Description
Product Characteristics: The monoclonal antibody HM104 recognizes the extracellular part of the Tumor Necrosis Factor Receptor type I (TNF-RI) of the membrane-bound as well as the soluble receptor. TNF-RI (~55-60 kDa) is present on most cell types and is considered to play a prominent role in cell stimulation by TNF- alpha. TNF-alpha activates inflammatory responses, induces apoptosis, regulates cellular proliferation, and may even promote cancer progression. The effects of TNF-alpha are mediated by TNF-R1 and TNF-R2, which have both distinct and overlapping downstream signaling cascades. Induction of cytotoxicity and other functions are mediated largely via TNF-RI. TNF-R1 is equally well activated by both the 17 kDa soluble and 26 kDa membrane-bound form, whereas TNF-R2 is efficiently activated only by the membrane bound form of TNF-alpha. TNF-R1 signaling is initiated when trimeric TNF-alpha binds TNF-R1 receptors. Subsequent TNF-R1 trimerization promotes the recruitment of a proximal signaling complex composed of TNF Receptor Associated protein with a Death Domain (TRADD), Receptor Interacting Protein (RIP), cellular Inhibitor of Apoptosis Protein 1 (cIAP1), TNF Receptor Associated Factor 2 (TRAF2), and likely TRAF5. Studies with TNF-R1-deficient mice indicate that TNF-R1 mediates most of the proliferation, pro-inflammatory, and apoptosis-activating pathways. CD120a, Tumor necrosis factor receptor superfamily member 1A, p55/p60, TNFR-1 Aliases Rat IgG2a
Target Information: The protein encoded by this gene is a member of the TNF-receptor superfamily. This protein is one of the major receptors for the tumor necrosis factor-alpha. This receptor can activate NF-kappaB, mediate apoptosis, and function as a regulator of inflammation. Antiapoptotic protein BCL2-associated athanogene 4 (BAG4/SODD) and adaptor proteins TRADD and TRAF2 have been shown to interact with this receptor, and thus play regulatory roles in the signal transduction mediated by the receptor. Germline mutations of the extracellular domains of this receptor were found to be associated with the autosomal dominant periodic fever syndrome. The impaired receptor clearance is thought to be a mechanism of the disease. [provided by RefSeq, Jul 2008]