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a-Synuclein (amino acids 1-140), an acidic neuronal protein of 140 amino acids, is extremely heat-resistant and is natively unfolded with an extended structure primarily composed of random coils. a-synuclein has been suggested to be implicated in the pathogenesis of Parkinson’s disease and related neurodegenerative disorders, and more recently, to be an important regulatory component of vesicular transport in neuronal cells. Moreover, recent studies have shown that a-synuclein has chaperone activity and that this activity is lost upon removing its C-terminal acidic tail (amino acids 96-140).

Adiponectin is a hormone exclusively expressed from adipose tissue. Many studies demonstrate that adiponectin has direct anti-diabetic, anti-atherogenic and anti-inflammatory functions. APM-1 can increase insulin sensitivity of skeletal muscle, attenuate hepatic lipogenesis and luconeogenesis, regulate NO production in endothelial cells, inhibit proliferation of smooth muscle cells and prevent lipid accumulation of macrophage cells.
In the circulation, adiponectin is present as three different oligomeric complexes, including the high molecular weight (HMW), the middle molecular weight (MMW, also called hexamer) and low molecular weigh (MMW, also called trimer) forms 8. Different oligomeric complex of adiponectin activates different signaling pathways and exerts distinct functions.

IFN-alpha is produced by macrophages and has antiviral activities. Interferon stimulates the production of two enzymes: protein kinase and an oligoadenylate synthetase.

IL-32 is part of the cytokine family and contains a tyrosine sulfation site, 3 potential N-myristoylation sites, multiple putative phosphorylation sites, and an RGD cell-attachment sequence. IL-32 expression is elevated after the activation of T-cells by mitogens or the activation of NK cells by IL-2. IL-32 induces the production of TNF-a from macrophage cells. IL-32 pro-inflammatory pathway is activated in response to influenza A virus infection. Dysregulation of IL-32 in myelodysplastic syndrome and chronic myelomonocytic leukemia modulates apoptosis and impairs NK function.
Induction of TNF, IL-1beta, and IL-6 by IL-32 is intervened by p38-MAPK. IL-32 induced monocyte-to-macrophage differentiation is mediated through nonapoptotic, caspase-3-dependent mechanisms. IL32 plays an important role in the pathogenesis of rheumatoid arthritis. IL-32 is involved in activation-induced cell death in T cells, through its intracellular actions. IL-32 is a cell-associated proinflammatory cytokine, which is particularly stimulated by mycobacteria through a caspase-1- and IL-18-dependent production of IFNgamma.
IL-32 is associated with TNF-a, IL-1beta, and IL-18. IL32 is involved in human rheumatoid arthritis and is a novel target in autoimmune diseases.

Tumor necrosis factor receptor superfamily member 8 (TNFRSF8) is a receptor for TNFSF8/CD30L. TNFRSF8 has a role in the regulation of cellular growth and transformation of activated lymphoblasts. In addition, the TNFRSF8 protein regulates gene expression via activation of NF-kappa-B. TNFRSF8 being a regulator of apoptosis, induces cell death or proliferation, depending on the cell type.

Sialic Acid Binding Ig Like Lectin 5, also known as SIGLEC5 is a member of the immunoglobulin superfamily and SIGLEC family. SIGLEC5 contains of 2 Ig-like C2-type domains and 1 Ig-like V-type domain. In addition, SIGLEC5 is expressed by monocytic/myeloid lineage cells. SIGLEC5 is expressed at high levels in peripheral blood leukocytes, spleen, and at lower levels in lymph node, appendix, pancreas, lung, and thymus.

Major pollen allergen Aln g 1 (Aln G 1.0101) causes an allergic reaction in humans.

Endoglin is a type I membrane glycoprotein located on cell surfaces and is part of the TGF beta receptor complex.
The Endoglin protein consists of a homodimer of 180 kDA with disulfide links. Endoglin has been found on endothelial cells, activated macrophages, fibroblasts, and smooth muscle cells. Furthermore, Endoglin has been found to be part of the TGF-beta1 receptor complex. Endoglin thus may be involved in the binding of TGF-beta1, TGF-beta3, activin-A, BMP-2, and BMP-7. Beside TGF-beta signaling endoglin may have other functions. It has been postulated that endoglin is involved in the cytoskeletal organization affecting cell morphology and migration. Endoglin has a role in the development of the cardiovascular system and in vascular remodeling. Endoglin expression is regulated during heart development . Experimental mice without the endoglin gene die due to cardiovascular abnormalities.

SARS or severe acute respiratory syndrome is a lethal kind of pneumonia generated by coronavirus. Coronaviruses are a family of viruses that causes a mild respiratory tract infection is a large type of creatures such as humans, pigs, cows, mice, cats etc. up to this day, the origin of the coronavirus is still unknown.

