli.

IL-7 is a cytokine important for B and T cell development. This cytokine and the hepatocyte growth factor (HGF) form a heterodimer that functions as a pre-pro-B cell growth-stimulating factor. This cytokine is found to be a cofactor for V(D)J rearrangement of the T cell receptor beta (TCRB) during early T cell development. This cytokine can be produced locally by intestinal epithelial and epithelial goblet cells, and may serve as a regulatory factor for intestinal mucosal lymphocytes. Knockout studies in mice suggested that this cytokine plays an essential role in lymphoid cell survival.

CBX3 takes part in transcriptional silencing in heterochromatin-like complexes. CBX3 identifies and binds histone H3 tails methylated at 'Lys-9', thereby create an epigenetic repression. Additionally, CBX3 takes part in the formation of functional kinetochore by interacting with MIS12 complex proteins.

Cyclin-G1 (CCNG1) belongs to the cyclin family and contains the cyclin box. CCNG1 may have a part in growth regulation and is associated with G2/M phase arrest in response to DNA damage. CCNG1 may be an intermediate by which p53 mediates its role as an inhibitor of cellular proliferation. The CCNG1 protein lacks the protein destabilizing (PEST) sequence which is present in other family members.

Polymerase (RNA) II (DNA directed) Polypeptide J (POLR2J) is a subunit of RNA polymerase II, the polymerase responsible for synthesizing messenger RNA in eukaryotes. The POLR2J protein occurs as a heterodimer with another polymerase subunit; together they develop a core subassembly unit of the polymerase. POLR2J is ubiquitously expressed, having a high expression in the heart and skeletal muscle.

Ras-related protein Rab-35 (RAB35) is restricted to the plasma membrane and endocytic compartments and controls a fast endocytic recycling pathway. Inhibition of Rab35 function leads to the accumulation of endocytic markers on numerous cytoplasmic vacuoles in cells that failed cytokinesis, which is consistent with a central requirement for Rab35-regulated recycling during cell division.

RAP1A is part of the family of RAS-related proteins which possess 50% amino acid identity with the classical RAS proteins and have various structural characteristics in common. RAP proteins differ from RAS proteins in their 61st amino acid, glutamine in RAS is replaced by threonine in RAP proteins. RAP1A induces morphological reversion of a cell line transformed by a Ras oncogene and counteracts the mitogenic function of Ras, since it can interact with Ras GAPs and RAF in a competitive manner.

Human immunodeficiency virus type-1 (HIV-1) regulatory Tat protein plays an crucial part in viral replication and infectivity. Throughout acute infection, Tat protein is released extracellularly by infected cells and is taken up by neighboring cells where it transactivates viral replication and inhances virus infectivity.
HIV-1 Tat activates transcription of HIV-1 viral genes by inducing phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII). Tat can also disturb cellular metabolism by inhibiting proliferation of antigen-specific T lymphocytes and by inducing cellular apoptosis. Tat-induced apoptosis of T-cells is attributed, in part, to the distortion of microtubules polymerization. LIS1 is a microtubule-associated protein that facilitates microtubule polymerization.

Human immunodeficiency virus type-1 (HIV-1) regulatory Tat protein plays an essential role in viral replication and infectivity. The HIV-1 TAT is a molecule of 86 aminoacids encoded by two exons. The product of the first exon is sufficient for the transactivation of the HIV-1 promoter. Biotin molecules can be coupled easily to either antigens (such as avidin, streptavidin, Fc binding proteins like Protein A or G) or antibodies and they can be used in a variety of detection systems.
Biotin can be conjugated to many proteins without significantly changing their biological activity. Biotin binds with high affinity to avidin, streptavidin and NeutrAvidin protein.
Every single protein can react with several molecules of biotin, each of which, in turn, can bind a molecule of avidin. This greatly increases the sensitivity of many assay procedures. The avidin-biotin interaction is the strongest known noncovalent biological interaction (Ka = 1015 M-1) between protein and ligand. The bound formation between biotin and avidin is very rapid and, once formed, withstands extremes of pH, organic solvents and other denaturing agents. The avidinbiotin complex can withstand up to 3 M guanidine•HCl. Biotin can be released by 8 M guanidine•HCl at pH 1.5, or by autoclaving.