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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.

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.

Chemokine (C-C motif) ligand 18 (CCL18) is a small cytokine belonging to the CC chemokine family that was previously called PARC (pulmonary and activation-regulated chemokine). CCL18 is approximately 60% identical in amino acid sequence to CCL3. It is expressed at high levels in lung and at lower levels in certain lymphoid tissues, such as the lymph nodes, and is chemotactic for activated T cells and non activated lymphocytes. The gene for human CCL18 contains three exons and is located on chromosome 17.

Short/branched chain specific acyl-CoA dehydrogenase (ACADSB) belongs to the acyl-CoA dehydrogenase family of enzymes which catalyze the dehydrogenation of acyl-CoA derivatives in the metabolism of fatty acids or branch chained amino acids. ACADSB catalyzes the degradation of L-isoleucine while having the highest affinity for (s)-2-methylbutyryl-CoA, isobutyryl-CoA and 2-methylhexanoyl-CoA as substrates. ACADSB may use valproyl-CoA as substrate. ACADSB gene defects cause the short/branched-chain acyl-CoA dehydrogenase deficiency (SBCADD), which is an autosomal recessive disorder characterized by an increase of 2-methylbutyrylglycine and 2-methylbutyrylcarnitine in blood and urine.

Synovial Sarcoma, X Breakpoint 1 (SSX1) is a member of a family of highly homologous synovial sarcoma X (SSX) breakpoint proteins. SSX proteins are localized to the nucleus and expressed in testis and some types of cancers and, hence, they are classified as C/T (cancer/testis) antigens. These proteins may serve as transcriptional repressors. SSX1 genes are involved in the t (X;18) translocation typically found in all synovial sarcomas. This translocation leads to the fusion of the synovial sarcoma translocation gene on chromosome 18 to one of the SSX genes on chromosome X. These hybrid proteins are most likely responsible for transforming activity.

WIF1 binds to wnt proteins and inhibits their activities. WIF1 plays a role in mesoderm segmentation. WNT proteins are extracellular signaling molecules that take part in the control of embryonic development & cancer. WIF1 protein contains a WNT inhibitory factor (WIF) domain and 5 epidermal growth factor (EGF)-like domains. WIF1 takes part in mesoderm segmentation. WIF1 protein is found to be present in fish, amphibia and mammals. WIF1 is a recurrent target in human salivary gland oncogenesis. Downregulation of WIF1 takes part in the development and progression of pleomorphic adenomas. WIF1 is a tumor suppressor, specifically in nonfunctioning pituitary tumors.

Alpha-synuclein or SNCA is a synuclein protein. SNCA mainly found in the brain, small concentration of the protein can also be located in other tissues such as heart and muscle. When looking in the brain tissue, SNCA is located in the end of the neuron, in an area called presynaptic terminal. In the presynaptic terminal SNCA has interaction with phospholipids & other proteins. Neurotransmitters are released from the synaptic vesicles in the Presynaptic terminals and act as messengers. Once released, the neurotransmitters send signals across the neurons that are crucial for the brain’s operation.

Enhancer of rudimentary homolog (ERH) is a ubiquitously expressed transcriptional coregulator which is highly conserved among eukaryotes. ERH may have a role in cell cycle regulation and pyrimidine biosynthesis. ERH has two casein kinase II phosphorylation sites which are thought to upset the ability of ERH to dimerize.

Syntaxin 4 (STX4) is a member of the syntaxin/epimorphin family of proteins. The Syntaxin family is cellular receptors for transport vesicles which participate in exocytosis in neutrophils. Syntaxin 4 is vital for normal regulation of glucose metabolism uptake in skeletal muscle and decline in STX4 protein levels lead to reduction of whole-body hormone-stimulated glucose metabolism. STX4 is expressed in neutrophils and neutrophil-differentiated HL-60 cells. The STX4 expression in neutrophils increases with differentiation.

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.

GMFB is part of the GMF subfamily of the larger actin-binding protein ADF family. GMFB is phosphorylated after phorbol ester stimulation, and is crucial for the nervous system. GMFB causes brain cell differentiation, stimulates neural regeneration and inhibits tumor cell proliferation. GMFB overexpression in astrocytes results in the increase of BDNF production. GMFB expression is increased by exercise, thus BDNF is important for exercise-induction of BDNF.

Salmonella Typhi is a pathogen causing typhoid fever, affecting over 17 million people with approximately 600,000 deaths annually worldwide. If untreated, typhoid fever cases result in mortality rates ranging from 12-30%.

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.

Borrelia belongs to a genus of bacteria of the spirochete phylum. Borrelia causes borreliosis, which is a zoonotic, vector-borne disease transmitted mainly by ticks and some by lice, depending on the species. Of the 36 known species of Borrelia, 12 are distinguished to cause Lyme disease or borreliosis and are transmitted by ticks. The main Borrelia species causing Lyme disease are Borrelia burgdorferi, Borrelia afzelii, and Borrelia garinii. The Borrelia genus members have a linear chromosome which is about 900 kbp in length as well as an excess of both linear and circular plasmids in the 5-220 kbp size range. The plasmids are atypical, as compared to most bacterial plasmids, since they contain many paralogous sequences, a large number of pseudogenes and, in some cases, essential genes. Moreover, a number of the plasmids have features suggesting that they are prophages.

