PR10A Protein, Coptis japonica, Recombinant (His & SUMO) is expressed in E. coli.

GLIPR1 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 25.7 kDa and the accession number is P48060-1.

GLIPR1 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 25.1 kDa and the accession number is Q4QQK5.

Involved in disease resistance. SAM22 Protein, Glycine max, Recombinant (His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 18.8 kDa and the accession number is P26987.

To assess whether beta-2 microglobulin (B2M) has effects on articular chondrocytes that would implicate B2M involvement in osteoarthritis (OA) pathogenesis.The average B2M level in OA synovial fluid is significantly higher than that found in normal synovial fluid. B2M is highly expressed in OA cartilage and synovial fluid compared to normal, and suggest that B2M may have effects on chondrocyte function that could contribute to OA pathogenesis.

TNFRSF11A, also known as receptor activator of NF-κB (RANK), activates several signaling pathways, such as NF-κB, JNK, ERK, p38α, and Akt/PKB. RANK/TNFRSF11A is a novel and frequent target for de novo methylation in gliomas, which affects apoptotic activity and focus formation thereby contributing to the molecular pathogenesis of gliomas. RANK/TNFRSF11A Protein, Human, Recombinant (aa 30-212, hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 46.85 kDa and the accession number is Q9Y6Q6-1.

Interleukin-13 (IL-13) is a monomeric 17 kDa immunoregulatory cytokine that plays a key role in the pathogenesis of allergy, cancer, and tissue fibrosis. It is secreted by several helper T cell subsets, NK cells, mast cells, eosinophils, basophils, and visceral smooth muscle cells. Inhibits inflammatory cytokine production. Synergizes with IL2 in regulating interferon-gamma synthesis. May be critical in regulating inflammatory and immune responses. Positively regulates IL31RA expression in macrophages (By similarity).

Recent studies have implicated chemokines in microglial activation and pathogenesis of neuropathic pain. C-X-C motif chemokine 13 (CXCL13) is a B lymphocyte chemoattractant that activates CXCR5. Using the spinal nerve ligation (SNL) model of neuropathic pain, CXCL13 was persistently upregulated in spinal cord neurons after SNL, resulting in spinal astrocyte activation via CXCR5 in mice. CXCL13/BCA-1 Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with N-hFc tag. The predicted molecular weight is 37.1 kDa and the accession number is O55038.

TNFSF13B is also known as B-cell activating factor (BAFF), BLyS and TNLG7A, is a member of TNF ligand superfamily. TNFSF/TNFRSF members function as key molecules in local and systemic inflammatory network, and the plasma TNFSF13B and TNFSF14 may be the potential local and systemic inflammatory indicators of severe HAdV pneumonia in pediatric patients. Identification of TNFSF13B as candidate causative genes supports conjectures on involvement of the immune system in BVVL and amyotrophic lateral sclerosis. It’s reported that APRIL, BAFF, and BAFF receptors play a major role in the pathogenesis of RA, and MSCT seems to inhibit these immunological factors.

Angiotensinogen is involved in maintaining blood pressure and in the pathogenesis of essential hypertension and preeclampsia. Genetic variations in Angiotensinogen are associated with susceptibility to essential hypertension, and can cause renal tubular dysgenesis, a severe disorder of renal tubular development. Defects in the encoding gene have also been associated with non-familial structural atrial fibrillation, and inflammatory bowel disease.

One of the virulence factors produced during swarmer cell differentiation of the bacteria, which seems to be associated with pathogenesis. The protease activity is limited to IgA1, IgA2, as well as IgG degradation. Serralysin Protein, Proteus mirabilis, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 68.4 kDa and the accession number is Q11137.

Cell surface-associated calcium-binding protein which plays an important role in adhesion and pathogenesis. Contributes to the resistance to killing by innate immune components in blood and thus attenuates bacterial clearance by interacting with host complement factor H/CFAH and modulating its activity. Inhibits also bacterial opsonization and killing by interacting with host complement regulator C4BPA and thus inhibiting classical complement pathway activation. SdrE Protein, S. aureus, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 64.5 kDa and the accession number is Q932F7.

