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CFLAR contains two death effector domains (DEDs) and a caspase-like domain. CFLAR may play a critical role between cell survival and cell death pathway in mammalian cells. CFLAR also interacts with adapter protein FADD and caspase-8 and -10, and potently inhibits apoptosis induced by all known death receptors DR3 (death receptor 3), TRAIL-R (TNF-related apoptosis-inducing ligand receptor) and TNFR1 (tumor necrosis factor receptor 1).

Alveolar Soft Part Sarcoma Chromosome Region, Candidate 1 (ASPSCR1) contains a UBX domain and interacts with glucose transporter type 4 (GLUT4). ASPSCR1 is a tether, which sequesters the GLUT4 in intracellular vesicles in muscle and fat cells, and redistributes the GLUT4 to the plasma membrane. Translocation t(X;17)(p11;q25) of this ASPSCR1 with transcription factor TFE3 gene ends with a ASPSCR1-TFE3 fusion protein in alveolar soft part sarcoma and in renal cell carcinomas.

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/ macrophagemigration, 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 mitogenesisand 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 are linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.

BAALC gene is found in patients with acute myeloid leukemia and is conserved among mammals and is not found in lower organisms. Tissues which express BAALC develop from the neuroectoderm. BAALC is located both in the membrane and in the cytoplasma, it exists as multiple alternatively spliced isoform. BAALC is expressed by hematopoetic and neural cells, BAALC interacts with CaMKII? and is involved in synaptic function at postsynaptic lipid rafts. Overexpression of BAALC concomitant forecast adverse clinical outcome and defines a significant risk factor in cytogenetically normal acute myeloid leukemia (AML).

SARS Coronavirus is an enveloped virus containing three outer structural proteins, namely the membrane (M), envelope (E), and spike (S) proteins. Spike (S)-glycoprotein of the virus interacts with a cellular receptor and mediates membrane fusion to allow viral entry into susceptible target cells. Accordingly, S-protein plays an important role in virus infection cycle and is the primary target of neutralizing antibodies.
It has recently been shown that SARS (severe acute respiratory syndrome) is caused by a human coronavirus. Human coronaviruses are the major cause of upper respiratory tract illness, such as the common cold, in humans. Coronaviruses are positive-stranded RNA viruses, featuring the largest viral RNA genomes known to date (27-31 kb). The first step in coronavirus infection is binding of the viral spike protein, a 139-kDa protein, to certain receptors on host cells. The spike protein is the main surface antigen of the coronavirus. The glycosilated spike protein (as well as the nucleocapsid protein) can be detected in infected cell culture supernatants with antisera from SARS patients.

The Fas receptor (CD95) mediates apoptotic signaling by Fas-ligand expressed on the surface of other cells. The Fas-FasL interaction plays an important role in the immune system and lack of this system leads to autoimmunity, indicating that Fas-mediated apoptosis removes self-reactive lymphocytes. Fas signaling is also involved in immune surveillance to remove transformed cells and virus infected cells. Binding of FAS to oligimerized FasL on another cell activates apoptotic signaling through a cytoplasmic domain termed the death domain that interacts with signaling adaptors including FAF, FADD and DAX to activate the caspase proteolytic cascade. Caspase-8 and caspase-10 are first activated, to then cleave and activate downstream caspases, and a variety of cellular substrates that lead to cell death. Caspases cleave nuclear lamins, causing the nucleus to break down and lose its normal structure and another caspase substrate is DFF, inducing cleavage and degradation of the genome. Other caspase substrates are involved in cytoskeletal structure, cell cycle regulation and signaling pathways. Activation of JNK kinase, activation of Jun, and production of ceramide may also play roles in Fas-mediated apoptosis. Activation of fas-mediated apoptosis is opposed by I-FLICE and FAP. Viruses and tumors may escape immune surveillance in part through suppression of fas-mediated apoptosis using similar mechanisms.

SARS Coronavirus is an enveloped virus containing three outer structural proteins, namely the membrane (M), envelope (E), and spike (S) proteins. Spike (S)-glycoprotein of the virus interacts with a cellular receptor and mediates membrane fusion to allow viral entry into susceptible target cells. Accordingly, S-protein plays an important role in virus infection cycle and is the primary target of neutralizing antibodies.

