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NRAS binds GDP/GTP and has intrinsic GTPase activity. NRAS is a membrane protein that shuttles between the Golgi apparatus and the plasma membrane. This transport is regulated through palmitoylation and depalmitoylation by the ZDHHC9-GOLGA7 complex. NRAS is activated to a GTP-bound form by a GTPase activating protein and inactivated to a GDP-bound form by a guanine nucleotide-exchange factor. Defects in this NRAS gene result in juvenile myelomonocytic leukemia.

SAA1 protein is an acute phase apolipoprotein reactant which is produced mostly by hepatocytes and under regulation of inflammatory cytokines. SAA1 (Serum amyloid A1) protein is produced mainly in the liver and circulates in low levels in the blood. The SAA1 seems to have a role in the immune system. SAA1 protein levels increase in the blood and other tissues under conditions of inflammation. SAA1 may facilitate the repair of injured tissues; it also acts as an antibacterial agent, and signals the migration of germ-fighting cells to sites of infection. SAA1 also functions as an apolipoprotein of the HDL complex.
Elevated levels of SAA1 ultimately affect secondary amyloidosis, extracellular amassing of amyloid fibrils, resulting from a circulating precursor, in a variety of tissues and organs. The most widespread type of amyloidosis appears secondary to chronic inflammatory disease, mainly rheumatoid arthritis. The SAA1 cleavage product a designated amyloid protein A is deposited systemically as amyloid in vital organs such as the liver, spleen, and kidneys in chronic inflammatory diseases patients. These deposits are extremely insoluble and resistant to proteolysis; they disrupt tissue structure and compromise performance.

Alanyl-tRNA synthetase is a member of the aminoacyl-tRNA synthetase family, key enzymes of protein biosynthesis which charge tRNA molecules with the respective amino acids. This 108 kDa protein is an autoantigen recognized by PL-12 antibodies which occur in a subset of patients with polymyositis and dermatomyositis. Preliminary data suggest that epitope spreading occurs in the autoimmune PL-12 response such that even antibodies to an isolated alanyl-tRNA molecule can develop.

African swine fever virus (ASFV) causes African swine fever (ASF), a disease of swine characterized by high morbidity and mortality. ASFV is a large DNA virus which belongs to Asfarviridae family. ASFV’s multilayered virion consists from up to 54 polypeptides while p30 is one of the early viral proteins. ASFV P30 is encoded by the CP204L gene and is one of the most antigenic structural proteinsi nvolved in ASFV entry.

H1N1 is a subtype specie of Influenza A virus. H1N1 Influenza Virus has mutated into various strains such as the Spanish Flu strain, mild human flu strains, endemic pigstrains, and various strains found in birds. The Influenza A Virus is a globular particle about 100nm in diameter, sheathed in a lipid bilayer derived from the plasma membrane of its host. Studded in the lipid bilayer are two integral membrane proteins some 500 molecules of hemagglutinin ("H") and some 100 molecules of neuraminidase ("N"). Within the lipid bilayer are 3000 molecules of matrix protein and 8 pieces of RNA. Each of the 8 RNA molecules is associated with many copies of a nucleoprotein, several molecules of the three subunits of its RNA polymerase some "non-structural" protein molecules of uncertain function.

H3N2 is a subtype of the influenza A virus. Its name derives from the forms of the two kinds of proteinson the surface of its coat, hemagglutinin(H) and neuraminidase(N). H3N2 exchanges genes for internal proteins with other influenza subtypes. H3N2 has tended to dominate in prevalence over H1N1, H1N2, and influenza B. H3N2 strain descended from H2N2by antigenic shift, in which genes from multiple subtypes re-assorted to form a new virus. Both the H2N2and H3N2 strains contained genesfrom avian influenzaviruses.

Lassa virus, which is a member of the Arenaviridae virus family, causes acute viral hemorrhagic fever. It was first reported in 1969 in the town of Lassa, in Borno State, Nigeria. Natal multimammate mouse is the primary reservoir of Lassa virus, found in sub-Saharan Africa. The virus is transmitted by contact with the feces or urine of animals, contributing to its high rate of incidence. Lassa fever occurs generally in West Africa. Lassa fever results in 300,000 to 500,000 cases annually and causes about 5,000 deaths each year. Outbreaks of this disease have been observed in Nigeria, Liberia, Sierra Leone, Guinea, and the Central African Republic. Protein structure: Lassa virus genome is comprised of two single-stranded RNA molecules defined as small (S) and large (L). Two genes on the S segment encode the nucleoprotein (NP) and two envelope glycoproteins (GP1 and GP2); while, the L segment encodes the viral polymerase (L protein) and RING finger Z matrix protein. GP1 subunit serves a putative role in receptor binding, while the structure of GP2 subunit is consistent with viral transmembrane fusion proteins. NP is a virion protein which binds and protects the viral RNA.