Human papillomavirus (HPV) 16 infection is a necessary condition for the pathogenesis and development of cervical cancer. The E6 protein is expressed by the HPV16 E6 gene and promotes malignant phenotype transformation, which is an important mechanism for the occurrence and development of cervical cancer.

The molecular features at the IL19 locus may modestly alter the establishment of HIV-1 infection. Interleukin (IL) 19, IL-20, and IL-24 belong to the IL-10 cytokine family and have been identified to play a role in the regulation of epidermal functions and inflammation. The expression of IL19 in biopsies of patients with active ulcerative colitis was increased compared with patients with quiescent ulcerative colitis and that colitis was attenuated in IL-19-deficient mice. The disruption of the epithelial barrier with dextran sodium sulfate leads to increased IL-19 expression. Attenuated colitis in IL-19-deficient animals was associated with reduced numbers of IL-6-producing macrophages in the inflamed colonic lamina propria. Microbial-driven expression of IL-19 by intestinal macrophages may contribute to the pathogenesis of inflammatory bowel disease.

Monocyte Chemoattractant Proteins 4 (MCP-4/CCL13) is a member of a distinct, structurally-related subclass of CC chemokines mainly involved in recruitment of eosinphils to inflammatory sites. CCL13/MCP-4, is a CC family chemokine that is chemoattractant for eosinophils, basophils, monocytes, macrophages, immature dendritic cells, and T cells, and its capable of inducing crucial immuno-modulatory responses through its effects on epithelial, muscular and endothelial cells. Similar to other CC chemokines, CCL13 binds to several chemokine receptors (CCR1, CCR2 and CCR3), allowing it to elicit different effects on its target cells. A number of studies have shown that CCL13 is involved in many chronic inflammatory diseases, in which it functions as a pivotal molecule involved in the selective recruitment of cell lineages to the inflamed tissues and their subsequent activation. MCP-4/CCL13 is secreted from chondrocytes and activates the proliferation of rheumatoid synovial cells, thereby leading to joint destruction in RA. The interferon-gamma in combination with interleukin-1beta/tumor necrosis factor-alpha activates the production of MCP-4/CCL13 from chondrocytes in RA joints, and that secreted MCP-4/CCL13 enhances fibroblast-like synoviocyte proliferation by activating the extracellular signal-regulated kinase mitogen-activated protein kinase cascade. CCL13 may have some role in the pathogenesis of systemic sclerosis (SSc).

Tissue kallikrein 13 (hK13), also known as KLK-L4 (kallikrein-like gene 4), is a member of the human tissue kallikrein family of serine proteases having diverse physiological functions in many tissues. The KLK13 gene resides on chromosome 19q13.3-4 along with other 14 members in a gene cluster and shares a high degree of homology. KLK13 is a trypsin-like, secreted serine protease expressed specifically in the testicular tissue including prostate, salivary gland, breast, and testis. Growing evidence suggests that many kallikreins are implicated in carcinogenesis and may play a role in metastasis. KLK13 may be involved in the pathogenesis and/or progression of breast and ovary cancers and is regarded as a novel cancer biomarker. Besides, KLK13 interacts and forms complexes with several serum protease inhibitors, such as alpha2-macroglobulin, and its expression is regulated by steroid hormones.

The recycling of citrulline by argininosuccinate synthase 1 (ASS1) and argininosuccinate lyase (ASL) is crucial to maintain arginine availability and nitric oxide (NO) production. Nitric oxide (NO) plays an established role in numerous physiological and pathological processes, but the specific cellular sources of NO in disease pathogenesis remain unclear, preventing the implementation of NO-related therapy. Argininosuccinate lyase (ASL) is the only enzyme able to produce arginine, the substrate for NO generation by nitric oxide synthase (NOS) isoforms. Induction of endogenous NO production by enterocytes with supplements that upregulate ASL expression and complement its substrates results in improved epithelial integrity and alleviation of colitis and of inflammation-associated colon cancer.