SARS Coronavirus is an enveloped virus containing three outer structural proteins, namely the membrane (M), envelope (E), and spike (S) proteins. Spike (S)-glycoprotein of the virus interacts with a cellular receptor and mediates membrane fusion to allow viral entry into susceptible target cells. Accordingly, S-protein plays an important role in virus infection cycle and is the primary target of neutralizing antibodies.

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/ macrophagemigration, 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 mitogenesisand 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 are linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.

GADD45GIP1 is a nuclear protein which takes part in apoptosis control. GADD45GIP1 is expressed in several tissues, such as heart, thyroid, trachea, kidney, ovary, pancreas, testis and stomach and acts as a negative regulator of G1 to S phase cell cycle production by collaborating with GADD45 proteins to inhibit the activity of cyclin-dependent kinases.

Human norovirus is classified into two groups, group 1& group 2. Norwalk virus is the species which belongs to group 1 and was discovered in 1968 at Ohio. Norovirus is a familiar virus which causes human gastroenteritis with the following symptoms vomiting, diarrhea and sickness. CDC report revealed that there are 19-21 million Americans infected by Nororvirus annually with 800 deaths, 1 in 15 people with infection. Around the world, this virus affects about 267 million people and causes over 200,000 deaths each year; these losses are mostly in less developed countries and in the very young, elderly and immuno-suppressed population, though, most cases are self-limited with a full recovery within just a few days.Norovirus is extremely contagious and can spread from human to human through infected food, water or contaminated surfaces. The outbreaks usually occur from November-April, while the peak is in January. Norovirus is a positive sense RNA virus with 7.5 kb nucleotides, encoding a major structural protein VP1 with 50-55kDa. The full length of VP1 capsid comprises the internal N-terminal, Hinge, shell (S) and protruding (P) domains. P domain from 225 to 520 forms P1- P2-P1 structure. Moreover, P domain has a receptor binding region which recognizes human histo-blood group antigens (HBGAs). P domain expressed in bacteria can spontaneously form a P dime as well as a P particle aggregated by 12 P dimmers. P particle displays an increased binding activity to HBGAs higher than virus-like particle (VLP) formed by the full-length capsid. For norovirus vaccine development, we consider P domain as a good candidate.

TBE is caused by tick-borne encephalitis virus (TBEV), a member of the family Flaviviridae.
A closely related virus in Far Eastern Eurasia, Russian spring-summer encephalitis virus (RSSEV).
The family Flaviviridae includes other tick-borne viruses are closely related to TBEV and RSSEV, such as Omsk hemorrhagic fever virus & Kyasanur Forest virus.
Louping ill virus is also a member of this family.

HTATIP2 is part of the short-chain dehydrogenases/reductases (SDR) family which acts as a tumor suppressor in metabolic suppression, inhibition of angiogenesis and induces the expression of apoptosis related genes Bad and Siva. HTATIP2 cooperates with the activation domain of HIV-1 TAT and enhances its transcription by phosphorylating RNA polymerase II (Pol II). Defects in HTATIP2 are related with hepatocellular carcinomas and apoptotic resistant tumor cells, implicating a probable use for HTATIP2 in antitumor therapy.

Endothelial cells express three different vascular endothelial growth factor (VEGF) receptors, belonging to the family of receptor tyrosine kinases (RTKs). They are named VEGFR-1 (Flt-1), VEGFR-2 (KDR/Flk-1), and VEGFR-3 (Flt-4). Their expression is almost exclusively restricted to endothelial cells, but VEGFR-1 can also be found on monocytes. All VEGF-receptors have seven immunoglobulin-like extracellular domains, a single transmembrane region and an intracellular split tyrosine kinase domain. VEGFR-2 has a lower affinity for VEGF than the Flt-1 receptor, but a higher signalling activity. Mitogenic activity in endothelial cells is mainly mediated by VEGFR-2 leading to their proliferation. Differential splicing of the flt-1 gene leads to the formation of a secreted, soluble variant of VEGFR-1 (sVEGFR-1). No naturally occurring, secreted forms of VEGFR-2 have so far been reported. The binding of VEGF165 to VEGFR-2 is dependent on heparin.