The secreted polypeptide noggin, encoded by the NOG gene, binds and inactivates members of the transforming growth factor-beta (TGF-beta) superfamily signaling proteins, such as bone morphogenetic protein-4 (BMP4). By diffusing through extracellular matrices more efficiently than members of the TGF-beta superfamily, noggin may have a principal role in creating morphogenic gradients. Noggin appears to have pleiotropic effect, both early in development as well as in later stages. It was originally isolated from Xenopus based on its ability to restore normal dorsal-ventral body axis in embryos that had been artificially ventralized by UV treatment. The results of the mouse knockout of noggin suggest that it is involved in numerous developmental processes, such as neural tube fusion and joint formation. Recently, several dominant human NOG mutations in unrelated families with proximal symphalangism (SYM1) and multiple synostoses syndrome (SYNS1) were identified; both SYM1 and SYNS1 have multiple joint fusion as their principal feature, and map to the same region (17q22) as NOG. All NOG mutations altered evolutionarily conserved amino acid residues. The amino acid sequence of human noggin is highly homologous to that of Xenopus, rat and mouse.

Poliovirus receptor, also known as PVR, is a Type I transmembrane glycoprotein which belongs to the immunoglobulin superfamily. PVR catalyzes a big structural modification in the virus which exposes membrane-binding protein chains. PVR regulates helper T cell differentiation as well as allergic diseases. PVR is expressed in many kinds of human cells and has various functions. PVR is potentially functional as a biomarker for cancer development as well as progression. PVR takes a vital part through both immunological & non-immunological mechanisms in pancreatic cancer.

Glycerol-3-phosphate dehydrogenase 1-like protein (GPD1L) converts sn-glycerol 3-phosphate to glycerone phosphate. GPD1L is found in the cytoplasm, associated with the plasma membrane, where it binds the sodium channel, voltage-gated, type V, alpha subunit (SCN5A). Mutations in the GPD1L gene are the cause of SIDS (sudden infant death syndrome) and Brugada syndrome type 2 (an autosomal dominant tachyarrhythmia).

NT3 a member of the neurotrophin family, that controls survival and differentiation of mammalian neurons. This protein is closely related to both nerve growth factor and brain-derived neurotrophic factor. It may be involved in the maintenance of the adult nervous system, and may affect development of neurons in the embryo when it is expressed in human placenta. NTF3-deficient mice generated by gene targeting display severe movement defects of the limbs. The mature peptide of this protein is identical in all mammals examined including human, pig, rat and mouse.

E-cadherin (uvomorulin, cell-CAM120/80) is a calcium dependent cell adhesion molecule expressed predominately in epithelial tissues. It plays an important role in the growth and development of cells via the mechanisms of control of tissue architecture and the maintenance of tissue integrity. Numerous studies have demonstrated that reduction and/or loss of Ecadherin expression in carcinomas correlates positively with the potential of these tumors for invasion and metastasis.

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.

SAA4 is a constitutively expressed protein which is a member of the SAA family. SAA4 is a major acute phase reactant and an apolipoprotein of the HDL complex. SAA4 is constitutively expressed only in humans and mice; it is connected almost completely with lipoproteins of the high density range. The physiological function of SAA4 is unknown, and its serum concentration has no association with those of other major apolipoproteins. SAA4 mRNA and protein occurrence in macrophage derived foam cells of coronary and carotid arteries implied a specific role of human SAA4 during inflammation including atherosclerosis.

SLAMF7 belongs to the CS2 family of cell surface receptors. SLAMF7 is a single-pass type 1 membrane protein, SLAMF7 Isoform 1 mediates NK cell activation via aSH2D1A-independent extracellular signal-regulated ERK-mediated pathway. SLAMF7 functions in lymphocyteadhesion. Furthermore, SLAMF7 can exert activating of inhibitory influences on cells of the immune system depending on cellular context as well as the availability of effector proteins.

Borrelia belongs to a genus of bacteria of the spirochete phylum. Borrelia causes borreliosis, which is a zoonotic, vector-borne disease transmitted mainly by ticks and some by lice, depending on the species. Of the 36 known species of Borrelia, 12 are distinguished to cause Lyme disease or borreliosis and are transmitted by ticks. The main Borrelia species causing Lyme disease are Borrelia burgdorferi, Borrelia afzelii, and Borrelia garinii. The Borrelia genus members have a linear chromosome which is about 900 kbp in length as well as an excess of both linear and circular plasmids in the 5-220 kbp size range. The plasmids are atypical, as compared to most bacterial plasmids, since they contain many paralogous sequences, a large number of pseudogenes and, in some cases, essential genes. Moreover, a number of the plasmids have features suggesting that they are prophages.