CTRL-1, also known as chymotrypsin-like protease, belongs to thepeptidase S1 family. CTRL-1 contains 1peptidase S1 domain. Its expression is increased in preeclampsia (PE). Placental-derived chymotrypsin-like protease is responsible for inducing endothelial inflammatory phenotypic changes possibly by upregulation of cell adhesion molecule expressions, activation of cellular protease, and induction of extracellular regulated kinase phosphorylation. Activated microglia have been observed in various neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis, and multiple sclerosis. Five structurally distinct inhibitors that are known to inhibit chymotrypsin-like proteases were partially protective. They might represent a novel class of drugs with benefit in diseases where overactivity of microglia contributes to the pathogenesis.

ARHI, also known as DIRAS3, belongs to the small GTPase superfamily, Di-Ras family. ARHI gene is a novel tumor suppressor gene located on chromosome 1p31. Downregulation of ARHI expression has been detected in many types of cancer. ARHI is expressed in normal ovarian and breast epithelial cells but not in ovarian and breast cancers. As a suppressor, ARHI is not only an important factor in the pathogenesis of gastric cancer, but also a potential factor for tumor aggravation. ARHI expression in gastric cancer can be employed to indicate favorable prognosis for the disease.

ADGRD1 (Adhesion G Protein-Coupled Receptor D1, also known as GPR133) is a Protein Coding gene. 4 alternatively spliced human isoforms have been reported. ADGRD1, an orphan member of the adhesion family of G-protein-coupled receptors, is a critical regulator of the response to hypoxia and tumor growth in Glioblastoma (GBM). ADGRD1 represents a novel molecular target in GBM and possibly other malignancies where hypoxia is fundamental to pathogenesis. Variations in the ADGRD1 locus are linked with differences in metabolism, human height, and heart frequency. ADGRD1 is a Gs protein-coupled receptor belonging to the class of adhesion GPCRs. The adhesion G-protein-coupled receptors (GPCRs), including GPR133, are membrane-bound proteins with long N termini containing multiple domains.

Tryptases are Trypsin-like Serine Proteases. β-Tryptases are the main isoenzymes in mast cells. Βtryptases form active tetramers with heparin proteoglycan. In the tetramer, the unique arrangement of the active sites facing a narrow central pore, β-Tryptases are resistant to macromolecule protease inhibitors . When mast cells are activated, β-Tryptases are released and participate in provoking inflammatory conditions . β-Tryptases have been implicated as mediators in the pathogenesis of asthma and other allergic disorders.

Gamma-Synuclein (SNCG) is a member of the Synuclein protein family. Gamma-Synuclein is mostly expressed in the peripheral nervous system and retina. Gamma-Synuclein plays a role in neurofilament network integrity and may be involved in modulating axonal architecture during development and in the adult. In addition, it may also function in modulating the keratin network in skin. SNCG expression in breast tumors has been as a marker for tumor progression. SNCG is also believed to be involved in the pathogenesis of neurodegenerative diseases.

Recent studies have implicated chemokines in microglial activation and pathogenesis of neuropathic pain. C-X-C motif chemokine 13 (CXCL13) is a B lymphocyte chemoattractant that activates CXCR5. Using the spinal nerve ligation (SNL) model of neuropathic pain, CXCL13 was persistently upregulated in spinal cord neurons after SNL, resulting in spinal astrocyte activation via CXCR5 in mice. CXCL13/BCA-1 Protein, Human, Recombinant (His & Sumo) is expressed in E. coli expression system with N-His-Sumo tag. The predicted molecular weight is 22.9 kDa and the accession number is O43927.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by a progressive decline in cognitive performance; Mild Cognitive Impairment (MCI) is instead an objective decline in cognitive performance that does not reach pathology. Paired immunoglobulin-like type 2 receptor alpha (PILRA) is a cell surface inhibitory receptor that was recently suggested to be involved in AD pathogenesis. In particular, the arginine-to-glycine substitution in position 78 (R78, rs1859788) was shown to be protective against AD.

