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TNFAIP3-interacting protein 1 (TNIP1) interacts with zinc finger protein A20/TNFAIP3 and inhibits TNF-induced NF-kappa-B-dependent gene expression by interfering with a RIP- or TRAF2-mediated transactivation signal. Furthermore, TNIP1 interacts with HIV-1 matrix protein and is packaged into virions and its overexpression can inhibit viral replication. TNIP1 can regulate matrix nuclear localization, both nuclear import of Preintegration complex (PIC) and export of GAG polyprotein and viral genomic RNA during virion production.

C1QBP binds to the globular "heads" of c1q thus inhibiting c1 activation. C1QBP interacts with a wide range of ligands and is implicated in cell signaling. C1QBP associates with C1r and C1s in order to yield the first component of the serum complement system. C1QBP protein has been identified as the p32 subunit of pre-mRNA splicing factor SF2, as well as a hyaluronic acid-binding protein.
C1QBP is a new marker of tumor cells and tumor-associated macrophages/myeloid cells in hypoxic/metabolically deprived areas of tumors.
Mitochondrial C1QBP is a critical mediator of p14ARF-induced apoptosis.
C1QBP functions as a chemotactic factor for immature dendritic cells, and migration is mediated through ligation of both C1QBP and cC1qR/CR.
C1QBP overexpression successfully blocks mRNA accumulation from the adenovirus major late transcription unit (MLTU) and stimulates RNA polymerase II carboxy-terminal domain phosphorylation in virus-infected cells.
C1QBP binds with Hepacivirus core protein on CD8+ and CD4+ positive t-cells and inactivates lck and akt.

SNRPD1 Human Recombinant produced in SF9 is a glycosylated, polypeptide chain having a calculated molecular mass of 16kDa.
SNRPD1 is expressed with a -6x His tag at N-terminus and purified by proprietary chromatographic techniques.

Complement Factor Properdin (CFP) which is a plasma glycoprotein, is a positive regulator of the alternative complement pathway of the innate immune system. CFP binds and stabilizes the C3- and C5-convertase enzyme complexes in a feedback loop that eventually ends with formation of the membrane attack complex and lysis of the target cell. Mutations in CFP lead to 2 forms of properdin deficiency that cause high susceptibility to meningococcal infections.

GREM1 belongs to the BMP (bone morphogenic protein) antagonist family. Like BMPs, BMP antagonists comprise cystine knots and usually form homo- and heterodimers. The CAN (cerberus and dan) subfamily of BMP antagonists, to which GREM1 belongs, is characterized by a C-terminal cystine knot with an eight-membered ring. The antagonistic effect of the secreted glycosylated protein is because of its direct binding to BMP proteins. As an antagonist of BMP, GREM1 takes a place in regulating organogenesis, body patterning, and tissue differentiation. In mouse, GREM1 has been shown to convey the sonic hedgehog (SHH) signal from the polarizing region to the apical ectodermal ridge during limb bud outgrowth. Alternatively merged transcript variants encoding different isoforms have been found for this gene.

Wheat Gliadin and related gluten components from barley, rye and possibly oats can cause an abnormal immune response called Celiac disease which is a chronic gastrointestinal disorder. Celiac disease characteristics are flattening of the jejunal mucosa and intestinal lesions of variable severity in hereditarily inclined individuals. Even though Celiac disease is not a classic autoimmune disease it is related to anti-tissue transglutaminase antibodies and gliadin antibodies tests are most recommended in screening populations at risk for CD and other gluten-sensitive enteropathies. In the past, serologic tests for gliadin antibodies usually were not very precise and were not enough for accurate diagnosis due to missing deamidated epitopes within the authentic gliadin fraction traditionally used in diagnostic test kits. ProSpec's deamidated Gliadin isoform matches to the deamidated neo-epitopes, which in the natural antigen are formed by transglutaminase-mediated glutamine side chain deamidation.

