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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 1124 amino acid (aa) residue precursor protein with an 18 residue putative signal peptide, a 727 residue extracellular domain and a 354 residue cytoplasmic domain. Whereas two ligands have been described for TIE-2 [angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2)], so far no ligand was found for TIE-1.

Eosinophil lysophospholipase (CLC) acts on biological membranes to regulate the multifunctional lysophospholipids. CLC is a lysophospholipase expressed in eosinophils and basophils. CLC hydrolyzes lysophosphatidylcholine to glycerophosphocholine and a free fatty acid. The CLC protein may possess carbohydrate or IgE-binding activities. CLC is both structurally and functionally related to the galectin family of beta-galactoside binding proteins. CLC may be linked with inflammation and some myeloid leukemias.

Galectins are a family of animal lectins with an affinity for beta-galactosides. This family has at least 14 identified members. Galectins share similarities in the CRD (the carbohydrate recognition domain). Galectins are synthesized as cytosolic proteins. Though localized principally in the cytoplasm and lacking a classical signal peptide, galectins can also be stimulated to secretion by non-classical pathways or alternatively targeted to the nucleus. Galectins are involved in modulating cell-cell and cell-matrix interactions. Human Galectin-7 belongs to the prototypical Galectins containing a single CRD, which is initially identified in human epidermis as a monomer. The Galectin-7 expression is induced by tumor suppressor protein p53 and associated with apoptosis. Galectin-7 is a pro-apoptotic protein which functions intracellularlly upstream of JNK activation and mitochondrial cytochrome c release. The correlation of Galectin-7 with the UV-induced apoptosis of keratinocytes presents a critical mechanism in the maintenance of epidermal homeostasis. Human Galectin-7 is localized in both nucleus and cytoplasm.

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.

Caused by one of four closely related virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. In cell culture experiments and mice Morpholino antisense oligos have shown specific activity against Dengue virus.

Caused by one of four closely related virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. In cell culture experiments and mice Morpholino antisense oligos have shown specific activity against Dengue virus.

HEXA is the alpha subunit of the lysosomal enzyme beta-hexosaminidase which, combined with the cofactor GM2 activator protein, catalyzes the degradation of the ganglioside GM2, and other molecules having N-acetyl hexosamines terminus. The two subunits composing Beta-hexosaminidase, alpha and beta, belong to the glycosyl hydrolases family and are encoded by distinct genes. Alpha subunit gene mutations can cause Tay-Sachs disease (GM2-gangliosidosis type I).

SDF-1 (stromal cell-derived factor-1) is small cytokine belonging to the chemokine family that is officially designated Chemokine (C-X-C motif) ligand 12 (CXCL12). It is produced in two forms, SDF-1?/CXCL12a and SDF-1?/CXCL12b, by alternate splicing of the same gene. Chemokines are characterized by the presence of four conserved cysteines, which form two disulfide bonds. The CXCL12 proteins belong to the group of CXC chemokines, whose initial pair of cysteines are separated by one intervening amino acid. CXCL12 is strongly chemotactic for lymphocytes and has been implicated as an important cell co-ordinator during development. During embryogenesis it directs the migration of hematopoietic cells from foetal liver to bone marrow. Mice which were knocked-out for CXCL12 gene were lethal before the birth or within just 1 hour of life. As another role, CXCL12a alters also the electrophysiology of neurons. CXCL12 was shown to be expressend in many tissues in mice (including brain, thymus, heart, lung, liver, kidney, spleen and bone marrow).
The receptor for this chemokine is CXCR4, which was previously called fusin. This CXCL12-CXCR4 interaction used to be considered exclusive (unlike for other chemokines and their receptors), but recently it was suggested that CXCL12 is also bound by CXCR7 receptor.
The gene for CXCL12 is located on human chromosome 10. In human and mouse both CXCL12 and CXCR4 show high identity of sequence: 99% and 90%, respectively.

Alpha 1 ACT is an early-stage acute-phase plasma protein and a serpin that preferentially inactivates chymotrypsin, cathepsin G, and chymase. Alpha-1-ACT, a serine protease inhibitor, is tightly associated with amyloid plaques in Alzheimer's disease (AD) and in normal aged human and monkey brain.
Regulation of the serine proteases and serine protease inhibitors plays an important role in neuromuscular differentiation. Prostate specific antigen (PSA), a chymotrypsin-like serine protease, is predominantly complexed to Alpha-1-ACT.

IFT20 is a fragment of intraflagellar transport (IFT) elements which takes part in ciliary process assembly. IFT20 is involved in the transferring of ciliary membrane proteins from the Golgi complex to the cilium and is expressed in virtually all tissues.

Transgelin 2 (TAGLN2) is one of the earliest markers of differentiated smooth muscle. TAGLN2 contains a calponin like repeat and a calponin-homology (CH) domain. TAGLN2 is downregulated in some transformed cell lines, indicating that a reduction of transgelin expression may be an early indicator of the onset of transformation. TAGLN2 also binds actin, causing actin fibers to gel within minutes of binding. The binding of transgelin to actin occurs at a ratio of 1:6 actin monomers.

LGALS2 is a soluble beta-galactoside binding lectin that controls cell-to-cell adhesion and cell-to-extracellular matrix interactions and takes part in tumor progression, pre-mRNA splicing and apoptosis. LGALS2 induces apoptosis in activated T cells and binds to the cytokine lymphotoxin-alpha (LTA) with threat of myocardial infarction.