Recent studies have implicated chemokines in microglial activation and pathogenesis of neuropathic pain. C-X-C motif chemokine 13 (CXCL13) is a B lymphocyte chemoattractant that activates CXCR5. Using the spinal nerve ligation (SNL) model of neuropathic pain, CXCL13 was persistently upregulated in spinal cord neurons after SNL, resulting in spinal astrocyte activation via CXCR5 in mice. CXCL13/BCA-1 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with N-His tag. The predicted molecular weight is 11.7 kDa and the accession number is O55038.

Chondroitin sulfate proteoglycan 5 (CSPG-5), also known as neuroglycan C, has been previously associated to differentiation since it shapes neurite growth and synapse forming. CSPG-5 expression shifts in brain areas of the default mode network of suicide victims, which may reflect an impact in the pathogenesis of psychiatric diseases or support diagnostic power.

Interleukin (IL)-1R3 is the co-receptor in three signaling pathways that involve six cytokines of the IL-1 family (IL-1α, IL-1β, IL-33, IL-36α, IL-36β and IL-36γ). In many diseases, multiple cytokines contribute to disease pathogenesis. For example, in asthma, both IL-33 and IL-1 are of major importance, as are IL-36 and IL-1 in psoriasis.

Induces local and distal defense responses (incompatible hypersensitive reaction) in plants from the solanaceae and cruciferae families. Elicits leaf necrosis and causes the accumulation of pathogenesis-related proteins. Might interact with the lipidic molecules of the plasma membrane. Beta-elicitin cryptogein Protein, Phytophthora cryptogea, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 17.3 kDa and the accession number is P15570.

Parvalbumins (PVALBs) are particularly abundant in the fast-contracting muscles and correlate positively with muscle relaxation speed in amphibians and fishes. The loss of PVALB plays a role in the pathogenesis of thyroid tumors. The mutations in the PVALB gene are not involved in GS patients who harbour a single or no mutant SLC12A3 allele.

Protein S100-A7, also known as S100 calcium-binding protein A7, Psoriasin, S100A7, and PSOR1, is a secreted protein which belongs to theS-100 family. S100A7 was first isolated from skin involved by psoriasis, which can be induced in cultured squamous epithelial cells. S100A7 is expressed by both normal cultured and malignant keratinocytes and malignant breast epithelial cells within ductal carcinoma in situ, suggesting an association with abnormal pathways of differentiation. S100A7 plays a role in the pathogenesis of inflammatory skin disease, as a chemotactic factor for hematopoietic cells. It also plays a role in early stages of breast tumor progression in association with the development of the invasive phenotype.

Protein-glutamine gamma-glutamyltransferase 2, also known as Tissue transglutaminase, Transglutaminase C, Transglutaminase-2, and TGM2, is a member of the transglutaminase superfamily. TGM2 plays a role in cell growth and survival through the anti-apoptosis signaling pathway. It is a calcium-dependent acyltransferase that also undergoes a GTP-binding/GTPase cycle even though it lacks any obvious sequence similarity with canonical GTP-binding (G) proteins. TGM2 is a multi-functional protein which catalyzes transamidation reactions or acts as a G-protein in intracellular signalling. As an enzyme which is responsible for the majority of transglutaminase (TG) activity in the brain, TGM2 is likely to play a modulatory role in nervous system development and has regulatory effect on neuronal cell death as well. Most importantly, numerous studies have presented data demonstrating that dysregulation of TGM2 may contribute to the pathogenesis of many neurodegenerative disorders, including Huntington's disease, Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis as well as nervous system injuries.