Leucine zipper down-regulated in cancer 1-like (LDOC1L) is a member of the LDOC1 family. LDOC1L is a nuclear protein containing a leucine zipper-like motif and a proline-rich region that shares noticeable similarity with an SH3-binding domain. LDOC1L localizes to the nucleus and is downregulated in certain cancer cell lines. LDOC1L is believed to regulate the transcriptional response mediated by the nuclear factor kB (NFkB).

Human papillomaviruses (HPVs) are a group family with more than 150 related viruses. HP 6 and 11 considered as low-risk HPVs can be sexually transmitted, causing warts to emerge on or around the genitals or anus, known as condylomata acuminate. HPV 11 major/large capsid antigen is used in clinical diagnosis to test the specific antibody to this virus induced by the virus infection, the positive reaction of this antibody is deemed as a marker for present and past infection. Furthermore, HPV 11 large capsid is used as a potential candiadate for vaccine development.

The Epstein-Barr virus (EBV), also called Human herpes virus 4 (HHV-4), is a virusof the herpes family(which includes Herpes simplex virusand Cytomegalovirus. On infecting the B-lymphocyte, the linear virus genome circularizes and the virus subsequently persists within the cell as an episome. The virus can execute several distinct programs of gene expressionwhich can be broadly categorized as being lytic cycle or latent cycle. The lytic cycleor productive infection results in staged expression of a host of viral proteinswith the ultimate objective of producing infectious virions. Formally, this phase of infection does not inevitably lead to lysis of the host cellas EBV virions are produced by budding from the infected cell. The latent cycle(lysogenic) programs are those that do not result in production of virions. A very limited, distinct set of viral proteins are produced during latent cycle infection. These include Epstein-Barr nuclear antigen(EBNA)-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, EBNA-leader protein (EBNA-LP) and latent membrane proteins(LMP)-1, LMP-2A and LMP-2B and the Epstein-Barr encoded RNAs(EBERs).

CMV belongs to the Betaherpesvirinae subfamily of Herpesviridae which includes herpes simplex virustypes 1 and 2, varicella-zoster virus, and Epstein-Barrvirus. The herpesviruses share a characteristic ability to remain latentover long periods. CMV is a double-stranded linear DNA virus with 162 hexagonal protein capsomeres surrounded by a lipid membrane. CMV has the largest genome of the herpes viruses, ranging from 230-240 kilobase pairs. Human CMV is composed of unique and inverted repeats that include the existence of 4 genome isomers caused by inversion of L-S genome components (class E). Replication may be divided into immediate early, delayed early, and late gene expression based on time of synthesis after infection. The DNA is replicated by rolling circles. In vitro, CMV replicates in human fibroblasts.

SERF2 (small EDRK-rich factor 2) is a member of the SERF family. SERF2 is a protein-coding gene. Among the diseases associated with SERF2 are spinal muscular atrophy, and muscular atrophy.

SARS Coronavirus is an enveloped virus containing three outer structural proteins, namely the membrane (M), envelope (E), and spike (S) proteins. Spike (S)-glycoprotein of the virus interacts with a cellular receptor and mediates membrane fusion to allow viral entry into susceptible target cells. Accordingly, S-protein plays an important role in virus infection cycle and is the primary target of neutralizing antibodies.

Chemokine (C-X-C motif) ligand 5 (CXCL5) is a small cytokine belonging to the CXC chemokine family that is also known as epithelial-derived neutrophil-activating peptide 78 (ENA-78). It is produced following stimulation of cells with the inflammatory cytokines interleukin-1 or tumor necrosis factor-alpha. Expression of CXCL5 has also been observed in eosinophils, and can be inhibited with the type II IFN. This chemokine stimulates the chemotaxis of neutrophils possesses angiogenic properties. It elicits these effects by interacting with the cell surface chemokine receptor CXCR2. The gene for CXCL5 is encoded on four exons and is located on human chromosome 4 amongst several other CXC chemokine genes. CXCL5 has been implicated in connective tissue remodelling.

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/ macrophagemigration, 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 mitogenesisand 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 are linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy.

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.