|Other Names||Tumor necrosis factor receptor superfamily member 1A, Tumor necrosis factor receptor 1, TNF-R1, Tumor necrosis factor receptor type I, TNF-RI, TNFR-I, p55, p60, CD120a, Tumor necrosis factor receptor superfamily member 1A, membrane form, Tumor necrosis factor-binding protein 1, TBPI, TNFRSF1A, TNFAR, TNFR1|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||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.|
|Cellular Location||Cell membrane; Single-pass type I membrane protein Golgi apparatus membrane; Single- pass type I membrane protein Secreted. Note=A secreted form is produced through proteolytic processing|
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The protein encoded by this gene is a member of theTNF-receptor superfamily. This protein is one of the majorreceptors for the tumor necrosis factor-alpha. This receptor canactivate NF-kappaB, mediate apoptosis, and function as a regulatorof inflammation. Antiapoptotic protein BCL2-associated athanogene 4(BAG4/SODD) and adaptor proteins TRADD and TRAF2 have been shown tointeract with this receptor, and thus play regulatory roles in thesignal transduction mediated by the receptor. Germline mutations ofthe extracellular domains of this receptor were found to beassociated with the autosomal dominant periodic fever syndrome. Theimpaired receptor clearance is thought to be a mechanism of thedisease.
Giroux, S., et al. Bone 47(5):975-981(2010)Romero, R., et al. Am. J. Obstet. Gynecol. 203 (4), 361 (2010) :Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)Wolanska, M., et al. Ginekol. Pol. 81(6):431-434(2010)Sainz, J., et al. Int J Immunopathol Pharmacol 23(2):423-436(2010)
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