Serpins are the largest and most diverse family of protease inhibitors. Most serpins control proteolytic cascades, certain serpins do not inhibit enzymes, but instead perform diverse functions such as storage (ovalbumin, in egg white), hormone carriage proteins (thyroxine-binding globulin, cortisol-binding globulin) and tumor suppressor genes (maspin). Most inhibitory serpins target chymotrypsin-like serine proteases. These enzymes are defined by the presence of a nucleophilic serine residue in their catalytic site. Some serpins inhibit other classes of protease. A number of such serpins have been shown to target cysteine proteases. These enzymes differ from serine proteases in that they are defined by the presence of a nucleophilic cysteine residue, rather than a serine residue, in their catalytic site.SerpinA12, also known as OL-64, Visceral adipose tissue-derived serine protease inhibitor, Vaspin, Visceral adipose-specific serpin and SERPINA12, is a secreted protein that belongs to the serpin family. SerpinA12 / Vaspin is expressed in visceral adipose tissues. It may modulate insulin action conceivably only in the presence of its yet undefined target proteases in white adipose tissues. SerpinA12 / Vaspin may be the compensatory molecule in the pathogenesis of metabolic syndrome and SerpinA12 / Vaspin recombinant protein or vaspin-mimicking agents such as vaspin analogs, antibodies or small molecule agents may be the link to drug discovery and development.

Atlastin-1, also known as Spastic paraplegia 3 protein A, Guanine nucleotide-binding protein 3, GTP-binding protein 3, GBP3, ATL1 and SPG3A, is a multi-pass membrane protein which belongs to theGBP family and atlastin subfamily. ATL1 / SPG3A is expressed predominantly in the adult and fetal central nervous system. Expression of ATL1 / SPG3A in adult brain is at least 5-fold higher than in other tissues. ATL1 / SPG3A is detected predominantly in pyramidal neurons in the cerebral cortex and the hippocampus of the brain. ATL1 / SPG3A is also expressed in upper and lower motor neurons (at protein level). A distinguishing feature of ATL1 / SPG3A is its frequent early onset, raising the possibility that developmental abnormalities may be involved in its pathogenesis. Missense SPG3A mutant atlastin-1 proteins have impaired GTPase activity and may act in a dominant-negative, loss-of-function manner by forming mixed oligomers with wild-type atlastin-1. Defects in ATL1 / SPG3A are the cause of spastic paraplegia autosomal dominant type 3 (SPG3), also known as Strumpell-Lorrain syndrome. Spastic paraplegia is a degenerative spinal cord disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs.

Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkB alpha, NFKBIA, or IKBA), is a member of the NF-kappa-B inhibitor family that function to inhibit the NF-kB transcription factor. NFKBIA inhibits NF-kB by masking the nuclear localization signals (NLS) of NF-kB proteins and keeping them sequestered in an inactive state in the cytoplasm. Also, NFKBIA blocks the ability of NF-κB transcription factors to bind to DNA, which is required for NF-kB's proper functioning. Signal-induced degradation of I kappa B alpha exposes the nuclear localization signal of NF-kappa B, thus allowing it to translocate into the nucleus and activate transcription from responsive genes. An autoregulatory loop is established when NF-kappa B induces expression of the I kappa B alpha gene and newly synthesized I kappa B alpha accumulates in the nucleus where it negatively regulates NF-kappa B-dependent transcription. As part of this post-induction repression, the nuclear export signal on I kappa B alpha mediates the transport of NF-kappa B-I kappa B alpha complexes from the nucleus to the cytoplasm. Deletion of NFKBIA has an effect that is similar to the effect of EGFR amplification in the pathogenesis of glioblastoma and is associated with comparatively short survival. Polymorphisms in NFKBIA may be important in pre-disposition to and outcome after treatment, of multiple myeloma (MM). The NFKBIA gene product, IkappaBalpha, binds to NF-kappaB preventing its activation and is important in mediating resistance to apoptosis in B-cell lymphoproliferative diseases.

