Datenblatt Neogen Elisa Screening

Description: Human IgG Subclass Screening Kit by Cygnus Technologies is available in Europe via Gentaur.

Description: A quantitative ELISA kit for measuring Human in samples from biological fluids.

Description: Screening Kit for detection of DPP4 Inhibitor in the research laboratory

Description: Receptor activator of nuclear factor kappa-B ligand (RANKL), also known as tumor necrosis factor ligand superfamily member 11 (TNFSF11), TNF-related activation-induced cytokine (TRANCE), osteoprotegerin ligand (OPGL), and osteoclast differentiation factor (ODF), is known as a type II membrane protein and is a member of the tumor necrosis factor (TNF) superfamily. RANKL, through its ability to stimulate osteoclast formation and activity, is a critical mediator of bone resorption and overall bone density. Some findings also suggestion some cancer cells, particularly prostate cancer cells, can activate an increase in bone remodeling and ultimately increase overall bone production. This increase in bone remodeling and bone production increases the overall growth of bone metastasizes. The overall control of bone remodeling is regulated by the binding of RANKL with its receptor or its decoy receptor, respectively, RANK and OPG.

Description: TNFRSF17 is a member of the TNF-receptor family, known as tumor necrosis factor receptor superfamily member 17, also known as B cell maturation antigen (BCMA or BCM) or CD269. It is a protein encoded by TNFRSF17 gene.  The receptor is expressed on the surface of B lymphocytes and plasma cells and is a marker protein of B lymphocyte maturation.The main ligands of BCMA are BAFF and APRIL. BCMA combined with BAFF could activate the classical and non-classical NF-κB and JNK signaling pathways, up-regulate the expression of anti-apoptotic protein and down-regulate the expression of pro-apoptotic protein. When BCMA binds to APRIL, the expression level of immune checkpoint is up-regulated, creating an immunosuppressed bone marrow microenvironment.

Description: BAFF receptor (B-cell activating factor receptor, BAFF-R), also known as tumor necrosis factor receptor superfamily member 13C (TNFRSF13C), is a membrane protein of the TNF receptor superfamily which recognizes BAFF. B-cell activating factor (BAFF) enhances B-cell survival in vitro and is a regulator of the peripheral B-cell population. Overexpression of BAFF in mice results in mature B-cell hyperplasia and symptoms of systemic lupus erythematosus (SLE). Also, some SLE patients have increased levels of BAFF in serum. Therefore, it has been proposed that abnormally high levels of BAFF may contribute to the pathogenesis of autoimmune diseases by enhancing the survival of autoreactive B cells.

Description: Cluster of Differentiation 70 (CD70) is also known as CD27 ligand (CD27L / CD27LG), TNFSF7, TNFSF7G, is a type II transmembrane glycoprotein belonging to the TNF superfamily (TNFSF) and is a surface antigen found on activated T-and B-lymphocytes and mature dendritic cells. Binding of CD70 to its receptor CD27 induces in priming, effector functions, differentiation and memory formation of T-cells, and thus is invloved in the biological processes including T-cell activation, the proliferation of costimulated T-cells, as well as the generation of cytolytic T-cells. CD70 on T cells provides costimulatory signals that are required for T cell proliferation, clonal expansion and the promotion of effector T cell formation. CD70 on mouse B cell has been shown to inhibit terminal differentiation of activated B cells into plasma cells and enhances commitment to memory B cell responses. CD70 induces proliferation and IFNγ production, on NK cells.

Description: BCMA (B cell maturation antigen), a member of the tumor necrosis factor receptor family. BCMA is mainly expressed on the surface of advanced B cells, short-lived proliferating plasmablasts and long-lived plasma cells, but not in naive B cells, CD34-positive hematopoietic stem cells and other normal tissue cells. With its specific expression ability, BCMA has become a good diagnostic marker and therapeutic target for multiple myeloma (MM).The main ligands of BCMA are BAFF and APRIL. When BCMA was combined with APRIL, the expression level of immune checkpoint was up-regulated to create an immunosuppressive bone marrow microenvironment. APRIL, as an important ligand of BCMA, is a member of the TNF(Tumor necrosis factor) receptor family (TNFSF-13A), which has 30% sequence homology with BAFF, another ligand of BCMA. But it has a higher affinity to interact with BCMA. It consists of 250 amino acids, of which 28 amino acids encode intracellular regions and 201 amino acids encode type II transmembrane proteins and their extracellular regions. The binding of APRIL to BCMA also induces both classical and non-classical NF-κB pathways, further promoting angiogenesis and metastasis, as well as tumor cell growth and proliferation.

Description: CD30 belongs to the tumor necrosis factor receptor (TNFR) superfamily, and the physiological functions of CD30 are in addition to the transmission of synergistic stimulation signals. CD30 ligand (CD30L) belongs to the tumor necrosis factor (TNF) superfamily, and CD30L is present in activated T cells, quiescent B cells, granulocytes, thymic medullary cells, and various leukemia cells. After crosslinking CD30 and CD30L, diverse physiological function signaling is led by TNFR correlation factors (TRAF), including TRAF1, 2, 3, 5. CD30 was originally found in Hodgkin's lymphoma and Reed Sternberg (RS) cells, and is now known to be expressed on the surface of some normal lymphocytes, virally infected lymphocytes, lymphocytes of lymphogenetic origin, and activated T cell subsets that produce Th2 cytokines.

Description: Tumor necrosis factor ligand superfamily member 14(LIGHT) is a tumor necrosis factor (TNF) superfamily ligand that regulates T cell immune responses by signaling through the herpes virus entry mediator (HVEM) and the lymphotoxin beta receptor (LTbetaR). LIGHT has emerged as a potent initiator of T cell co-stimulation signals effecting CTL-mediated tumor rejection, allograft rejection and graft versus host disease. Constitutive expression of LIGHT leads to tissue destruction and autoimmune-like disease syndromes.