H1N1 is subtype specie of Influenza A virus. H1N1 Influenza Virus has mutated into various strains such as the Spanish Flu strain, mild human flu strains, endemic pig strains, and various strains found in birds.
The Influenza A Virus is a globular particle about 100nm in diameter, sheathed in a lipid bilayer derived from the plasma membrane of its host. Studded in the lipid bilayer are two integral membrane proteins some 500 molecules of hemagglutinin ("H") and some 100 molecules of neuraminidase ("N"). Within the lipid bilayer are 3000 molecules of matrix protein and 8 pieces of RNA. Each of the 8 RNA molecules is associated with many copies of a nucleoprotein, several molecules of the three subunits of its RNA polymerase some "non-structural" protein molecules of uncertain function.

HBsAg is the surface antigenof the Hepatitis-B-Virus (HBV). The capsidof a virus has different surface proteins from the rest of the virus. The antigen is a protein that binds specifically on one of these surface proteins. It is commonly referred to as the Australian Antigen.

Caused by one of four closely related virusserotypesof 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 Morpholinoantisense oligos have shown specific activity against Dengue virus.

H1N1 is a subtype specie of Influenza A virus. H1N1 Influenza Virus has mutated into various strains such as the Spanish Flu strain, mild human flu strains, endemic pig strains, and various strains found in birds.
The Influenza A Virus is a globular particle about 100nm in diameter, sheathed in a lipid bilayer derived from the plasma membrane of its host. Studded in the lipid bilayer are two integral membrane proteins some 500 molecules of hemagglutinin ("H") and some 100 molecules of neuraminidase ("N"). Within the lipid bilayer are 3000 molecules of matrix protein and 8 pieces of RNA. Each of the 8 RNA molecules is associated with many copies of a nucleoprotein, several molecules of the three subunits of its RNA polymerase some "non-structural" protein molecules of uncertain function.

Yellow fever virus is a part of Flaviviridaeis virus family. Yellow Fever Virusis a 40–50nm enveloped RNA virus, transmitted by mosquitoe. Recombinant yellow fever virus protein is derived from its envelope domain III.

Dengue NS1 is an early marker for dengue infection from the first day of fever and lasting about one week. Dengue IgM is usually detected early on the first day to 5 days of infection. Dengue NS1 could be detected from both primary and secondary infection for all four subtypes.

The OmpA protein is one of the main outer-membrane proteins of a large array of Gram-negative bacteria such as A.salmonicida, Shigella dysenteriae and E.coli.OmpA’s major physiological functions include maintenance of the structural integrity and morphology of the cells and porin activity, as well as a role in conjugation and bacteriophage binding.Achromogenic atypical Aeromonas salmonicida is the causative agent of goldfish ulcer disease.Virulence of this bacterium is associated with the production of a paracrystalline outer membrane A-layer protein.The species specific structural gene for the monomeric form of A-protein was cloned into a pET-3d plasmid in order to express and produce a recombinant form of the protein in E.coli BL21(DE3). The induced protein was isolated from inclusion bodies by a simple solubilization-renaturation procedure and purified by ion exchange chromatography on Q-Sepharose to over 95% pure monomeric protein.Recombinant A-protein was compared by biochemical, immunological and molecular methods with the A-protein isolated from atypical A.salmonicida bacterial cells by the glycine and the membrane extraction methods.

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.

Entry of HSV into the host cell involves interactions of several viral glycoproteins with cell surface receptors. The virus particle is covered by an envelope which, when bound to specific receptors on the cell surface, will fuse with the cell membrane and create an opening, or pore, through which the virus enters the host cell. The sequential stages of HSV entry are analagous to those of other viruses. At first, complementary receptors on the virus and cell surface bring the two membranes into proximity. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Finally, a stable entry pore is formed through which the viral envelope contents are introduced to the host cell.

Arylsulfatase A (ARSA) hydrolyzes cerebrosidesulfate to cerebroside and sulfate. ARSA is inhibited by phosphate. The phosphate develops a covalent bond with the active site 3-oxoalanine. ARSA gene defects cause metachromatic leucodystrophy (MLD), a progressive demyelination disease which results in various neurological symptoms and ultimately death.

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.

Entry of HSV into the host cell involves interactions of several viral glycoproteins with cell surface receptors. The virus particle is covered by an envelope which, when bound to specific receptors on the cell surface, will fuse with the cell membrane and create an opening, or pore, through which the virus enters the host cell. The sequential stages of HSV entry are analagous to those of other viruses. At first, complementary receptors on the virus and cell surface bring the two membranes into proximity. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Finally, a stable entry pore is formed through which the viral envelope contents are introduced to the host cell.