Koebnerisin is also known as protein S100-A7A (S100A7A), S100 calcium-binding protein A7-like 1 (S100A7L1) or S100 calcium-binding protein A15 (S100A15). Human S100A7A / S100A15 is a novel member of the S100 family of EF-hand calcium-binding proteins and was recently identified in psoriasis, where it is significantly upregulated in lesional skin. S100A7 is expressed by both normal cultured and malignant keratinocytes and malignant breast epithelial cells within ductal carcinoma in situ, suggesting an association with abnormal pathways of differentiation. S100A7 plays a role in the pathogenesis of inflammatory skin disease, as a chemotactic factor for hematopoietic cells. It also plays a role in early stages of breast tumor progression in association with the development of the invasive phenotype. The association of the 11.2 kDa S100A7A / S100A15 with psoriasis suggests that it contributes to the pathogenesis of the disease and could provide a molecular target for therapy.

SMAD3 belongs to the SMAD family. Members of this family mediate signal transduction by the TGF-beta/activin/BMP-2/4 cytokine superfamily from receptor Ser/Thr protein kinases at the cell surface to the nucleus. SMAD3 is involved in cell signalling. It modulates signals of activin and TGFβ's. Binding of SMAD3 with SMAD4 enables its transmigration into the nucleus where it forms complexes with other proteins and acts as a transcription factor. SMAD3 is a receptor-regulated SMAD (R-SMAD). In mice, mutation of SMAD3 has been linked to colorectal adenocarcinoma, increased systemic inflammation, and accelerated wound healing. Increased SMAD3 activity has been implicated in the pathogenesis of scleroderma. Smad3 is also a multifaceted regulator in adipose physiology and the pathogenesis of obesity and type 2 diabetes.

Angiopoietin-like protein 1 (ANGPTL1) has been reported to suppress migration and invasion in lung and breast cancer, acting as a novel tumor suppressor candidate. Downregulation of tumor suppressor signaling plays an important role in the pathogenesis of hepatocellular carcinoma (HCC).The downregulation of the angiopoietin-like protein ANGPTL1 is associated with vascular invasion, tumor thrombus, metastasis, and poor prognosis in HCC. Ectopic expression of ANGPTL1 in HCC cells effectively decreased their in vitro and in vivotumorigenicity, cell motility, and angiogenesis. shRNA-mediated depletion of ANGPTL1 exerted opposing effects. ANGPTL1 promoted apoptosis via inhibition of the STAT3/Bcl-2-mediated antiapoptotic pathway and decreased cell migration and invasion via downregulation of transcription factors SNAIL and SLUG. Furthermore, ANGPTL1 inhibited angiogenesis by attenuating ERK and AKT signaling and interacted with integrin α1β1 receptor to suppress the downstream FAK/Src-JAK-STAT3 signaling pathway. Taken together, these results suggest ANGPTL1 as a prognostic biomarker and novel therapeutic agent in HCC. ANGPTL1 expression was down-regulated in CRC tissues and inversely correlated with poor survival. ANGPTL1 repressed migration and invasion of CRC cells, and microRNA-138 was involved in this process. Angiopoietin-like protein 1 (ANGPTL1) has been shown to act as a tumor suppressor by inhibiting angiogenesis, cancer invasion, and metastasis.

MSH2 is a key DNA mismatch repair protein, which plays an important role in genomic stability. In addition to its DNA repair function, MSH2 serves as a sensor for DNA base analogs-provoked DNA replication errors and binds to various DNA damage-induced adducts to trigger cell cycle arrest or apoptosis. Loss or depletion of MSH2 from cells renders resistance to certain DNA-damaging agents. Therefore, the level of MSH2 determines the DNA damage response.MSH2 is a central component of the mismatch repair pathway that targets mismatches arising during DNA replication, homologous recombination (HR), and in response to genotoxic stresses.MSH2 rearrangements are involved in approximately 10% of hereditary non-polyposis colorectal cancer (HNPCC) families, and in most of the rearrangements, exon 1 is deleted. Loss of human MSH2 (hMSH2) protein might be involved in the multistep pathogenesis of hematological malignancies associated with genetic instability.

