1. Measured by its ability to bind mouse IL1B in a functional ELISA. Immobilized mouse IL1A at 10 μg/mL (100 μl/well) can bind mouse IL1R1, The EC50 of mouse IL1R1 is 0.13 μg/mL. 2. Measured by its ability to inhibit Interferon gamma secretion by human natural killer lymphoma NK-92 cells in the presence of 20 ng/mL rmIL1α. The EC50 for this effect is typically 20-80 ng/mL.

IL-1R1 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 38.7 kDa and the accession number is P13504.

Mouse

HEK293 Cells

interleukin 1 receptor, type I,IL-iR,Il1r-1,IL-1R1,CD121b,CD121a

A DNA sequence encoding the mouse IL1R1 (P13504) extracellular domain (Met 1-Lys 338) was expressed, with a C-terminal polyhistidine tag. Predicted N terminal: Leu 20

> 95 % as determined by SDS-PAGE

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

Interleukin 1 receptor, type I (IL-1R1) also known as CD121a (Cluster of Differentiation 121a), is an interleukin receptor. IL-1R1/CD121a is a cytokine receptor that belongs to the interleukin 1 receptor family. This protein is a receptor for interleukin alpha (IL1A), interleukin beta (IL1B), and interleukin 1 receptor, type I (IL1R1/IL1RA). IL-1R1/CD121a is an important mediator involved in many cytokines induced immune and inflammatory responses. This protein has been characterized by pharmacological and molecular techniques in the mouse brain. The spindle-shaped astrocytes enclose the wound, separating the healthy from damaged neural tissue. The shape change and subsequent repair processes are IL-1β activity-dependent, acting through the IL-1 type 1 receptor (IL-1R1), as co-application of the IL-1type 1 receptor antagonist protein (IL-1ra) blocks IL-1β induced effects. In the spleen, a slight increase in IL-1R ACP and IL-1R1 was observed during the first hours following LPS stimulation. In conclusion, IL-1R AcP mRNA is expressed in the brain and in other tissues where IL-1R1/CD121a transcripts are found. However, the regulation of its expression is distinct from IL-1R1/CD121a. The high level of expression and the lack of regulation of IL-1R AcP transcripts in the brain under inflammatory conditions suggest that the protein might be constitutively expressed in excess.