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GT15064100 ug$365.00Buy Now | Add to Cart
 
Type: Goat IgG
 
Applications: IHC; WB; E
E=ELISA; FC=Flow Cytometry; ICC=Immunocytochemistry; IF=Immunofluorescence; IP=Immunoprecipitation; IHC=Immunohistochemistry; SE=Sandwich ELISA; WB=Western blotting; NB=Neutralization of Bioactivity; FACS; FPLC=Fast Protein Liquid Chromatography; GF=Gravity Flow; BSM=Biosactive Small Molecule or Peptide; HPLC=High Performance Liquid Chromatography; TPE=Targeted Protein Expression; AC=Adherent Cell Assays; NAC=Non-adherent Cell Assays; CDM=Cell Differentiation Media; BSC-CM5= Biacore Sensor Chip CM5; FM=Fluorescent Micsroscopy; ; ; ; ; ; ; ; ; ; ; Health and Fitness
Species Reactivity: R
B=Bovine; Ca=Cat; Ch=Chicken; D=Dog; EQ=Equine; GP=Guinea Pig; H=Human; M=Mouse; P=Porcine; Pr=Primate; R=Rat; Rb=Rabbit; Y=Yeast; Xe=Xenopus; Ze=Zebrafish; ; ; ; NA-Not Applicable; STP=Step-Tactin Proteins; All
Format: Affinity Purified - liquid
 
Immunogen: Recombinant rat tumor necrosis factor alpha
 
Description/Data:
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Image: TNF-alpha in cryostat tissue sections of rat spinal cord.

Tumor necrosis factor receptor 1 and 2 (TNF-R1 and TNF-R2), are 55 and 75 kDa members of a family cell surface molecules including nerve growth factor receptor, Fas/Apo-1, CD30, Ox40 and 4-1BB, which are characterized by cysteine rich motifs in the extracellular domain. While TNF-R1 and TNF-R2 share 28% sequence identity in their extracellular domains, their intracellular domains lack sequence homology which suggests that they differ in their internal signal transduction pathways. TNF-R1 initiates the majority of TNF.s activities, which includes triggering apoptosis of certain tumor cells, mediating the inflammatory response and regulating immune function (Chen). Each pathway is characterized by TNF-induced formation of a multi-protein signaling complex at the cell membrane. TNF and TNF-R1 binding initiates a series of intracellular events that result in activation of the transcription factors NF kappa B and c-Jun. TNF and TNF-R1 binding triggers release of the 80 residue inhibitory protein silencer of death domains (SODD) from the C-terminal intracellular domain of TNF-R1. This domain interacts with TNF receptor-associated death domain (TRADD) which in turn recruits receptor-interacting protein (RIP) TNF-R-associated factor 2 (TRAF2) and Fas-associated death domain (FADD). These three proteins recruit enzymes responsible for initiating signaling events. For example, interaction of SODD with TRADD, and subsequent interactions with FADD initiates Caspase-8 mediated apoptosis. TRAF2 links TNF-R1 with stress activated protein kinase (SAPK) and p38 mitogen activated protein kinases via germinal center kinase (GCK) and receptor interacting protein (RIP). The cytoplasmic domain of TNF-R1 can directly interact with Jak kinases.

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