MDC (CCL22) is a small cytokine that belongs to the CC chemokine family. CCL22 is one of several Cys-Cys (CC) cytokine genes clustered on the q arm of chromosome 16.
MDC shows chemotactic activity for natural killer cells, chronically activated T lymphocytes, monocytes and dendritic cells. On the other hand, MDC shows a mild activity for primary activated T lymphocytes and has no chemoattractant activity for neutrophils, eosinophils and resting T lymphocytes. MDC may also have a role in the trafficking of activated T lymphocytes to inflammatory sites and other aspects of activated T lymphocyte physiology. MDC interacts with cell surface chemokine receptors CCR4.
CCL22 is vastly expressed in macrophage and in monocyte-derived dendritic cells, and thymus. CCL22 is also found in the lymph node, appendix, activated monocytes, resting and activated macrophages. Lower expression of CCL22 can be seen in the lung and the spleen and very weak expression in the small intestine. In the lymph node CCL22 is expressed in a mature subset of Langerhans' cells (CD1a+ and CD83+).
Furthermore, CCL22 is expressed in atopic dermatitis, allergic contact dermatitis skin, and psoriasis, in both the epidermis and dermis. In addition, MDC has a role in hindering progression of lung cancer. Moreover, significantly higher CCL22 expression is linked to gastric cancer.

Interleukin-22 (IL-22), also known as IL-10-related T cell-derived inducible factor (IL-TIF) was initially identified as a gene induced by IL-9 in mouse T cells and mast cells. Mouse IL-22 cDNA encodes a 179 amino acid residue protein with a putative 33 amino acids signal peptide that is cleaved to generate a 147 aa mature protein that shares approximately 79% and 22% aa sequence identity with human IL-22 and IL-10, respectively. IL-22 has been shown to activate STAT-1 and STAT-3 in several hepatoma cell lines and upregulate the production of acute phase proteins. IL-22 is produced by normal mouse T cells upon Con A activation. Mouse IL-22 expression is also induced in various organs upon lipopolysaccharide injection, suggesting that IL-22 may be involved in inflammatory responses. The functional IL-22 receptor complex consists of two receptor subunits, IL-22R (previously an orphan receptor named CRF2-9) and IL-10Rβ (previously known as CRF2-4), belonging to the class II cytokine recep

SERPINA1 is secreted and is a serine protease inhibitor which its targets include elastase, plasmin, collagenase, leucocytic proteases, trypsin, chymotrypsin, and plasminogen activator. Defects in SERPINA1 gene can cause emphysema or liver disease. SERPINA1 is an endogenous inhibitor of serine proteases and inhibits the catalytic domain of human recombinant matriptase in vitro. Rise in SERPINA1 occurs as an acute phase response to tissue necrosis and inflammation. mutations in SERPINA1 and SLC11A1 genes change the balance between elastase produced by leukocytes during phagocytosis.

Fucosidase Alpha-L- 1 Plasma, also known as FUCA1 is a member of the glycosyl hydrolase 29 family which is responsible for hydrolyzing the alpha-1,6-linked fucose joined to the reducing-end N-acetylglucosamine of the carbohydrate moieties of glycoproteins. Fucosidosis is an autosomal recessive lysosomal storage disease caused by the absence of alpha-L-fucosidase activity.

Human immunodeficiency virus (HIV) is a retrovirusthat can lead to a condition in which the immune systembegins to fail, leading to opportunistic infections. HIV primarily infects vital cells in the humanimmune systemsuch as helper T cells(specifically CD4+ T cells), macrophagesand dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosisin infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytesthat recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunityis lost, and the body becomes progressively more susceptible to opportunistic infections. HIV was classified as a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry of the target cell, the viral RNA genomeis converted to double-stranded DNAby a virally encoded reverse transcriptasethat is present in the virus particle. This viral DNA is then integrated into the cellular DNA by a virally encoded integraseso that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latentand the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells.

Caused by one of four closely related virus serotypes of the genus Flavivirus, family Flaviviridae, each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. In cell culture experiments and mice Morpholino antisense oligos have shown specific activity against Dengue virus.

Peroxisome proliferators are non-genotoxic carcinogens which are purported to exert their effect on cells through their interaction with members of the nuclear hormone receptor family termed peroxisome proliferators activated receptors (PPARs). Nuclear hormone receptors are ligand-dependent intracellular proteins that stimulate transcription of specific genes by binding to specific DNA sequences following activation by the appropriate ligand. Studies indicate that PPARs are activated by peroxisome proliferators such as clofibric acid, nafenopin, and WY-14,643, as well as by some fatty acids.

Zika virus (ZIKV) belongs to the family Flaviviridae and the genus Flavivirus, it is transmitted by daytime-active Aedes mosquitoes, such as A. aegypti and A. albopictus. The Zika virus is related to the dengue, yellow fever, Japanese encephalitis, and West Nile viruses. Much like the other flaviviruses, Zika virus is enveloped and icosahedral and has a nonsegmented, single-stranded, positive-sense RNA genome. Zika fever is an infection, which often causes no symptoms or only mild ones, like a mild form of dengue fever, and it is treated by rest. As of February 2016, there has been mounting evidence that Zika fever in pregnant women can cause abnormal brain development in their fetuses by mother-to-child transmission, which may result in miscarriage or microcephaly, however it is not yet known whether Zika virus causes microcephaly. Furthermore, a connection has been established with neurologic conditions in infected adults, including Guillain–Barre syndrome.