Mitochondrial antiviral signaling protein (MAVS) is vital for innate immune defense against viruses. MAVS is an intermediary protein essential in the virus-triggered IFN-beta signaling pathways. MAVS is involved in activation of transcription factors that regulate expression of IFN-beta and contributes to antiviral immunity.

Signal-Regulatory Protein Alpha, SIRPA belongs to the signal-regulatory-protein (SIRP) family, as well as theimmunoglobulin super family. The members of the SIRP family are receptor-type transmembrane glycoproteins which areinvolved in the negative regulation of receptor tyrosine kinase-coupled signaling processes. SIRPA can bephosphorylated by tyrosine kinases. The phospho-tyrosine residues of this PTP have been shown to recruit SH2domain containing tyrosine phosphatases (PTP), and perform as substrates of PTPs. SIRPA take part insignal transduction mediated by a variety of growth factor receptors. CD47 has been shown to be a ligand for SIRPA.

NHP2 belongs to the H/ACA snoRNPs (small nucleolar ribonucleoproteins) gene family. snoRNPs are involved in various aspects of rRNA processing and modification and have been organized into 2 families: C/D and H/ACA. NHP2 (NOLA2) forms a small ribonucleoprotein particle with GAR1 (NOLA1), Nop10 for the isomerization of uridine to pseudouridine. NHP2 is involved in a variety of aspects of rRNA processing and modification. NHP2 localizes to the dense fibrillar component of the nucleolus and in nuclear Cajal bodies.

IFIH1 is a DEAD box protein which is upregulated in response to treatment with beta-interferon and a protein kinase C-activating compound, mezerein. Irreversible reprogramming of melanomas can be attained by therapy with both these agents; treatment with either agent alone only achieves reversible differentiation. DEAD box proteins are implicated in several cellular processes involving alteration of RNA secondary structure such as translation initiation, nuclear and mitochondrial splicing, and ribosome and spliceosome assembly.

Methylosome subunit pICln (CLNS1A), is a member of the pICln (TC 1.A.47) family. CLNS1A takes part in multiple regulatory pathways. CLNS1A interaction with Sm proteins, inhibits their compilation on U RNA and interferes with snRNP biogenesis. CLNS1A inhibits the binding of survival motor neuron protein (SMN) to Sm proteins. Methylosome subunit pICln is related with the plasma membrane where it functions as a chloride present regulator.

ARL5A is a member of the ARF family of GTP-binding proteins. ARFs are vital in eukaryotic vesicular trafficking pathways and have a crucial part in the activation of phospholipase D. Different from ARF family members, ARL5 is believed to lack ADP-ribosylation enhancing activity. ARL5A is developmentally regulated and has a role in nuclear dynamics and signaling cascades during embryonic development.

Phosphoglycerate kinase 1, also referred to PGK1, is an X-linked enzyme whichfunctions in the glycolytic pathway.The gene encoding the erythrocyte enzyme PGK1 & it seems that PGK-1 plays a role as a polymerase alpha cofactor protein (primer recognition protein) as a glyxolytic enzyme role. The PGK1 catalyzes the reversible conversion of 1, 3-diphosphoglycerate to 3-phosphoglycerate during glycolysis, generating one molecule of ATP.

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 probably 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.

HB-EGF is an EGF related growth factor which signals via the EGF receptor, and stimulates the proliferation of SMC (smooth muscle cells), fibroblasts, epithelial cells and keratinocytes. HB-EGF is expressed in various cell types and tissues, including vascular endothelial cells and SMC, macrophages, skeletal muscle, keratinocytes and particular tumor cells. HB-EGF’s ability to explicitly bind heparin and heparin sulfate proteoglycans is dissimilar from other EGF-like molecules, and might be related to the enhanced mitogenic activity, relative to EGF, that HB-EGF exerts on smooth muscle cells.

Sarcoglycan Delta (SGCD) is one of the four known components of the sarcoglycan complex, which is a subcomplex of the dystrophin-glycoprotein complex (DGC) and is expressed mainly in skeletal and cardiac muscle. DGC forms a link between the F-actin cytoskeleton and the extracellular matrix. SGCD protein’s mutations have been associated with autosomal recessive limb-girdle muscular dystrophy and dilated cardiomyopathy. SGCD gene expression is regulated by MITF In melanocytic cells.