Coronavirus encodes the 2’-O-MTase (2'O Methyltransferase) that is composed of the catalytic subunit nsp16 and the stimulatory subunit nsp10 and plays an important role in virus genome replication and evasion from innate immunity during viral infection. Nonstructural protein 16 (NSP16) / viral 2'O-methyltransferase (2'O-MTase) is highly conserved. The conserved 2'O-MTase activity is important for CoV pathogenesis and NSP16 is a conserved universal target for rapid live attenuated vaccine design in an expanding Coronavirus outbreak setting, such as COVID-19. Targeting the 2'O-methylation pathway on SARS-CoV replication and pathogenesis can be the treatment options for vaccine and anti-viral drug development which can against SARS-CoV-2，SARS-CoV, MERS-CoV or other RNA and DNA viruses.

Small ubiquitin-like modifier (SUMO), also known as SUMO homologue and SMT3, is a member of the superfamily of ubiquitin-like polypeptides that become covalently attached to various intracellular target proteins as a way to alter their function, location, and/or half-life. Small ubiquitin-like modifiers include SUMO1, SUMO2, SUMO3, and SUMO4. Except for SUMO4, all other SUMOs are ubiquitously expressed, including in the brain. In human, SUMO2 and SUMO3 are two highly homologous proteins, collectively called SUMO2/3. Several studies suggest that SUMO3 are associated with pathogenesis in several neurological diseases, including Alzheimer's disease, Parkinson's disease, and cerebral ischemia/stroke.

IFN-α, a cytokine expressed in human islets from individuals affected by type 1 diabetes, plays a key role in the pathogenesis of diabetes by upregulating inflammation, endoplasmic reticulum (ER) stress and MHC class I overexpression, three hallmarks of islet histology in early type 1 diabetes. IFN-alpha 1/IFNA1 Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with C-hFc tag. The predicted molecular weight is 46.14 kDa and the accession number is P01562.

Tissue-type plasminogen activator (PLAT) is a protein that secreted into extracellular space. PLAT contains five domains: EGF-like domain, fibronectin type-I domain, 2 kringle domains and peptidase S1 domain. It belongs to the peptidase S1 family. The main function of this protein is to convert plasminogen into biologically active plasmin. As a protease, PLAT plays a crucial role in regulating blood fibrinolysis, maintaining the homeostasis of extracellular matrix and in modulating the post-translational activation of growth factors. PLAT is found not only in the blood, where its primary function is as a thrombolytic enzyme, but also in the central nervous system (CNS). It participates in a number of physiological and pathological events in the CNS, as well as the role of neuroserpin as the natural regulator of PLAT's activity in these processes. Increased or decreased activity of PLAT leads to hyperfibrinolysis or hypofibrinolysis, respectively. In addition, as a cytokine, PLAT plays a pivotal role in the pathogenesis of renal interstitial fibrosis through diverse mechanisms. Thus, as a fibrogenic cytokine, it promotes the progression of kidney diseases.

C-X-C motif chemokine 2 (CXCL2,MIP-2) belongs to the intercrine alpha (chemokine CxC) family. It was originally identified as a heparin-binding protein secreted from a murine macrophage cell line in response to endotoxin stimulation. The expression of mouse MIP-2 is stimulated by endotoxin. The mouse MIP-2 shares approximately 63% aa sequence identity with murine KC, another mouse alpha chemokine, which is induced by PDGF. It has been suggested that mouse KC and MIP-2 are the homologs of the human GROs and rat CINCs. Chemotactic for human polymorphonuclear leukocytes but does not induce chemokinesis or an oxidative burst. The expression of MIP-2 was found to be associated with neutrophil influx in pulmonary inflammation and glomerulonephritis, suggesting that MIP-2 may contribute to the pathogenesis of inflammatory diseases.