Yersinia enterocolitica is a Gram-negative bacillus-shaped bacterium, which is a member of the Enterobacteriaceae family. Y.Enterocolitica is motile at temperatures between 22-29°C, however becomes non-motile at normal human body temperature. Y. Enterocolitica infection causes the yersiniosis disease, which is an animal-borne disease occurring in humans, as well as in a various groups of animals such as cattle, deer, pigs, and birds. Yersinia enterocolitica is a heterogeneous group of strains, which are conventionally classified by bio-typing into six bio-groups on the basis of phenotypic characteristics, and by serotyping into more than 57 “O” serogroups, on the basis of their O (lipopolysaccharide or LPS) surface antigen. Five of the six biogroups (1B and 2–5) are considered as pathogens. Nevertheless, only a few of these serogroups have been linked with disease in either humans or animals. Strains which belong to serogroups O:3 (biogroup 4), O:5,27 (biogroups 2 and 3), O:8 (biogroup 1B), and O:9 (biogroup 2) are most frequently isolated worldwide from human samples. Still, the main Y. enterocolitica serogroup in many European countries is serogroup O:3 followed by O:9, whereas the serogroup O:8 is mostly detected in the United States.

CD86 type I membrane protein is a member of the immunoglobulin superfamily which is expressed by antigen-presenting cells, and acts as the ligand for two proteins at the cell surface of T cells, CD28 antigen and cytotoxic T-lymphocyte-associated protein 4. CD86 binding with CD28 protein is a co-stimulatory signal for initiation of the T-cell. CD86 binding with CTLA-4 negatively regulates T-cell activation and diminishes the immune response.

CCL15, a new human CC chemokine, was isolated from a human fetal spleen cDNA library. CCL15 cDNA encodes a predicted 113 amino acid (aa) protein containing a putative signal peptide of 21 amino acids that is cleaved to generate a 92 aa residue mature protein. Within the CC family members, human CCL15 shares 45%, 44%, 35%, and 30% aa homology with mouse C10, human MPIF-1, human HCC-1, and mouse MIP-1?, respectively. The gene for MIP-5 is found on chromosome 17 where the genes for most of the human CC chemokines are located. Human CCL15 is expressed in T and B lymphocytes, NK cells, monocytes and monocyte-derived dendritic cells. Human MIP-5 is chemotactic for T cells and monocytes and has been shown to induce calcium flux in human CCR-1-transfected cells.

Apoptosis-Inducing Factor, Mitochondrion-Associated, 1 (AIFM1) is a mitochondrial protein which translocates to the nucleus once apoptosis has been initiated. AIFM1 causes DNA fragmentation and chromatin condensation and also triggers the release of cytochrome c and caspase-9 from mitochondria. Bcl-2 overexpression prevents the release of AIFM1 from mitochondria, but doesn’t block its apoptogenic activity.

Interleukin-1 ra is a member of the interleukin 1 cytokine family. IL1RAinhibits the activities of interleukin 1, alpha (IL1A) and interleukin 1, beta (IL1B), and modulates a variety of interleukin 1 related immune and inflammatory responses. IL1RAand five other closely related cytokine genes form a gene cluster spanning approximately 400 kb on chromosome 2. A polymorphism of this gene is reported to be associated with increased risk of osteoporotic fractures and gastric cancer.

Coagulation factor VIII participates in the intrinsic pathway of blood coagulation; factor VIII is a cofactor for factor IXa which, in the presence of Ca+2 and phospholipids, converts factor X to the activated form Xa. This gene produces two alternatively spliced transcripts. Transcript variant 1 encodes a large glycoprotein, isoform a, which circulates in plasma and associates with von Willebrand factor in a noncovalent complex. This protein undergoes multiple cleavage events. Transcript variant 2 encodes a putative small protein, isoform b, which consists primarily of the phospholipid binding domain of factor VIIIc. This binding domain is essential for coagulant activity. Defects in this gene results in hemophilia A, a common recessive X-linked coagulation disorder.

A human infecting coronavirus (viral pneumonia) called 2019 novel coronavirus, 2019-nCoV was found in the fish market at the city of Wuhan, Hubei province of China on December 2019.

The 2019-nCoV shares an 87% identity to the 2 bat-derived severe acute respiratory syndrome 2018 SARS-CoV-2 located in Zhoushan of eastern China. 2019-nCoV has an analogous receptor-BD-structure to that of 2018 SARS-CoV, even though there is a.a. diversity so thus the 2019-nCoV might bind to ACE2 receptor protein (angiotensin-converting enzyme 2) in humans.

