CD120a (TNF Receptor I) Monoclonal Antibody (TBP-1), eBioscience™, Invitrogen™

Description

• Description: The monoclonal antibody TBP-1 recognizes Tumor Necrosis Factor Receptor type I (TNF-RI) TNF-receptors have been demonstrated on a wide variety of human somatic cells including fibroblasts, endothelial cells, adipocytes, liver membranes, granulocytes and several tumor cell lines
• Based on gel filtration experiments the receptor appears to be a complex of different proteins with a molecular weight of 350 kDa
• In a variety of cell lines two different types of TNF receptors with 75-80 and 55-60 kDa respectively have been identified
• The cDNAs encoding the two different TNF receptors have been cloned
• The exact mechanism of signal transduction after binding of TNF to the receptor is still unclear
• The extracellular fragment of the 60 kDa TNF receptor, with a molecular mass of about 30 kDa was purified, partially sequenced, and the respective cDNA was cloned
• This TNF binding protein is liberated from the intact molecule by proteolytic cleavage and comprises most of the extracellular portion of the receptor, including all three N-glycosylation sites
• Applications Tested: ELISA
• TNFR1 (Tumor necrosis factor receptor 1) belongs to the tumor necrosis factor superfamily, and is one of the major TNF-alpha receptors
• TNFR1 plays an important role in mediating, in cytokine mediated signaling, positive regulation of the NF-Kb pathway, positive regulation of angiogenesis, and negative regulation of gene expression
• The extracellular domain of TNFR1 is also released into the circulatory system as soluble TNFR1 (sTNFR1)
• In humans, the TNFR1 gene is located on chromosome 12
• Anti-apoptotic protein BCL2-associated athanogene 4 (BAG4/SODD) and adaptor proteins TRADD and TRAF2 have been shown to interact with TNFR1, and thus play regulatory roles in the signal transduction mediated by the receptor
• Germline mutations of the extracellular domains of TNFR1 were found to be associated with the autosomal dominant periodic fever syndrome, and the impaired receptor clearance is thought to be a mechanism of the disease.