Tumor necrosis factor receptor superfamily, member 13C (TNFRSF13C) also known as B-cell-activating factor receptor (BAFFR) and CD268 antigen, is a member of the tumor necrosis factor receptor superfamily. BAFF promotes the survival of B cells and is essential for B cell maturation. BAFF binds to three TNF receptor superfamily members: B-cell maturation antigen (BCMA/TNFRSF17), transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI/TNFRSF13B) and BAFF receptor (BAFF R/BR3/TNFRSF13C). These receptors are type III transmembrane proteins that lack a signal peptide. BAFF R is highly expressed in spleen, lymph node and resting B cells. It is also expressed at lower levels in activated B cell, in resting CD4+ T cells, in thymus and peripheral blood leukocytes. BAFF knockout mice lack mature B cells. Similarly, A/WySnJ mice that are defective in BAFF-R intracellular signaling also lack mature B cells, suggesting that BAFF R is the critical receptor for BAFF during B lymphopoiesis. It has been proposed that abnormally high levels of BAFFR/TNFRSF13C (CD268) may contribute to the pathogenesis of autoimmune diseases by enhancing the survival of autoreactive B cells.

May be involved in epidermal differentiation and inflammation and might therefore be important for the pathogenesis of psoriasis and other diseases. S100A7A Protein, Human, Recombinant (His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 13.2 kDa and the accession number is Q86SG5.

Essential virulence determinant. This protein is a protein tyrosine phosphatase. The essential function of YopH in Yersinia pathogenesis is host-protein dephosphorylation. It contributes to the ability of the bacteria to resist phagocytosis by peritoneal macrophages.

CCL18 is a chemotactic cytokine involved in the pathogenesis and progression of various disorders, including cancer. Proof showed high levels of CCL18 in the serum of epithelial ovarian carcinoma patients suggesting its potential as a circulating biomarker. CCL18 chemokine has an important role in chemokine-mediated tumor metastasis, and may serve as a potential predictor for poor survival outcomes for ovarian cancer. (CCL18) is predominantly secreted by M2-tumor associated macrophages (TAMs) and promotes malignant behaviors of various human cancer types. CCL18 has a correlation with cardiac function in patients with AAMI and it might be considered as an indicator of poor LVEF in patients with AAMI. Circulating and WAT-secreted CCL18 correlates with insulin resistance and metabolic risk score. Because CCL18 is macrophage-specific and associates with adipose immune gene expression, it may constitute a marker of WAT inflammation. Macrophages are thought to be the main source of CCL18, and the effect of pirfenidone, an anti-fibrotic agent for idiopathic pulmonary fibrosis, on the expression of CCL18 in macrophages warrants investigation.

The PRAC gene is located on chromosome 17 at position 17q21, about 4 kbp downstream from the homeodomain Hoxb-13 gene. The pathogenesis of PCa may be due to the expression levels of PRAC protein, and this protein can serve as a potential biomarker for the management of PCa.

KLK6 (kallikrein-related peptidase 6), also known as Klk7, belongs to the peptidase S1 family, Kallikrein subfamily. Kallikreins are a subgroup of serine proteases having diverse physiological functions. Growing evidence suggests that many kallikreins are implicated in carcinogenesis and some have potential as novel cancer and other disease biomarkers. KLK6 is a serine protease that exhibits a preference for Arg over Lys in the substrate P1 position and for Ser or Pro in the P2 position. Klk7 shows activity against amyloid precursor protein, myelin basic protein, gelatin, casein, and extracellular matrix proteins such as fibronectin, laminin, vitronectin, and collagen. KLK6 degrades alpha-synuclein and prevents its polymerization, indicating that KLK6 may be involved in the pathogenesis of Parkinson's disease and other synucleinopathies. Klk7 may be involved in the regulation of axon outgrowth following spinal cord injury. Tumor cells treated with a neutralizing KLK6 antibody migrate less than control cells, suggesting a role in invasion and metastasis.

BACE2, also known as beta secretase 2, belongs to the peptidase A1 family. It is a protease known to be an important enzyme involved in the cellular pathways. BACE2 has been shown to interact with GGA1 and GGA2. It is the major β-secretase in vivo. BACE2 is located on chromosome 21 and may play a role in alzheimer's disease pathogenesis in down syndrome(DS). Overexpression of BACE2 by lentivirus markedly reduced amyloid β protein production in primary neurons. Despite an extra copy of the BACE2 gene in DS and the increase of its transcription, BACE2 protein levels are unchanged.