While bats are possibly the host of 2019-nCoV, researchers suspect that animal from the ocean sold at the seafood market was an intermediate host. RSCU analysis proposes that the 2019-nCoV is a recombinant within the viral spike glycoprotein between the bat coronavirus and an unknown coronavirus.

Ataxin 3 is otherwise known as Machado-Joseph disease protein 1. Machado–Joseph disease is a hereditary autosomal dominant neurodegenerative disorder. ATXN3 contains trinucleotide CAG repeats in the coding region, and the expansion of these repeats from the normal 13-36 to 68-79 causes the Machado-Joseph disease. ATXN3 is a poly-ubiquitin-binding protein whose cellular turnover is regulated by its catalytic activity.
In addition, ATXN3 is a proteasome-associated factor which mediates the degradation of ubiquitinated proteins. ATXN3 folds reversibly using a single intermediate; partial destabilization of ATXN3 by chemical denaturation causes the formation of fibrillar aggregates by the non-pathological variant.
Ataxin-3 interacts with the major histone acetyltransferases cAMP-response-element binding protein (CREB)-binding protein, p300, and p300/CREB-binding protein-associated factor and hinders transcription by these coactivators.

Active IL-12 is a p70 disulphide-linked dimer composed of p35 and p40 subunits. The protein is a pleiotropic cytokine produced primarily by antigen presenting cells and has multiple effects on T lymphocytes and natural killer cells in terms of stimulating cytotoxicity, proliferation, production of other cytokines and Th1 subset differentiation.

Osteoprotegerin acts as decoy receptor for rankl and thereby neutralizes its function in osteoclastogenesis. OPG inhibits the activation of osteoclasts and promotes osteoclast apoptosis in vitro. Bone homeostasis seems to depend on the local rankl/opg ratio. Osteoprotegerin may also play a role in preventing arterial calcification. May act as decoy receptor for trail and protect against apoptosis. Trail binding blocks the inhibition of osteoclastogenesis.

Killer Cell Lectin-like Receptor Subfamily G, Member 1 (KLRG1) is a member of the killer cell lectin-like receptor (KLR) family, which is a group of transmembrane proteins preferentially expressed in NK cells. Natural killer (NK) cells are lymphocytes which mediate lysis of certain tumor cells and virus-infected cells without previous activation. NK cells can also regulate specific humoral and cell-mediated immunity. The cell surface expression of KLRG1 is up-regulated by MHC class I molecules expression.

Procalcitonin is a peptide hormone mainly produced by the C cells of the thyroid and certain endocrine cells of the lung. Under normal expression conditions, procalcitonin is immediately cleaved into three specific fragments, an N terminal residue, calcitonin and katacalcin. Levels of unprocessed procalcitonin rise significantly after bacterial infection, trauma or shock.

Since April 2012, cases of the Middle East Respiratory Syndrome Coronavirus (MERS-CoV) have been identified in various countries. Coronaviruses are the cause of the common cold, SARS (severe acute respiratory syndrome) and other severe illnesses with high mortality rates, all are classified into coronavirus family. MERS-CoV is a new type of SARS found in the coronavirus family causing severe pneumonia with sudden and serious respiratory illness with high mortality rates as well. Since January 27th 2015, the WHO has reported 956 human cases, including 351 deaths. More cases of the new coronavirus strain are expected. Like in other coronaviruses, large surface spike glycoprotein is a central structural protein of this virus; it is located above the virion surface to bind and enter into the target cell. Spike protein has 2 domains- S1 and S2. The S1 domain is responsible for cellular tropism and interaction with target cell, while the S2 domain is responsible for membrane fusion. The C-terminal of S1 domain contains a receptor binding domain, and is also a potential target for vaccine development and an antigen for diagnosis.

Glucagon is an important hormone involved in carbohydrate metabolism. The hormone is synthesized and secreted from alpha cells (?-cells) of the islets of Langerhans, which are located in the endocrine portion of the pancreas. Glucagon is released when the glucose level in the blood is low (hypoglycemia), causing the liver to convert stored glycogen into glucose and release it into the bloodstream. The action of glucagon is thus opposite to that of insulin, which instructs the body's cells to take in glucose from the blood in times of satiation.
Glucagon is beneficial for the culture of some cell types. It has been used in some biochemical regulation studies of glycogenolysis in hepatocytes. It has been also been found to induce DNA replication in primary cultures of adult rat hepatocytes when used in combinations with EGF and Insulin. Glucagon increases the blood glucose concentration by promoting rapid breakdown of liver glycogen, and also acts to relax smooth muscle such as the gastrointestinal tract.