Chemokine (C-X-C motif) ligand (CXCL7) is a small cytokine belonging to the CXC chemokine family. It is a protein that is released in large amounts from platelets following their activation. It stimulates various processes including mitogenesis, synthesis of extracellular matrix, glucose metabolism and synthesis of plasminogen activator.

Platelet factor-4 is a 70-amino acid protein that is released from the alpha-granules of activated platelets and binds with high affinity to heparin. Its major physiologic role appears to be neutralization of heparin-like molecules on the endothelial surface of blood vessels, thereby inhibiting local antithrombin III activity and promoting coagulation. As a strong chemoattractant for neutrophils and fibroblasts, PF4 probably has a role in inflammation and wound repair. Oncostatin-A is a member of the CXC chemokine family. Human PF4 is used for the proof of heparin-induced thrombocytopenia. Furthermore it is used as an inhibitor in the angiogenesis during tumor therapy.

Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) was first characterized as a growth factor that supports the in-vitro colony formation of granulocytes-macrophages progenitor cells. It is a pleiotropic cytokine and a member of a family of endogenous cytokines of the hematopoietic system. GM-CSF is produced as a response to immune or inflammatory stimuli by activated cells of the hematopoietic system such as T cells, B cells, macrophages, mast cells and also fibroblasts and alveolar epithelial cells. It plays an important role in regulating the proliferation, differentiation, survival and activation of hematopoietic cells such as granulocytes and monocytes ,neutrophiles, basophiles and eosonophoiles, erythroid cells, megakaryocytes and T cells.
Human and mouse GM-CSF have about 56% homology and are species specific. Human GM-CSF is not active on mouse cells and vice versa. It is active on canine and feline cells.
GMCSF is 144 amino acids, 22kDa glycoprotein. It is composed of four bundles alpha helices. Its receptor is heterodimers with a ligand-specific alpha subunit and a betac subunit that is shared with the interleukin IL-3 and IL-5 receptors. This unusual form of receptor assembly likely applies also to IL-3 and IL-5 receptors. Cross-linking the two receptor subunits is required for receptor activation and signaling .
GMCSF has been shown to be involved in maturation, mobilization and antigen presentation of myeloid dentritic cells (DCs) in-vivo or ex-vivo. This function promotes Th1 immune responses, cytotoxcity, anti-angiogenesis as well as allergic inflammation, and the development of autoimmunity. Therefore GMCSF can be used in immunotherapy for the treatment of immune suppressed and immune-compromised patients as well as in veterinary medicine for the same purpose. GM-CSF is also important in regulation of embryo development and pregnancy and specifically in embryo implantation and subsequent development .

Galectin-3 mediates with the alpha-3, beta-1 integrin the stimulation by cspg4 of endothelial cells migration. Galectin-3 plays an necessary part during the acquisition of vasculogenic mimicry and angiogenic properties associated with melanoma progression. LGALS3 overexpression is highly expressed in early stages of papillary carcinoma, and its expression intensity declines during tumor progression. Serum levels of LGALS3 are high in patients with thyroid malignancy but there is considerable overlap in serum LGALS3 concentrations between those with benign and malignant nodular thyroid disease. LGLAS3 takes part as an immune regulator to inhibit T-cell immune responses and promote tumor growth, as a result providing a new mechanism for tumor immune tolerance.

Reticulon 4 Receptor, also known as RTN4R, plays a role as a receptor for RTN4, OMG and MAG. RTN4R is a glycosylphosphoinositol (GPI)-anchored protein which is a part from the Nogo recptor family. RTN4R is expressed mainly in neurons and their axons and is regulates axonal regeneration and plasticity in the adult central nervous system. RTN4R is a potential drug target for treating various neurological cases such as spinal cord injury, CNS lesions, stroke and Alzheimer's disease.