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< 1.0 EU per 1 microgram of protein (determined by LAL method)
Purity
> 90% by SDS - PAGE
Storage
Can be stored at +4centigrade short term (1-2 weeks). For long term storage, aliquot and store at -20Centigrade or -70Centigrade. Avoid repeated freezing and thawing cycles.
Concentration
0.5mg/ml (determined by Absorbance at 280nm)
Warning
For research use only!
Background
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.
References
Zola H., et al. (2007) J Immunol Methods. 318:1-5. Cottin V., et al. (2002) J Immunol. 168:4095-4102.
Tag
hIgG-His tag
Species
Human
Source
Insect cells
BACKGROUND
Background
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.
References
Zola H., et al. (2007) J Immunol Methods. 318:1-5. Cottin V., et al. (2002) J Immunol. 168:4095-4102.
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