The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
ab109144 blocks TNF-alpha-mediated biological effect with an inhibitory activity in a concentration range of 0.1 to 1µg/ml. Binds Human and Mouse TNF-alpha.
< 0.100 Eu/µg
After reconstitution, prepare aliquots and store at -20°C. Avoid freeze/thaw cycles. PBS containing at least 0.1% BSA should be used for further dilutions.
Concentration information loading...
Shipped at 4°C. Store at 4°C (up to 6 months). Store at -20°C.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
Reconstitute with 50µl sterile water to give a final concentration of 1mg/ml.
TNF R I
Tumor necrosis factor alpha receptor
Tumor necrosis factor binding protein 1
Tumor necrosis factor receptor 1
Tumor necrosis factor receptor superfamily member 1A
Tumor necrosis factor receptor type 1
Tumor necrosis factor receptor type I
Tumor necrosis factor-binding protein 1
Receptor for TNFSF2/TNF-alpha and homotrimeric TNFSF1/lymphotoxin-alpha. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. Contributes to the induction of non-cytocidal TNF effects including anti-viral state and activation of the acid sphingomyelinase.
Defects in TNFRSF1A are the cause of familial hibernian fever (FHF) [MIM:142680]; also known as tumor necrosis factor receptor-associated periodic syndrome (TRAPS). FHF is a hereditary periodic fever syndrome characterized by recurrent fever, abdominal pain, localized tender skin lesions and myalgia. Reactive amyloidosis is the main complication and occurs in 25% of cases.
Contains 1 death domain. Contains 4 TNFR-Cys repeats.
The domain that induces A-SMASE is probably identical to the death domain. The N-SMASE activation domain (NSD) is both necessary and sufficient for activation of N-SMASE. Both the cytoplasmic membrane-proximal region and the C-terminal region containing the death domain are involved in the interaction with TRPC4AP.
The soluble form is produced from the membrane form by proteolytic processing.